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Psychopharmacology (from Greek ψῡχή, psȳkhē, 'breath, life, soul'; φάρμακον, pharmakon, 'drug'; and -λογία, -logia) is the scientific study of the effects drugs have on mood, sensation, thinking, behavior, judgment and evaluation, and memory. It is distinguished from neuropsychopharmacology, which emphasizes the correlation between drug-induced changes in the functioning of cells in the nervous system and changes in consciousness and behavior.^[1]

The field of psychopharmacology studies a wide range of substances with various types of psychoactive properties, focusing primarily on the chemical interactions with the brain. The term "psychopharmacology" was likely first coined by David Macht in 1920. Psychoactive drugs interact with particular target sites or receptors found in the nervous system to induce widespread changes in physiological or psychological functions. The specific interaction between drugs and their receptors is referred to as "drug action", and the widespread changes in physiological or psychological function is referred to as "drug effect".^[2] These drugs may originate from natural sources such as plants and animals, or from artificial sources such as chemical synthesis in the laboratory.

Historical overview

Early psychopharmacology

Not often mentioned or included in the field of psychopharmacology today are psychoactive substances not identified as useful in modern mental health settings or references. These substances are naturally occurring, but nonetheless psychoactive, and are compounds identified through the work of ethnobotanists and ethnomycologists (and others who study the native use of naturally occurring psychoactive drugs). However, although these substances have been used throughout history by various cultures, and have a profound effect on mentality and brain function, they have not always attained the degree of scrutinous evaluation that lab-made compounds have. Nevertheless, some, such as psilocybin and mescaline, have provided a basis of study for the compounds that are used and examined in the field today. Hunter-gatherer societies tended to favor hallucinogens, and today their use can still be observed in many surviving tribal cultures. The exact drug used depends on what the particular ecosystem a given tribe lives in can support, and are typically found growing wild. Such drugs include various psychoactive mushrooms containing psilocybin or muscimol and cacti containing mescaline and other chemicals, along with myriad other plants containing psychoactive chemicals. These societies generally attach spiritual significance to such drug use, and often incorporate it into their religious practices. With the dawn of the Neolithic and the proliferation of agriculture, new psychoactives came into use as a natural by-product of farming. Among them were opium, cannabis, and alcohol derived from the fermentation of cereals and fruits. Most societies began developing herblores, lists of herbs which were good for treating various physical and mental ailments. For example, St. John's wort was traditionally prescribed in parts of Europe for depression (in addition to use as a general-purpose tea), and Chinese medicine developed elaborate lists of herbs and preparations. These and various other substances that have an effect on the brain are still used as remedies in many cultures.^[3]

Modern psychopharmacology

The dawn of contemporary psychopharmacology marked the beginning of the use of psychiatric drugs to treat psychological illnesses. It brought with it the use of opiates and barbiturates for the management of acute behavioral issues in patients. In the early stages, psychopharmacology was primarily used for sedation. With the 1950s came the establishment of lithium for mania, chlorpromazine for psychoses, and then in rapid succession, the development of tricyclic antidepressants, monoamine oxidase inhibitors, and benzodiazepines, among other antipsychotics and antidepressants. A defining feature of this era includes an evolution of research methods, with the establishment of placebo-controlled, double-blind studies, and the development of methods for analyzing blood levels with respect to clinical outcome and increased sophistication in clinical trials. The early 1960s revealed a revolutionary model by Julius Axelrod describing nerve signals and synaptic transmission, which was followed by a drastic increase of biochemical brain research into the effects of psychotropic agents on brain chemistry.^[4] After the 1960s, the field of psychiatry shifted to incorporate the indications for and efficacy of pharmacological treatments, and began to focus on the use and toxicities of these medications.^[5]^[6] The 1970s and 1980s were further marked by a better understanding of the synaptic aspects of the action mechanisms of drugs. However, the model has its critics, too – notably Joanna Moncrieff and the Critical Psychiatry Network.^{[citation needed]}

Chemical signaling

Neurotransmitters

Psychoactive drugs exert their sensory and behavioral effects almost entirely by acting on neurotransmitters and by modifying one or more aspects of synaptic transmission. Neurotransmitters can be viewed as chemicals through which neurons primarily communicate; psychoactive drugs affect the mind by altering this communication. Drugs may act by 1) serving as a precursor to a neurotransmitter; 2) inhibiting neurotransmitter synthesis; 3) preventing storage of neurotransmitters in the presynaptic vesicle; 4) stimulating or inhibiting neurotransmitter release; 5) stimulating or blocking post-synaptic receptors; 6) stimulating autoreceptors, inhibiting neurotransmitter release; 7) blocking autoreceptors, increasing neurotransmitter release; 8) inhibiting neurotransmission breakdown; or 9) blocking neurotransmitter reuptake by the presynaptic neuron.^[1]

Hormones

The other central method through which drugs act is by affecting communications between cells through hormones. Neurotransmitters can usually only travel a microscopic distance before reaching their target at the other side of the synaptic cleft, while hormones can travel long distances before reaching target cells anywhere in the body. Thus, the endocrine system is a critical focus of psychopharmacology because 1) drugs can alter the secretion of many hormones; 2) hormones may alter the behavioral responses to drugs; 3) hormones themselves sometimes have psychoactive properties; and 4) the secretion of some hormones, especially those dependent on the pituitary gland, is controlled by neurotransmitter systems in the brain.^[1]

Psychopharmacological substances

Alcohol

Alcohol is a depressant, the effects of which may vary according to dosage amount, frequency, and chronicity. As a member of the sedative-hypnotic class, at the lowest doses, the individual feels relaxed and less anxious. In quiet settings, the user may feel drowsy, but in settings with increased sensory stimulation, individuals may feel uninhibited and more confident. High doses of alcohol rapidly consumed may produce amnesia for the events that occur during intoxication. Other effects include reduced coordination, which leads to slurred speech, impaired fine-motor skills, and delayed reaction time. The effects of alcohol on the body's neurochemistry are more difficult to examine than some other drugs. This is because the chemical nature of the substance makes it easy to penetrate into the brain, and it also influences the phospholipid bilayer of neurons. This allows alcohol to have a widespread impact on many normal cell functions and modifies the actions of several neurotransmitter systems. Alcohol inhibits glutamate (a major excitatory neurotransmitter in the nervous system) neurotransmission by reducing the effectiveness at the NMDA receptor, which is related to memory loss associated with intoxication. It also modulates the function of GABA, a major inhibitory amino acid neurotransmitter. Abuse of alcohol has also been correlated with thiamine deficiencies within the brain, leading to lasting neurological conditions that affect primarily the ability of the brain to effectively store memories.^[7] One such neurological condition is called Korsakoff's syndrome, for which very few effective treatment modalities have been found.^[7]^[8] The reinforcing qualities of alcohol leading to repeated use – and thus also the mechanisms of withdrawal from chronic alcohol use – are partially due to the substance's action on the dopamine system. This is also due to alcohol's effect on the opioid systems, or endorphins, that have opiate-like effects, such as modulating pain, mood, feeding, reinforcement, and response to stress.^[1]

Antidepressants

Antidepressants reduce symptoms of mood disorders primarily through the regulation of norepinephrine and serotonin (particularly the 5-HT receptors). After chronic use, neurons adapt to the change in biochemistry, resulting in a change in pre- and postsynaptic receptor density and second messenger function.^[1] The Monoamine Theory of Depression and Anxiety, which states that the disruption of the activity of nitrogen containing neurotransmitters (i.e. serotonin, norepinephrine, and dopamine) is strongly correlated with the presence of depressive symptoms.^[9] Despite its longstanding prominence in pharmaceutical advertising, the myth that low serotonin levels cause depression is not supported by scientific evidence.^[10]^[11]^[12]

Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressants. They inhibit monoamine oxidase, the enzyme that metabolizes the monoamine neurotransmitters in the presynaptic terminals that are not contained in protective synaptic vesicles. The inhibition of the enzyme increases the amount of neurotransmitter available for release. It increases norepinephrine, dopamine, and 5-HT, thus increasing the action of the transmitters at their receptors. MAOIs have been somewhat disfavored because of their reputation for more serious side effects.^[1]

Tricyclic antidepressants (TCAs) work through binding to the presynaptic transporter proteins and blocking the reuptake of norepinephrine or 5-HT into the presynaptic terminal, prolonging the duration of transmitter action at the synapse.

Selective serotonin reuptake inhibitors (SSRIs) selectively block the reuptake of serotonin (5-HT) through their inhibiting effects on the sodium/potassium ATP-dependent serotonin transporter in presynaptic neurons. This increases the availability of 5-HT in the synaptic cleft.^[13] The main parameters to consider in choosing an antidepressant are side effects and safety. Most SSRIs are available generically and are relatively inexpensive. Older antidepressants such as TCAs and MAOIs usually require more visits and monitoring, which may offset the low expense of the drugs. SSRIs are relatively safe in overdoses and better tolerated than TCAs and MAOIs for most patients.^[13]

Antipsychotics

All proven antipsychotics are postsynaptic dopamine receptor blockers (dopamine antagonists). For an antipsychotic to be effective, it generally requires a dopamine antagonism of 60%–80% of dopamine D₂ receptors.^[13]

First generation (typical) antipsychotics: Traditional neuroleptics modify several neurotransmitter systems, but their clinical effectiveness is most likely due to their ability to antagonize dopamine transmission by competitively blocking the receptors or by inhibiting dopamine release. The most serious and troublesome side effects of these classical antipsychotics are movement disorders that resemble the symptoms of Parkinson's disease, because the neuroleptics antagonize dopamine receptors broadly, also reducing the normal dopamine-mediated inhibition of cholinergic cells in the striatum.^[1]

Second-generation (atypical) antipsychotics: The concept of "atypicality" is from the finding that second generation antipsychotics (SGAs) have a greater serotonin/dopamine ratio than earlier drugs, and might be associated with improved efficacy (particularly for the negative symptoms of psychosis) and reduced extrapyramidal side effects. Some of the efficacy of atypical antipsychotics may be due to 5-HT₂ antagonism or the blockade of other dopamine receptors. Agents that purely block 5-HT₂ or dopamine receptors other than D₂ have often failed as effective antipsychotics.^[13]

Benzodiazepines

Benzodiazepines are often used to reduce anxiety symptoms, muscle tension, seizure disorders, insomnia, symptoms of alcohol withdrawal, and panic attack symptoms. Their action is primarily on specific benzodiazepine sites on the GABA_A receptor. This receptor complex is thought to mediate the anxiolytic, sedative, and anticonvulsant actions of the benzodiazepines.^[13] Use of benzodiazepines carries the risk of tolerance (necessitating increased dosage), dependence, and abuse. Taking these drugs for a long period of time can lead to severe withdrawal symptoms upon abrupt discontinuation.^[14]

Hallucinogens

Classical serotonergic psychedelics

Psychedelics cause perceptual and cognitive distortions without delirium. The state of intoxication is often called a "trip". Onset is the first stage after an individual ingests (LSD, psilocybin, ayahuasca, and mescaline) or smokes (dimethyltryptamine) the substance. This stage may consist of visual effects, with an intensification of colors and the appearance of geometric patterns that can be seen with one's eyes closed. This is followed by a plateau phase, where the subjective sense of time begins to slow and the visual effects increase in intensity. The user may experience synesthesia, a crossing-over of sensations (for example, one may "see" sounds and "hear" colors). These outward sensory effects have been referred to as the "mystical experience", and current research suggests that this state could be beneficial to the treatment of some mental illnesses, such as depression and possibly addiction.^[15] In instances where some patients have seen a lack of improvement from the use of antidepressants, serotonergic hallucinogens have been observed to be rather effective in treatment.^[16] In addition to the sensory-perceptual effects, hallucinogenic substances may induce feelings of depersonalization, emotional shifts to a euphoric or anxious/fearful state, and a disruption of logical thought. Hallucinogens are classified chemically as either indolamines (specifically tryptamines), sharing a common structure with serotonin, or as phenethylamines, which share a common structure with norepinephrine. Both classes of these drugs are agonists at the 5-HT₂ receptors; this is thought to be the central component of their hallucinogenic properties. Activation of 5-HT_2A may be particularly important for hallucinogenic activity. However, repeated exposure to hallucinogens leads to rapid tolerance, likely through down-regulation of these receptors in specific target cells.^[1] Research suggests that hallucinogens affect many of these receptor sites around the brain and that through these interactions, hallucinogenic substances may be capable of inducing positive introspective experiences.^[16] The current research implies that many of the effects that can be observed occur in the occipital lobe and the frontomedial cortex; however, they also present many secondary global effects in the brain that have not yet been connected to the substance's biochemical mechanism of action.^[16]

Dissociative hallucinogens

Another class of hallucinogens, known as dissociatives, includes drugs such as ketamine, phencyclidine (PCP), and Salvia divinorum. Drugs such as these are thought to interact predominantly with glutamate receptors within the brain. Specifically, ketamine is thought to block NMDA receptors that are responsible for signalling in the glutamate pathways.^[17] Ketamine's more tranquilizing effects can be seen in the central nervous system through interactions with parts of the thalamus by inhibition of certain functions.^[17] Ketamine has become a major drug of research for the treatment of depression.^[18] These antidepressant effects are thought to be related to the drug's action on the glutamate receptor system and the relative spike in glutamate levels, as well as its interaction with mTOR, which is an enzymatic protein involved in catabolic processes in the human body.^[19]^[18] Phencyclidine's biochemical properties are still mostly unknown; however, its use has been associated with dissociation, hallucinations, and in some cases seizures and death.^[20] Salvia divinorum, a plant native to Mexico, has strong dissociative and hallucinogenic properties when the dry leaves are smoked or chewed.^[21] The qualitative value of these effects, whether negative or positive, has been observed to vary between individuals with many other factors to consider.^[21]

Hypnotics

Hypnotics are often used to treat the symptoms of insomnia or other sleep disorders. Benzodiazepines are still among the most widely prescribed sedative-hypnotics in the United States today. Certain non-benzodiazepine drugs are used as hypnotics as well. Although they lack the chemical structure of the benzodiazepines, their sedative effect is similarly through action on the GABA_A receptor. They also have a reputation of being less addictive than benzodiazepines. Melatonin, a naturally-occurring hormone, is often used over the counter (OTC) to treat insomnia and jet lag. This hormone appears to be excreted by the pineal gland early during the sleep cycle and may contribute to human circadian rhythms. Because OTC melatonin supplements are not subject to careful and consistent manufacturing, more specific melatonin agonists are sometimes preferred. They are used for their action on melatonin receptors in the suprachiasmatic nucleus, responsible for sleep-wake cycles. Many barbiturates have or had an FDA-approved indication for use as sedative-hypnotics, but have become less widely used because of their limited safety margin in overdose, their potential for dependence, and the degree of central nervous system depression they induce. The amino-acid L-tryptophan is also available OTC, and seems to be free of dependence or abuse liability. However, it is not as powerful as the traditional hypnotics. Because of the possible role of serotonin in sleep patterns, a new generation of 5-HT₂ antagonists are in current development as hypnotics.^[13]

Cannabis and the cannabinoids

Cannabis consumption produces a dose-dependent state of intoxication in humans. There is commonly increased blood flow to the skin, which leads to an increased heart rate and sensations of warmth or flushing. It also frequently induces increased hunger.^[1] Iversen (2000) categorized the subjective and behavioral effects often associated with cannabis into three stages. The first is the "buzz", a brief period of initial responding where the main effects are lightheadedness or slight dizziness, in addition to possible tingling sensations in the extremities or other parts of the body. The "high" is characterized by feelings of euphoria and exhilaration characterized by mild psychedelia as well as a sense of disinhibition. If the individual has taken a sufficiently large dose of cannabis, the level of intoxication progresses to the stage of being "stoned", and the user may feel calm, relaxed, and possibly in a dreamlike state. Sensory reactions may include the feeling of floating, enhanced visual and auditory perception, visual illusions, or the perception of the slowing of time passage, which are somewhat psychedelic in nature.^[22]

There exist two primary CNS cannabinoid receptors, on which marijuana and the cannabinoids act. Both the CB₁ and CB₂ receptor are found in the brain. The CB₂ receptor is also found in the immune system. CB₁ is expressed at high densities in the basal ganglia, cerebellum, hippocampus, and cerebral cortex. Receptor activation can inhibit cAMP formation, inhibit voltage-sensitive calcium ion channels, and activate potassium ion channels. Many CB₁ receptors are located on axon terminals, where they act to inhibit the release of various neurotransmitters. In combination, these chemical actions work to alter various functions of the central nervous system, including the motor system, memory, and various cognitive processes.^[1]

Opioids

The opioid category of drugs – including drugs such as heroin, morphine, and oxycodone – belong to the class of narcotic analgesics, which reduce pain without producing unconsciousness but do produce a sense of relaxation and sleep, and at high doses may result in coma and death. The ability of opioids (both endogenous and exogenous) to relieve pain depends on a complex set of neuronal pathways at the spinal cord level, as well as various locations above the spinal cord. Small endorphin neurons in the spinal cord act on receptors to decrease the conduction of pain signals from the spinal cord to higher brain centers. Descending neurons originating in the periaqueductal gray give rise to two pathways that further block pain signals in the spinal cord. The pathways begin in the locus coeruleus (noradrenaline) and the nucleus of raphe (serotonin). Similar to other abused substances, opioid drugs increase dopamine release in the nucleus accumbens.^[1] Opioids are more likely to produce physical dependence than any other class of psychoactive drugs, and can lead to painful withdrawal symptoms if discontinued abruptly after regular use.

Stimulants

Cocaine is one of the more common stimulants and is a complex drug that interacts with various neurotransmitter systems. It commonly causes heightened alertness, increased confidence, feelings of exhilaration, reduced fatigue, and a generalized sense of well-being. The effects of cocaine are similar to those of amphetamines, though cocaine tends to have a shorter duration of effect. In high doses or with prolonged use, cocaine can result in a number of negative effects, including irritability, anxiety, exhaustion, total insomnia, and even psychotic symptomatology. Most of the behavioral and physiological actions of cocaine can be explained by its ability to block the reuptake of the two catecholamines, dopamine and norepinephrine, as well as serotonin. Cocaine binds to transporters that normally clear these transmitters from the synaptic cleft, inhibiting their function. This leads to increased levels of neurotransmitter in the cleft and transmission at the synapses.^[1] Based on in-vitro studies using rat brain tissue, cocaine binds most strongly to the serotonin transporter, followed by the dopamine transporter, and then the norepinephrine transporter.^[23]

Amphetamines tend to cause the same behavioral and subjective effects of cocaine. Various forms of amphetamine are commonly used to treat the symptoms of attention deficit hyperactivity disorder (ADHD) and narcolepsy, or are used recreationally. Amphetamine and methamphetamine are indirect agonists of the catecholaminergic systems. They block catecholamine reuptake, in addition to releasing catecholamines from nerve terminals. There is evidence that dopamine receptors play a central role in the behavioral responses of animals to cocaine, amphetamines, and other psychostimulant drugs. One action causes the dopamine molecules to be released from inside the vesicles into the cytoplasm of the nerve terminal, which are then transported outside by the mesolimbic dopamine pathway to the nucleus accumbens. This plays a key role in the rewarding and reinforcing effects of cocaine and amphetamine in animals, and is the primary mechanism for amphetamine dependence.^{[citation needed]}

Psychopharmacological research

In psychopharmacology, researchers are interested in any substance that crosses the blood–brain barrier and thus has an effect on behavior, mood, or cognition. Drugs are researched for their physiochemical properties, physical side effects, and psychological side effects. Researchers in psychopharmacology study a variety of different psychoactive substances, including alcohol, cannabinoids, club drugs, psychedelics, opiates, nicotine, caffeine, psychomotor stimulants, inhalants, and anabolic–androgenic steroids. They also study drugs used in the treatment of affective and anxiety disorders, as well as schizophrenia.

Clinical studies are often very specific, typically beginning with animal testing and ending with human testing. In the human testing phase, there is often a group of subjects: one group is given a placebo, and the other is administered a carefully measured therapeutic dose of the drug in question. After all of the testing is completed, the drug is proposed to the concerned regulatory authority (e.g. the U.S. FDA), and is either commercially introduced to the public via prescription, or deemed safe enough for over-the-counter sale.

Though particular drugs are prescribed for specific symptoms or syndromes, they are usually not specific to the treatment of any single mental disorder.

A somewhat controversial application of psychopharmacology is "cosmetic psychiatry": persons who do not meet criteria for any psychiatric disorder are nevertheless prescribed psychotropic medication. The antidepressant bupropion is then prescribed to increase perceived energy levels and assertiveness while diminishing the need for sleep. The antihypertensive compound propranolol is sometimes chosen to eliminate the discomfort of day-to-day anxiety. Fluoxetine in nondepressed people can produce a feeling of generalized well-being. Pramipexole, a treatment for restless leg syndrome, can dramatically increase libido in women. These and other off-label lifestyle applications of medications are not uncommon. Although occasionally reported in the medical literature, no guidelines for such usage have been developed.^[24] There is also a potential for the misuse of prescription psychoactive drugs by elderly persons, who may have multiple drug prescriptions.^[25]^[26]

References

^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l Meyer JS, Quenzer LF (2005). Psychopharmacology: Drugs, The Brain, and Behavior (First ed.). Sunderland, MA: Sinauer Associates. ISBN 0-87893-534-7. LCCN 2004020935.
^ Hart CL (2017). Drugs, society & human behavior. McGraw Hill Education. ISBN 978-1-260-71105-9. OCLC 1201695043.
^ Goodman J, Sherratt A, Lovejoy PE, eds. (1995). Consuming Habits: Global and Historical Perspectives on How Cultures Define Drugs (First ed.). London: Routledge. doi:10.4324/9780203993163. ISBN 978-0-203-99316-3. LCCN 94042752.
^ Arana GW, Rames L (1995). "Chapter Three: Psychopharmacology". In Mogul KM, Dickstein LJ (eds.). Career Planning for Psychiatrists. Issues in Psychiatry. Washington, D.C.: American Psychiatric Press. pp. 25–34. ISBN 978-0-88048-197-7. LCCN 95001384.
^ Coryell W (July 1987). "Shifts in attitudes among psychiatric residents: serial measures over 10 years". The American Journal of Psychiatry. 144 (7): 913–917. doi:10.1176/ajp.144.7.913. PMID 3605403.
^ Garfinkel PE, Cameron P, Kingstone E (November 1979). "Psychopharmacology education in psychiatry". Canadian Journal of Psychiatry. 24 (7): 644–651. doi:10.1177/070674377902400708. PMID 519630. S2CID 208220503.
^ ^a ^b Fouarge E, Maquet P (May 2019). "[Neurological consequences of alcoholism]". Revue Médicale de Liège. 74 (5–6): 310–313. PMID 31206272.
^ Thomson AD, Marshall EJ (2006-03-01). "The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis". Alcohol and Alcoholism. 41 (2): 151–158. doi:10.1093/alcalc/agh249. PMID 16384871.
^ Wagner H (2014-02-25). The Psychobiology of Human Motivation. doi:10.4324/9781315812328. ISBN 9781317798200. S2CID 141555822.
^ Whitaker, R., Cosgrove, L. (23 April 2015). Psychiatry Under the Influence: Institutional Corruption, Social Injury, and Prescriptions for Reform. Palgrave Macmillan US. ISBN 9781137506924.
^ Moncrieff, J., Cooper, R. E., Stockmann, T., Amendola, S., Hengartner, M. P., Horowitz, M. A. (20 July 2022). "The serotonin theory of depression: a systematic umbrella review of the evidence". Molecular Psychiatry. Nature Publishing Group: 1–14. doi:10.1038/s41380-022-01661-0. ISSN 1359-4184. PMC 10618090. PMID 35854107. S2CID 250646781. Retrieved 2 May 2023.
^ Ghaemi, N., M., P. H. (2022), Has the Serotonin Hypothesis Been Debunked?, retrieved 2 May 2023
^ ^a ^b ^c ^d ^e ^f Schatzberg AF, Cole JO, DeBattista C (2010). Manual of Clinical Psychopharmacology (Seventh ed.). Washington, D.C.: American Psychiatric Publishing. ISBN 978-1-58562-377-8. LCCN 2010006867.
^ Schacter DL, Gilbert DT, Wegner DM (2010). Psychology. New York: Worth Publishers. ISBN 978-1-4292-3719-2. LCCN 2010940234.
^ Pollan M (2019). How to Change Your Mind: What the New Science of Psychedelics Teaches Us About Consciousness, Dying, Addiction, Depression, and Transcendence. Penguin Books. ISBN 9780735224155.
^ ^a ^b ^c Dos Santos RG, Osório FL, Crippa JA, Hallak JE (December 2016). "Classical hallucinogens and neuroimaging: A systematic review of human studies: Hallucinogens and neuroimaging". Neuroscience and Biobehavioral Reviews. 71: 715–728. doi:10.1016/j.neubiorev.2016.10.026. PMID 27810345. S2CID 5261758.
^ ^a ^b Liu GL, Cui YF, Lu C, Zhao P (March 2020). "Ketamine a dissociative anesthetic: Neurobiology and biomolecular exploration in depression". Chemico-Biological Interactions. 319: 109006. doi:10.1016/j.cbi.2020.109006. PMID 32084352. S2CID 211245150.
^ ^a ^b De Maricourt P, Jay T, Goncalvès P, Lôo H, Gaillard R (February 2014). "[Ketamine's antidepressant effect: focus on ketamine mechanisms of action]". L'Encéphale (in French). 40 (1): 48–55. doi:10.1016/j.encep.2013.09.002. PMID 24434007.
^ Sabatini DM (November 2017). "Twenty-five years of mTOR: Uncovering the link from nutrients to growth". Proceedings of the National Academy of Sciences of the United States of America. 114 (45): 11818–11825. Bibcode:2017PNAS..11411818S. doi:10.1073/pnas.1716173114. PMC 5692607. PMID 29078414.
^ "UNODC - Bulletin on Narcotics - 1974 Issue 4 - 002". United Nations : Office on Drugs and Crime. Retrieved 2022-04-16.
^ ^a ^b Dalgarno P (June 2007). "Subjective effects of Salvia divinorum". Journal of Psychoactive Drugs. 39 (2): 143–149. doi:10.1080/02791072.2007.10399872. PMID 17703708. S2CID 40477640.
^ Iversen LL (2000). The Science of Marijuana. New York: Oxford University Press. ISBN 978-0-19-513123-9. LCCN 99032747.
^ Ritz MC, Cone EJ, Kuhar MJ (1990). "Cocaine inhibition of ligand binding at dopamine, norepinephrine and serotonin transporters: a structure-activity study". Life Sciences. 46 (9): 635–645. doi:10.1016/0024-3205(90)90132-B. PMID 2308472.
^ Giannini AJ (June 2004). "The Case for Cosmetic Psychiatry: Treatment Without Diagnosis". Psychiatric Times. Vol. 21, no. 7. pp. 1–2. Archived from the original on January 17, 2019.
^ Blow FC, Oslin DW, Barry KL (Spring 2002). "Misuse of abuse of alcohol, illicit drugs, and psychoactive medication among older people". Generations. 26 (1): 50–54. ISSN 0738-7806.
^ Hilmer SN, McLachlan AJ, Le Couteur DG (June 2007). "Clinical pharmacology in the geriatric patient". Fundamental & Clinical Pharmacology. 21 (3): 217–230. doi:10.1111/j.1472-8206.2007.00473.x. PMID 17521291.

External links

Psychopharmacology: The Fourth Generation of Progress — American College of Neuropsychopharmacology (ACNP)
Bibliographical history of Psychopharmacology and Pharmacopsychology — Advances in the History of Psychology, York University
Monograph Psychopharmacology Today
British Association for Psychopharmacology (BAP)
Psychopharmacology Institute: Video lectures and tutorials on psychotropic medications.

[Psychopharm-1] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l Meyer JS, Quenzer LF (2005). Psychopharmacology: Drugs, The Brain, and Behavior (First ed.). Sunderland, MA: Sinauer Associates. ISBN 0-87893-534-7. LCCN 2004020935.

[2] Hart CL (2017). Drugs, society & human behavior. McGraw Hill Education. ISBN 978-1-260-71105-9. OCLC 1201695043.

[3] Goodman J, Sherratt A, Lovejoy PE, eds. (1995). Consuming Habits: Global and Historical Perspectives on How Cultures Define Drugs (First ed.). London: Routledge. doi:10.4324/9780203993163. ISBN 978-0-203-99316-3. LCCN 94042752.

[4] Arana GW, Rames L (1995). "Chapter Three: Psychopharmacology". In Mogul KM, Dickstein LJ (eds.). Career Planning for Psychiatrists. Issues in Psychiatry. Washington, D.C.: American Psychiatric Press. pp. 25–34. ISBN 978-0-88048-197-7. LCCN 95001384.

[5] Coryell W (July 1987). "Shifts in attitudes among psychiatric residents: serial measures over 10 years". The American Journal of Psychiatry. 144 (7): 913–917. doi:10.1176/ajp.144.7.913. PMID 3605403.

[6] Garfinkel PE, Cameron P, Kingstone E (November 1979). "Psychopharmacology education in psychiatry". Canadian Journal of Psychiatry. 24 (7): 644–651. doi:10.1177/070674377902400708. PMID 519630. S2CID 208220503.

[:02-7] Fouarge E, Maquet P (May 2019). "[Neurological consequences of alcoholism]". Revue Médicale de Liège. 74 (5–6): 310–313. PMID 31206272.

[8] Thomson AD, Marshall EJ (2006-03-01). "The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis". Alcohol and Alcoholism. 41 (2): 151–158. doi:10.1093/alcalc/agh249. PMID 16384871.

[9] Wagner H (2014-02-25). The Psychobiology of Human Motivation. doi:10.4324/9781315812328. ISBN 9781317798200. S2CID 141555822.

[10] Whitaker, R., Cosgrove, L. (23 April 2015). Psychiatry Under the Influence: Institutional Corruption, Social Injury, and Prescriptions for Reform. Palgrave Macmillan US. ISBN 9781137506924.

[11] Moncrieff, J., Cooper, R. E., Stockmann, T., Amendola, S., Hengartner, M. P., Horowitz, M. A. (20 July 2022). "The serotonin theory of depression: a systematic umbrella review of the evidence". Molecular Psychiatry. Nature Publishing Group: 1–14. doi:10.1038/s41380-022-01661-0. ISSN 1359-4184. PMC 10618090. PMID 35854107. S2CID 250646781. Retrieved 2 May 2023.

[12] Ghaemi, N., M., P. H. (2022), Has the Serotonin Hypothesis Been Debunked?, retrieved 2 May 2023

[Clinical-13] ^ ^a ^b ^c ^d ^e ^f Schatzberg AF, Cole JO, DeBattista C (2010). Manual of Clinical Psychopharmacology (Seventh ed.). Washington, D.C.: American Psychiatric Publishing. ISBN 978-1-58562-377-8. LCCN 2010006867.

[14] Schacter DL, Gilbert DT, Wegner DM (2010). Psychology. New York: Worth Publishers. ISBN 978-1-4292-3719-2. LCCN 2010940234.

[15] Pollan M (2019). How to Change Your Mind: What the New Science of Psychedelics Teaches Us About Consciousness, Dying, Addiction, Depression, and Transcendence. Penguin Books. ISBN 9780735224155.

[:12-16] Dos Santos RG, Osório FL, Crippa JA, Hallak JE (December 2016). "Classical hallucinogens and neuroimaging: A systematic review of human studies: Hallucinogens and neuroimaging". Neuroscience and Biobehavioral Reviews. 71: 715–728. doi:10.1016/j.neubiorev.2016.10.026. PMID 27810345. S2CID 5261758.

[:0-17] Liu GL, Cui YF, Lu C, Zhao P (March 2020). "Ketamine a dissociative anesthetic: Neurobiology and biomolecular exploration in depression". Chemico-Biological Interactions. 319: 109006. doi:10.1016/j.cbi.2020.109006. PMID 32084352. S2CID 211245150.

[:1-18] De Maricourt P, Jay T, Goncalvès P, Lôo H, Gaillard R (February 2014). "[Ketamine's antidepressant effect: focus on ketamine mechanisms of action]". L'Encéphale (in French). 40 (1): 48–55. doi:10.1016/j.encep.2013.09.002. PMID 24434007.

[19] Sabatini DM (November 2017). "Twenty-five years of mTOR: Uncovering the link from nutrients to growth". Proceedings of the National Academy of Sciences of the United States of America. 114 (45): 11818–11825. Bibcode:2017PNAS..11411818S. doi:10.1073/pnas.1716173114. PMC 5692607. PMID 29078414.

[20] "UNODC - Bulletin on Narcotics - 1974 Issue 4 - 002". United Nations : Office on Drugs and Crime. Retrieved 2022-04-16.

[:2-21] Dalgarno P (June 2007). "Subjective effects of Salvia divinorum". Journal of Psychoactive Drugs. 39 (2): 143–149. doi:10.1080/02791072.2007.10399872. PMID 17703708. S2CID 40477640.

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[24] Giannini AJ (June 2004). "The Case for Cosmetic Psychiatry: Treatment Without Diagnosis". Psychiatric Times. Vol. 21, no. 7. pp. 1–2. Archived from the original on January 17, 2019.

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+{{Short description|Study of the effects of psychoactive drugs}}
-'''Psychopharmacology''' is the study of the effects of any psychoactive [[drug]] that acts upon the [[mind]] by affecting [[brain]] chemistry. [[Fly agaric]] can be regarded as the first such drug, being known from at least 10000 BCE.
+{{for multi|the journal|Psychopharmacology (journal){{!}}''Psychopharmacology'' (journal)|the album|Psychopharmacology (album){{!}}''Psychopharmacology'' (album)}}
+[[Image:Psychoactive Drugs.jpg|right|thumb|Various [[psychoactive]] drugs]]
+'''Psychopharmacology''' (from [[Ancient Greek|Greek]] {{langx|grc|[[wiktionary:ψῡχή|ψῡχή]]|psȳkhē|breath, life, soul|label=none}}; {{langx|grc|[[wiktionary:φάρμακον|φάρμακον]]|pharmakon|drug|label=none}}; and {{langx|grc|[[wiktionary:-λογία|-λογία]]|[[-logia]]|label=none}}) is the scientific study of the effects [[drug]]s have on [[Mood (psychology)|mood]], [[Sensation (psychology)|sensation]], [[Cognition|thinking]], [[behavior]], [[Value judgment|judgment]] and [[evaluation]], and [[memory]]. It is distinguished from [[neuropsychopharmacology]], which emphasizes the correlation between drug-induced changes in the functioning of [[Cell (biology)|cells]] in the [[nervous system]] and changes in [[consciousness]] and behavior.<ref name="Psychopharm">{{cite book|title=Psychopharmacology: Drugs, The Brain, and Behavior| vauthors = Meyer JS, Quenzer LF |publisher=Sinauer Associates|year=2005|isbn=0-87893-534-7|edition=First|location=Sunderland, MA|lccn=2004020935|author-link1=John S. Meyer}}</ref>
-Generally [[hallucinogenic drugs]] were used in hunter-gatherer societies, which can still be observed today. With the dawn of the [[Neolithic]], drugs which require a longer time for production followed, mainly [[narcotic]] drugs such as [[alcohol]] and [[opium]], but also [[cannabis]].
+The field of psychopharmacology studies a wide range of substances with various types of [[psychoactive]] properties, focusing primarily on the chemical interactions with the brain. The term "psychopharmacology" was likely first coined by [[David Macht]] in 1920. Psychoactive drugs interact with particular target sites or receptors found in the [[nervous system]] to induce widespread changes in physiological or psychological functions. The specific interaction between drugs and their receptors is referred to as "[[drug action]]", and the widespread changes in physiological or psychological function is referred to as "[[Pharmacodynamics|drug effect]]".<ref>{{Cite book| vauthors = Hart CL |url=http://worldcat.org/oclc/1201695043|title=Drugs, society & human behavior|publisher=McGraw Hill Education|year=2017|isbn=978-1-260-71105-9|oclc=1201695043}}</ref> These drugs may originate from natural sources such as plants and animals, or from artificial sources such as [[chemical synthesis]] in the laboratory.
-However, the use of '''psychiatric drugs''' to restore mental health, or at least limit aberrant behaviour, has only been widespread since the 1950s when a number of new classes of drugs were discovered, notably [[tranquillizer]]s and [[antidepressant]]s.
+==Historical overview==
-Following their discovery some of these drugs gained  popularity amongst [[psychiatrist]]s and [[general practitioner]]s. Some once-popular drugs are now out of favor, and there are fashions in psychiatric drugs, as with any other kind of drug.
+===Early psychopharmacology===
+[[Image:Amanita muscaria 3 vliegenzwammen op rij.jpg|thumb|left|250px|The common [[muscimol]]-bearing mushroom ''[[Amanita muscaria]]'' (fly agaric)]]
+Not often mentioned or included in the field of psychopharmacology today are [[psychoactive]] substances not identified as useful in modern [[mental health]] settings or references. These substances are naturally occurring, but nonetheless psychoactive, and are compounds identified through the work of [[ethnobotanists]] and [[Ethnomycology|ethnomycologists]] (and others who study the native use of naturally occurring psychoactive drugs). However, although these substances have been used throughout history by various cultures, and have a profound effect on mentality and brain function, they have not always attained the degree of scrutinous evaluation that lab-made compounds have. Nevertheless, some, such as [[psilocybin]] and [[mescaline]], have provided a basis of study for the compounds that are used and examined in the field today. [[Hunter-gatherer]] societies tended to favor [[hallucinogen]]s, and today their use can still be observed in many surviving [[tribe|tribal]] cultures. The exact drug used depends on what the particular [[ecosystem]] a given tribe lives in can support, and are typically found growing wild. Such drugs include various [[psychoactive mushroom]]s containing psilocybin or [[muscimol]] and [[Psychoactive cactus|cacti]] containing mescaline and other chemicals, along with myriad other [[psychoactive plant|plants containing psychoactive chemicals]]. These societies generally attach spiritual significance to such drug use, and often incorporate it into their religious practices.
+With the dawn of the [[Neolithic]] and the proliferation of agriculture, new psychoactives came into use as a natural by-product of farming. Among them were [[opium]], [[cannabis (drug)|cannabis]], and [[ethanol|alcohol]] derived from the fermentation of cereals and fruits. Most societies began developing [[herblores]], lists of herbs which were good for treating various physical and mental ailments. For example, [[St. John's wort]] was traditionally prescribed in parts of Europe for depression (in addition to use as a general-purpose tea), and [[Chinese medicine]] developed elaborate lists of [[herbal remedies|herbs]] and preparations. These and various other substances that have an effect on the brain are still used as remedies in many cultures.<ref>{{Cite book|title=Consuming Habits: Global and Historical Perspectives on How Cultures Define Drugs|publisher=Routledge|year=1995|isbn=978-0-203-99316-3| veditors = Goodman J, Sherratt A, Lovejoy PE |editor-link2=Andrew Sherratt |edition=First |location=London |doi=10.4324/9780203993163|lccn=94042752 }}</ref>
+{{clear}}
+===Modern psychopharmacology===
-==Reduction of anxiety==
+The dawn of contemporary psychopharmacology marked the beginning of the use of psychiatric drugs to treat psychological illnesses. It brought with it the use of opiates and barbiturates for the management of acute behavioral issues in patients. In the early stages, psychopharmacology was primarily used for sedation. With the 1950s came the establishment of [[lithium (medication)|lithium]] for [[mania]], [[chlorpromazine]] for [[Psychosis|psychoses]], and then in rapid succession, the development of tricyclic antidepressants, monoamine oxidase inhibitors, and benzodiazepines, among other antipsychotics and antidepressants. A defining feature of this era includes an evolution of research methods, with the establishment of [[placebo-controlled]], [[blinded experiment|double-blind]] studies, and the development of methods for analyzing blood levels with respect to clinical outcome and increased sophistication in clinical trials. The early 1960s revealed a revolutionary model by [[Julius Axelrod]] describing nerve signals and [[synaptic transmission]], which was followed by a drastic increase of biochemical brain research into the effects of psychotropic agents on brain chemistry.<ref>{{Cite book|title=Career Planning for Psychiatrists| vauthors = Arana GW, Rames L |publisher=American Psychiatric Press|year=1995|isbn=978-0-88048-197-7| veditors = Mogul KM, Dickstein LJ |series=Issues in Psychiatry|location=Washington, D.C.|pages=25–34|chapter=Chapter Three: Psychopharmacology|lccn=95001384}}</ref> After the 1960s, the field of psychiatry shifted to incorporate the indications for and efficacy of pharmacological treatments, and began to focus on the use and toxicities of these medications.<ref>{{cite journal | vauthors = Coryell W | title = Shifts in attitudes among psychiatric residents: serial measures over 10 years | journal = The American Journal of Psychiatry | volume = 144 | issue = 7 | pages = 913–917 | date = July 1987 | pmid = 3605403 | doi = 10.1176/ajp.144.7.913 }}</ref><ref>{{cite journal | vauthors = Garfinkel PE, Cameron P, Kingstone E | title = Psychopharmacology education in psychiatry | journal = Canadian Journal of Psychiatry | volume = 24 | issue = 7 | pages = 644–651 | date = November 1979 | pmid = 519630 | doi = 10.1177/070674377902400708 | s2cid = 208220503 }}</ref> The 1970s and 1980s were further marked by a better understanding of the synaptic aspects of the action mechanisms of drugs. However, the model has its critics, too – notably [[Joanna Moncrieff]] and the [[Critical Psychiatry Network]].{{Citation needed|date=December 2019}}
+==Chemical signaling==
-[[Barbiturate]]s were used as [[hypnotic]]s and as [[anxiolytic]]s, but the development of the safer [[benzodiazepine]]s (Lowell Randall and Leo Sternbach, 1957) in the 1960s and 1970s led to billions of doses being consumed annually under tradenames like Mogadon, Valium (diazepam, 1963) or Librium (chlordiazepoxide). However, the problems of chronic use and dependence led to the use of other drugs, such as the [[azapirone]]s.
+===Neurotransmitters===
-==Antipsychotic drugs==
+Psychoactive drugs exert their sensory and behavioral effects almost entirely by acting on [[neurotransmitter]]s and by modifying one or more aspects of synaptic transmission. Neurotransmitters can be viewed as chemicals through which [[neuron]]s primarily communicate; psychoactive drugs affect the mind by altering this communication. Drugs may act by 1) serving as a [[precursor (chemistry)|precursor]] to a neurotransmitter; 2) inhibiting neurotransmitter synthesis; 3) preventing storage of neurotransmitters in the pre[[synaptic vesicle]]; 4) stimulating or inhibiting neurotransmitter release; 5) stimulating or blocking post-synaptic receptors; 6) stimulating [[autoreceptor]]s, inhibiting neurotransmitter release; 7) blocking autoreceptors, increasing neurotransmitter release; 8) inhibiting neurotransmission breakdown; or 9) blocking neurotransmitter [[reuptake]] by the presynaptic neuron.<ref name=Psychopharm />
+===Hormones===
-Outside of the more popular drugs there was success in the treatment of some of the symptoms of [[psychosis]] and [[Clinical depression|depression]]. The first [[antipsychotic]] compound, for the treatment of the symptoms of [[schizophrenia]], was [[chlorpromazine]] (known by tradenames like Largactil (Chlorpromazine hydrochloride) or Thorazine) in 1953. It went beyond simple sedation, with patients showing improvements in thinking and emotional behaviour, and over 100 million patients were treated. From chlopromazine a number of other similar [[antidopaminergic]] compounds were developed, such as the [[phenothiazine]]s. Such drugs had a revolutionary role in transforming mental institutions from an almost purely custodial role. But the limited knowledge of brain chemistry means that even more modern compounds cause a range of [[extrapyramidal side-effect]]s and while effective at controlling acute symptoms are of less value in treating chronic symptoms.  Enthusiasm for the first generation of anti-psychotic medications peaked in the late 1960s, but the image of the drugs plummeted in the mid-1970s, as studies emerged showing high rates of [[tardive dyskinesia]] (a typically permanent [[neurological disorder]] involving involuntary movements) in chronic users.
+The other central method through which drugs act is by affecting communications between cells through [[hormone]]s. Neurotransmitters can usually only travel a microscopic distance before reaching their target at the other side of the [[synaptic cleft]], while hormones can travel long distances before reaching target cells anywhere in the body. Thus, the [[endocrine system]] is a critical focus of psychopharmacology because 1) drugs can alter the secretion of many hormones; 2) hormones may alter the behavioral responses to drugs; 3) hormones themselves sometimes have psychoactive properties; and 4) the secretion of some hormones, especially those dependent on the [[pituitary gland]], is controlled by neurotransmitter systems in the brain.<ref name=Psychopharm />
+==Psychopharmacological substances==
+{{main|Psychiatric medication|Psychoactive drug}}
-==LSD==
+===Alcohol===
+[[Alcohol (drug)|Alcohol]] is a [[depressant]], the effects of which may vary according to dosage amount, frequency, and chronicity. As a member of the sedative-hypnotic class, at the lowest doses, the individual feels relaxed and less anxious. In quiet settings, the user may feel drowsy, but in settings with increased sensory stimulation, individuals may feel uninhibited and more confident. High doses of alcohol rapidly consumed may produce [[amnesia]] for the events that occur during intoxication. Other effects include reduced coordination, which leads to slurred speech, impaired fine-motor skills, and delayed reaction time. The effects of alcohol on the body's neurochemistry are more difficult to examine than some other drugs. This is because the chemical nature of the substance makes it easy to penetrate into the brain, and it also influences the [[phospholipid bilayer]] of neurons. This allows alcohol to have a widespread impact on many normal cell functions and modifies the actions of several neurotransmitter systems. Alcohol inhibits [[glutamate]] (a major excitatory neurotransmitter in the nervous system) neurotransmission by reducing the effectiveness at the [[NMDA]] receptor, which is related to memory loss associated with intoxication. It also modulates the function of [[GABA]], a major inhibitory amino acid neurotransmitter. Abuse of alcohol has also been correlated with thiamine deficiencies within the brain, leading to lasting neurological conditions that affect primarily the ability of the brain to effectively store memories.<ref name=":02">{{cite journal | vauthors = Fouarge E, Maquet P | title = [Neurological consequences of alcoholism] | journal = Revue Médicale de Liège | volume = 74 | issue = 5–6 | pages = 310–313 | date = May 2019 | pmid = 31206272 | url = https://pubmed.ncbi.nlm.nih.gov/31206272 }}</ref> One such neurological condition is called [[Korsakoff's syndrome]], for which very few effective treatment modalities have been found.<ref name=":02" /><ref>{{cite journal | vauthors = Thomson AD, Marshall EJ | title = The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis | journal = Alcohol and Alcoholism | volume = 41 | issue = 2 | pages = 151–158 | date = 2006-03-01 | pmid = 16384871 | doi = 10.1093/alcalc/agh249 }}</ref> The reinforcing qualities of alcohol leading to repeated use – and thus also the mechanisms of withdrawal from chronic alcohol use – are partially due to the substance's action on the [[dopamine]] system. This is also due to alcohol's effect on the [[opioid]] systems, or [[endorphins]], that have opiate-like effects, such as modulating pain, mood, feeding, reinforcement, and response to stress.<ref name=Psychopharm />
-[[LSD]] was promoted in the [[1950s]] as a psychiatric cure-all, useful for treating schizophrenia, [[criminal]] behavior, sexual deviancy, [[alcoholism]], and a wide variety of other mental ailments. Drug manufacturer [[Sandoz Laboratories]] suggested in its literature that psychiatrists take LSD themselves, to gain a better subjective understanding of the schizophrenic experience. Many users have reported profound, life-transforming experiences as a result of taking LSD, while others have experienced intensely negative "bad trips", and a few have devolved into states of [[LSD psychosis]]. While scientific research into the effects and potential uses of LSD was common in the 1950s, it gradually declined as LSD became increasingly associated with spiritual experiences and [[hippie]]s in the [[1960s]].
+===Antidepressants===
-Several researchers, most prominently erstwhile [[Harvard]] professor Dr. [[Timothy Leary]], dissociated themselves from the mainstream mental health research establishment as its support for LSD research declined and transitioned to roles as spiritual gurus, advocating the use of LSD for personal spiritual growth. LSD was prohibited in the [[United States]] in [[1967]], and systematic research since that time has been uncommon.
+[[Antidepressant]]s reduce symptoms of mood disorders primarily through the regulation of [[norepinephrine]] and [[serotonin]] (particularly the [[5-HT receptor]]s). After chronic use, neurons adapt to the change in biochemistry, resulting in a change in pre- and postsynaptic receptor density and second messenger function.<ref name=Psychopharm /> The Monoamine Theory of Depression and Anxiety, which states that the disruption of the activity of nitrogen containing neurotransmitters (i.e. serotonin, norepinephrine, and dopamine) is strongly correlated with the presence of depressive symptoms.<ref>{{Cite book | vauthors = Wagner H |date=2014-02-25 |title=The Psychobiology of Human Motivation |url=http://dx.doi.org/10.4324/9781315812328 |doi=10.4324/9781315812328|isbn=9781317798200 |s2cid=141555822 }}</ref> Despite its longstanding prominence in pharmaceutical advertising, the myth that low serotonin levels cause depression is not supported by scientific evidence.<ref>{{cite book | vauthors=((Whitaker, R.)), ((Cosgrove, L.)) | date=23 April 2015 | title=Psychiatry Under the Influence: Institutional Corruption, Social Injury, and Prescriptions for Reform | publisher=Palgrave Macmillan US | url=https://play.google.com/store/books/details?id=QYwEogEACAAJ | isbn=9781137506924}}</ref><ref>{{cite journal | vauthors=((Moncrieff, J.)), ((Cooper, R. E.)), ((Stockmann, T.)), ((Amendola, S.)), ((Hengartner, M. P.)), ((Horowitz, M. A.)) | journal=Molecular Psychiatry | title=The serotonin theory of depression: a systematic umbrella review of the evidence | pages=1–14 | publisher=Nature Publishing Group | date=20 July 2022 | url=https://www.nature.com/articles/s41380-022-01661-0 | issn=1359-4184 | doi=10.1038/s41380-022-01661-0 | pmid=35854107 | s2cid=250646781 | access-date=2 May 2023| doi-access=free | pmc=10618090 }}</ref><ref>{{Citation | vauthors=((Ghaemi, N.)), ((M., P. H.)) | year=2022 | title=Has the Serotonin Hypothesis Been Debunked? | url=https://www.psychologytoday.com/us/blog/mood-swings/202210/has-the-serotonin-hypothesis-been-debunked | access-date=2 May 2023}}</ref>
+[[Monoamine oxidase inhibitor]]s (MAOIs) are the oldest class of antidepressants. They inhibit [[monoamine oxidase]], the enzyme that metabolizes the monoamine neurotransmitters in the presynaptic terminals that are not contained in protective synaptic vesicles. The inhibition of the enzyme increases the amount of neurotransmitter available for release. It increases norepinephrine, dopamine, and 5-HT, thus increasing the action of the transmitters at their receptors. MAOIs have been somewhat disfavored because of their reputation for more serious side effects.<ref name=Psychopharm />
-==MDMA==
-MDMA, commonly known as [[Ecstasy]], was popularized as an adjucant to talk therapy in the [[1960s]] and [[1970s]] by Dr. [[Alexander Shulgin]]. One primary effect of Ecstasy is diminution of inhibitions, rendering users extremely comfortable talking about themselves and others.
+[[Tricyclic antidepressant]]s (TCAs) work through binding to the presynaptic transporter proteins and blocking the reuptake of norepinephrine or 5-HT into the presynaptic terminal, prolonging the duration of transmitter action at the synapse.
-Potential theraputic uses of MDMA have been overshadowed by its popularity as a [[recreational drug]] and research indicating that even casual MDMA use results in the shearing of axons in the [[central nervous system]]. This deterioration in the CNS is primarily located within serotonergic pathways (the same pathways that account for the drug's psychological effects). Because of this damage, heavy users often report suffering from severe, long-term depression.
+[[Selective serotonin reuptake inhibitor]]s (SSRIs) selectively block the reuptake of serotonin (5-HT) through their inhibiting effects on the sodium/potassium [[Adenosine triphosphate|ATP]]-dependent serotonin transporter in presynaptic neurons. This increases the availability of 5-HT in the synaptic cleft.<ref name="Clinical">{{cite book|title=Manual of Clinical Psychopharmacology| vauthors = Schatzberg AF, Cole JO, DeBattista C |publisher=American Psychiatric Publishing|year=2010|isbn=978-1-58562-377-8|edition=Seventh|location=Washington, D.C.|lccn=2010006867}}</ref> The main parameters to consider in choosing an antidepressant are side effects and safety. Most SSRIs are available generically and are relatively inexpensive. Older antidepressants such as TCAs and MAOIs usually require more visits and monitoring, which may offset the low expense of the drugs. SSRIs are relatively safe in overdoses and better tolerated than TCAs and MAOIs for most patients.<ref name=Clinical />
-==Antidepressant drugs==
+===Antipsychotics===
-For [[Clinical depression|depression]] two major classes of drugs were developed in the late 1950s, one group based on iproniazid (an [[MAOI]] developed at Hoffman-LaRoche, 1956) the other on imipramine (a [[tricyclic antidepressant]] developed by R. Kuhn at Geigy Labs in 1958). Improvements were effected but the results were less marked than with anti-psychotic drugs. This category also includes [[tetracyclic antidepressant]]s or [[selective serotonin reuptake inhibitor|SSRI]]s such as  [[Fluoxetine|Prozac]] (discovered by D. T. Wong at Eli Lilly labs in 1974, [[FDA]] approved in 1987).
+All proven antipsychotics are postsynaptic dopamine receptor blockers (dopamine [[Receptor antagonist|antagonist]]s). For an antipsychotic to be effective, it generally requires a dopamine antagonism of 60%–80% of dopamine D<sub>2</sub> receptors.<ref name=Clinical />
+[[Typical antipsychotic|First generation (typical) antipsychotics]]: Traditional [[neuroleptics]] modify several neurotransmitter systems, but their clinical effectiveness is most likely due to their ability to antagonize dopamine transmission by competitively blocking the receptors or by inhibiting dopamine release. The most serious and troublesome side effects of these classical antipsychotics are movement disorders that resemble the symptoms of [[Parkinson's disease]], because the neuroleptics antagonize dopamine receptors broadly, also reducing the normal dopamine-mediated inhibition of [[cholinergic]] cells in the [[striatum]].<ref name=Psychopharm />
-==Mood stabilizers==
+[[Atypical antipsychotic|Second-generation (atypical) antipsychotics]]: The concept of "atypicality" is from the finding that second generation antipsychotics (SGAs) have a greater serotonin/dopamine ratio than earlier drugs, and might be associated with improved efficacy (particularly for the [[negative symptoms]] of psychosis) and reduced [[extrapyramidal symptoms|extrapyramidal side effects]]. Some of the efficacy of atypical antipsychotics may be due to 5-HT<sub>2</sub> antagonism or the blockade of other dopamine receptors. Agents that purely block 5-HT<sub>2</sub> or dopamine receptors other than D<sub>2</sub> have often failed as effective antipsychotics.<ref name=Clinical />
-In [[1949]], the Australian [[John Cade]] discovered that [[lithium salt]]s could control [[mania]], reducing the frequency and severity of manic episodes. It did not take long for others to discover that these drugs also reduced the frequency and severity of depressive episodes.
-Other [[mood stabilizer]]s include [[Valproic acid]], [[Carbamazepine]], lamotrigine, and topiramate.
+===Benzodiazepines===
-==Treatment of addiction==
+[[Benzodiazepine]]s are often used to reduce anxiety symptoms, muscle tension, seizure disorders, insomnia, symptoms of alcohol withdrawal, and panic attack symptoms. Their action is primarily on specific benzodiazepine sites on the GABA<sub>A</sub> receptor. This receptor complex is thought to mediate the [[anxiolytic]], sedative, and [[anticonvulsant]] actions of the benzodiazepines.<ref name=Clinical /> Use of benzodiazepines carries the risk of tolerance (necessitating increased dosage), dependence, and abuse. Taking these drugs for a long period of time can lead to [[Benzodiazepine withdrawal syndrome|severe withdrawal symptoms]] upon abrupt discontinuation.<ref>{{Cite book|title=Psychology| vauthors = Schacter DL, Gilbert DT, Wegner DM |publisher=Worth Publishers|year=2010|isbn=978-1-4292-3719-2|location=New York|lccn=2010940234|author-link=Daniel Schacter|author-link2=Daniel Gilbert (psychologist)|author-link3=Daniel Wegner|url-access=registration|url=https://archive.org/details/psychology0000scha}}</ref>
+===Hallucinogens===
-Research with the drug [[ibogaine]] to treat heroin addiction has shown much promise in eliminating physical withdrawal symptoms. The drug is obtained from an African plant and was used as early as the 1960s by Claudio Naranjo.
+==== Classical serotonergic psychedelics ====
+[[Psychedelics]] cause perceptual and cognitive distortions without delirium. The state of intoxication is often called a "trip". Onset is the first stage after an individual ingests ([[LSD]], [[psilocybin]], [[ayahuasca]], and [[mescaline]]) or smokes ([[dimethyltryptamine]]) the substance. This stage may consist of visual effects, with an intensification of colors and the appearance of geometric patterns that can be seen with one's eyes closed. This is followed by a plateau phase, where the subjective sense of time begins to slow and the visual effects increase in intensity. The user may experience [[synesthesia]], a crossing-over of sensations (for example, one may "see" sounds and "hear" colors). These outward sensory effects have been referred to as the "mystical experience", and current research suggests that this state could be beneficial to the treatment of some mental illnesses, such as depression and possibly addiction.<ref>{{Cite book | vauthors = Pollan M |title=How to Change Your Mind: What the New Science of Psychedelics Teaches Us About Consciousness, Dying, Addiction, Depression, and Transcendence |publisher=Penguin Books |year=2019 |isbn=9780735224155}}</ref> In instances where some patients have seen a lack of improvement from the use of antidepressants, serotonergic hallucinogens have been observed to be rather effective in treatment.<ref name=":12">{{cite journal | vauthors = Dos Santos RG, Osório FL, Crippa JA, Hallak JE | title = Classical hallucinogens and neuroimaging: A systematic review of human studies: Hallucinogens and neuroimaging | journal = Neuroscience and Biobehavioral Reviews | volume = 71 | pages = 715–728 | date = December 2016 | pmid = 27810345 | doi = 10.1016/j.neubiorev.2016.10.026 | s2cid = 5261758 }}</ref> In addition to the sensory-perceptual effects, hallucinogenic substances may induce feelings of depersonalization, emotional shifts to a euphoric or anxious/fearful state, and a disruption of logical thought. Hallucinogens are classified chemically as either [[indolamines]] (specifically [[tryptamines]]), sharing a common structure with serotonin, or as [[phenethylamines]], which share a common structure with norepinephrine. Both classes of these drugs are [[agonist]]s at the 5-HT<sub>2</sub> receptors; this is thought to be the central component of their hallucinogenic properties. Activation of 5-HT<sub>2A</sub> may be particularly important for hallucinogenic activity. However, repeated exposure to hallucinogens leads to rapid tolerance, likely through down-regulation of these receptors in specific target cells.<ref name=Psychopharm /> Research suggests that hallucinogens affect many of these receptor sites around the brain and that through these interactions, hallucinogenic substances may be capable of inducing positive introspective experiences.<ref name=":12"/> The current research implies that many of the effects that can be observed occur in the occipital lobe and the frontomedial cortex; however, they also present many secondary global effects in the brain that have not yet been connected to the substance's biochemical mechanism of action.<ref name=":12" />
+==== Dissociative hallucinogens ====
+Another class of hallucinogens, known as [[dissociative]]s, includes drugs such as [[ketamine]], [[phencyclidine]] (PCP), and ''[[Salvia divinorum]]''. Drugs such as these are thought to interact predominantly with glutamate receptors within the brain. Specifically, ketamine is thought to block NMDA receptors that are responsible for signalling in the glutamate pathways.<ref name=":0">{{cite journal | vauthors = Liu GL, Cui YF, Lu C, Zhao P | title = Ketamine a dissociative anesthetic: Neurobiology and biomolecular exploration in depression | journal = Chemico-Biological Interactions | volume = 319 | pages = 109006 | date = March 2020 | pmid = 32084352 | doi = 10.1016/j.cbi.2020.109006 | s2cid = 211245150 }}</ref> Ketamine's more tranquilizing effects can be seen in the central nervous system through interactions with parts of the thalamus by inhibition of certain functions.<ref name=":0" /> Ketamine has become a major drug of research for the treatment of depression.<ref name=":1">{{cite journal | vauthors = De Maricourt P, Jay T, Goncalvès P, Lôo H, Gaillard R | title = [Ketamine's antidepressant effect: focus on ketamine mechanisms of action] | language = French | journal = L'Encéphale | volume = 40 | issue = 1 | pages = 48–55 | date = February 2014 | pmid = 24434007 | doi = 10.1016/j.encep.2013.09.002 }}</ref> These antidepressant effects are thought to be related to the drug's action on the glutamate receptor system and the relative spike in glutamate levels, as well as its interaction with mTOR, which is an enzymatic protein involved in catabolic processes in the human body.<ref>{{cite journal | vauthors = Sabatini DM | title = Twenty-five years of mTOR: Uncovering the link from nutrients to growth | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 114 | issue = 45 | pages = 11818–11825 | date = November 2017 | pmid = 29078414 | pmc = 5692607 | doi = 10.1073/pnas.1716173114 | bibcode = 2017PNAS..11411818S | doi-access = free }}</ref><ref name=":1" /> Phencyclidine's biochemical properties are still mostly unknown; however, its use has been associated with dissociation, hallucinations, and in some cases seizures and death.<ref>{{Cite web |title=UNODC - Bulletin on Narcotics - 1974 Issue 4 - 002 |url=https://www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1974-01-01_4_page003.html |access-date=2022-04-16 |website=United Nations : Office on Drugs and Crime |language=en}}</ref> ''Salvia divinorum'', a plant native to Mexico, has strong dissociative and hallucinogenic properties when the dry leaves are smoked or chewed.<ref name=":2">{{cite journal | vauthors = Dalgarno P | title = Subjective effects of Salvia divinorum | journal = Journal of Psychoactive Drugs | volume = 39 | issue = 2 | pages = 143–149 | date = June 2007 | pmid = 17703708 | doi = 10.1080/02791072.2007.10399872 | s2cid = 40477640 }}</ref> The qualitative value of these effects, whether negative or positive, has been observed to vary between individuals with many other factors to consider.<ref name=":2" />
+===Hypnotics===
+[[Hypnotic]]s are often used to treat the symptoms of insomnia or other sleep disorders. Benzodiazepines are still among the most widely prescribed sedative-hypnotics in the United States today. Certain non-benzodiazepine drugs are used as hypnotics as well. Although they lack the chemical structure of the benzodiazepines, their sedative effect is similarly through action on the GABA<sub>A</sub> receptor. They also have a reputation of being less addictive than benzodiazepines. [[Melatonin]], a naturally-occurring hormone, is often used over the counter (OTC) to treat insomnia and jet lag. This hormone appears to be excreted by the pineal gland early during the sleep cycle and may contribute to human [[circadian rhythm]]s. Because OTC melatonin supplements are not subject to careful and consistent manufacturing, more specific melatonin agonists are sometimes preferred. They are used for their action on melatonin receptors in the [[suprachiasmatic nucleus]], responsible for sleep-wake cycles. Many barbiturates have or had an FDA-approved indication for use as sedative-hypnotics, but have become less widely used because of their limited safety margin in overdose, their potential for dependence, and the degree of [[central nervous system depression]] they induce. The amino-acid [[L-tryptophan]] is also available OTC, and seems to be free of dependence or abuse liability. However, it is not as powerful as the traditional hypnotics. Because of the possible role of serotonin in sleep patterns, a new generation of 5-HT<sub>2</sub> antagonists are in current development as hypnotics.<ref name=Clinical />
+===Cannabis and the cannabinoids===
+[[Cannabis (drug)|Cannabis]] consumption produces a dose-dependent state of intoxication in humans. There is commonly increased blood flow to the skin, which leads to an increased heart rate and sensations of warmth or flushing. It also frequently induces increased hunger.<ref name=Psychopharm /> Iversen (2000) categorized the subjective and behavioral effects often associated with cannabis into three stages. The first is the "buzz", a brief period of initial responding where the main effects are lightheadedness or slight dizziness, in addition to possible tingling sensations in the extremities or other parts of the body. The "high" is characterized by feelings of euphoria and exhilaration characterized by mild psychedelia as well as a sense of disinhibition. If the individual has taken a sufficiently large dose of cannabis, the level of intoxication progresses to the stage of being "stoned", and the user may feel calm, relaxed, and possibly in a dreamlike state. Sensory reactions may include the feeling of floating, enhanced visual and auditory perception, visual illusions, or the perception of the slowing of time passage, which are somewhat psychedelic in nature.<ref name="Cannabis">{{cite book|url=https://archive.org/details/scienceofmarijua00iver|title=The Science of Marijuana| vauthors = Iversen LL |publisher=Oxford University Press|year=2000|isbn=978-0-19-513123-9|location=New York|lccn=99032747|url-access=registration}}</ref>
+There exist two primary CNS cannabinoid receptors, on which marijuana and the cannabinoids act. Both the [[CB1 receptor|CB<sub>1</sub>]] and [[CB2 receptor|CB<sub>2</sub> receptor]] are found in the brain. The CB<sub>2</sub> receptor is also found in the immune system. CB<sub>1</sub> is expressed at high densities in the [[basal ganglia]], [[cerebellum]], [[hippocampus]], and [[cerebral cortex]]. Receptor activation can inhibit [[Cyclic adenosine monophosphate|cAMP]] formation, inhibit voltage-sensitive calcium ion channels, and activate potassium ion channels. Many CB<sub>1</sub> receptors are located on axon terminals, where they act to inhibit the release of various neurotransmitters. In combination, these chemical actions work to alter various functions of the central nervous system, including the motor system, memory, and various cognitive processes.<ref name=Psychopharm />
+===Opioids===
+The [[opioid]] category of drugs – including drugs such as [[heroin]], [[morphine]], and [[oxycodone]] – belong to the class of [[narcotic]] [[analgesic]]s, which reduce pain without producing unconsciousness but do produce a sense of relaxation and sleep, and at high doses may result in coma and death. The ability of opioids (both [[endogenous]] and [[exogenous]]) to relieve pain depends on a complex set of neuronal pathways at the spinal cord level, as well as various locations above the spinal cord. Small [[endorphin]] neurons in the spinal cord act on receptors to decrease the conduction of pain signals from the spinal cord to higher brain centers. Descending neurons originating in the [[periaqueductal gray]] give rise to two pathways that further block pain signals in the spinal cord. The pathways begin in the locus coeruleus (noradrenaline) and the nucleus of raphe (serotonin). Similar to other abused substances, opioid drugs increase dopamine release in the [[nucleus accumbens]].<ref name=Psychopharm /> Opioids are more likely to produce [[physical dependence]] than any other class of psychoactive drugs, and can lead to painful withdrawal symptoms if discontinued abruptly after regular use.
+===Stimulants===
+[[Cocaine]] is one of the more common stimulants and is a complex drug that interacts with various neurotransmitter systems. It commonly causes heightened alertness, increased confidence, feelings of exhilaration, reduced fatigue, and a generalized sense of well-being. The effects of cocaine are similar to those of amphetamines, though cocaine tends to have a shorter duration of effect. In high doses or with prolonged use, cocaine can result in a number of negative effects, including irritability, anxiety, exhaustion, total insomnia, and even psychotic symptomatology. Most of the behavioral and physiological actions of cocaine can be explained by its ability to block the reuptake of the two [[catecholamine]]s, dopamine and norepinephrine, as well as serotonin. Cocaine binds to transporters that normally clear these transmitters from the synaptic cleft, inhibiting their function. This leads to increased levels of neurotransmitter in the cleft and transmission at the synapses.<ref name=Psychopharm /> Based on in-vitro studies using rat brain tissue, cocaine binds most strongly to the serotonin transporter, followed by the dopamine transporter, and then the norepinephrine transporter.<ref name="Cocaine">{{cite journal | vauthors = Ritz MC, Cone EJ, Kuhar MJ | title = Cocaine inhibition of ligand binding at dopamine, norepinephrine and serotonin transporters: a structure-activity study | journal = Life Sciences | volume = 46 | issue = 9 | pages = 635–645 | year = 1990 | pmid = 2308472 | doi = 10.1016/0024-3205(90)90132-B | url = https://zenodo.org/record/1253964 | author-link3 = Michael J. Kuhar }}</ref>
+[[Amphetamines]] tend to cause the same behavioral and subjective effects of cocaine. Various forms of amphetamine are commonly used to treat the symptoms of [[attention deficit hyperactivity disorder]] (ADHD) and [[narcolepsy]], or are used recreationally. Amphetamine and [[methamphetamine]] are indirect agonists of the catecholaminergic systems. They block catecholamine reuptake, in addition to releasing catecholamines from nerve terminals. There is evidence that dopamine receptors play a central role in the behavioral responses of animals to cocaine, amphetamines, and other psychostimulant drugs. One action causes the dopamine molecules to be released from inside the vesicles into the cytoplasm of the nerve terminal, which are then transported outside by the [[mesolimbic]] dopamine pathway to the nucleus accumbens. This plays a key role in the rewarding and reinforcing effects of cocaine and amphetamine in animals, and is the primary mechanism for amphetamine dependence.{{Citation needed|date=December 2019}}
+==Psychopharmacological research==
+{{main|Psychoactive substances|Psychiatric medication}}
+In psychopharmacology, researchers are interested in any substance that crosses the [[blood–brain barrier]] and thus has an effect on behavior, mood, or cognition. Drugs are researched for their physiochemical properties, physical [[adverse effect|side effects]], and psychological side effects. Researchers in psychopharmacology study a variety of different psychoactive substances, including alcohol, cannabinoids, [[club drug]]s, psychedelics, opiates, [[nicotine]], [[caffeine]], [[psychomotor stimulants]], [[inhalant]]s, and [[anabolic–androgenic steroid]]s. They also study drugs used in the treatment of affective and anxiety disorders, as well as [[schizophrenia]].
+Clinical studies are often very specific, typically beginning with animal testing and ending with human testing. In the human testing phase, there is often a group of subjects: one group is given a placebo, and the other is administered a carefully measured [[therapeutic dose]] of the drug in question. After all of the testing is completed, the drug is proposed to the concerned regulatory authority (e.g. the U.S. [[FDA]]), and is either commercially introduced to the public via [[Medical prescription|prescription]], or deemed safe enough for [[Over-the-counter drug|over-the-counter]] sale.
+Though particular drugs are prescribed for specific symptoms or syndromes, they are usually not specific to the treatment of any single mental disorder.
+A somewhat controversial application of psychopharmacology is "cosmetic psychiatry": persons who do not meet criteria for any psychiatric disorder are nevertheless prescribed psychotropic medication. The antidepressant [[bupropion]] is then prescribed to increase perceived energy levels and assertiveness while diminishing the need for sleep. The antihypertensive compound [[propranolol]] is sometimes chosen to eliminate the discomfort of day-to-day anxiety. [[Fluoxetine]] in nondepressed people can produce a feeling of generalized well-being. [[Pramipexole]], a treatment for restless leg syndrome, can dramatically increase libido in women. These and other off-label lifestyle applications of medications are not uncommon. Although occasionally reported in the medical literature, no guidelines for such usage have been developed.<ref>{{Cite magazine| vauthors = Giannini AJ |date=June 2004|title=The Case for Cosmetic Psychiatry: Treatment Without Diagnosis|url=https://www.psychiatrictimes.com/dependent-personality-disorder/case-cosmetic-psychiatry-treatment-without-diagnosis|magazine=[[Psychiatric Times]]|volume=21|issue=7|pages=1–2|archive-url=https://web.archive.org/web/20190117051806/https://www.psychiatrictimes.com/dependent-personality-disorder/case-cosmetic-psychiatry-treatment-without-diagnosis|archive-date=January 17, 2019|url-status=live}}</ref> There is also a potential for the misuse of prescription psychoactive drugs by elderly persons, who may have multiple drug prescriptions.<ref>{{Cite journal| vauthors = Blow FC, Oslin DW, Barry KL |date=Spring 2002|title=Misuse of abuse of alcohol, illicit drugs, and psychoactive medication among older people|url=https://www.questia.com/library/journal/1P3-128577291/misuse-and-abuse-of-alcohol-illicit-drugs-and-psychoactive|journal=Generations|volume=26|issue=1|pages=50–54|issn=0738-7806}}</ref><ref>{{cite journal | vauthors = Hilmer SN, McLachlan AJ, Le Couteur DG | title = Clinical pharmacology in the geriatric patient | journal = Fundamental & Clinical Pharmacology | volume = 21 | issue = 3 | pages = 217–230 | date = June 2007 | pmid = 17521291 | doi = 10.1111/j.1472-8206.2007.00473.x | doi-access = free }}</ref>
+== See also ==
+{{Portal|Psychiatry}}
+*[[Pharmacology]]
+*[[Neuropharmacology]]
+*[[Neuropsychopharmacology]]
+*[[Psychiatry]]
+*[[History of pharmacy]]
+*[[Mental health]]
+*[[Recreational drug use]]
+*[[Nathan S. Kline]]
+*[[Prescriptive authority for psychologists movement]]
+== References ==
+{{reflist|30em}}
+== Further reading ==
+{{refbegin}}
+*{{Cite book|title=Psychopharmacology: From Theory to Practice|publisher=Oxford University Press|year=1977|isbn=0-19-502215-7| veditors = Barchas JD, Berger PA, Ciaranello RD, Elliott GR |editor-link1=Jack Barchas|location=New York|lccn=76057489}}, an introductory text with detailed examples of treatment protocols and problems.
+*{{Cite book|title=Psychopharmacology: A Generation of Progress|publisher=Raven Press|year=1978|isbn=0-89004-191-1| veditors = Lipton MA, DiMascio A, Killam KF |location=New York|lccn=77083697}}, a general historical analysis.
+*{{Cite book|title=The Psychopharmacology of Addiction|publisher=Oxford University Press|year=1988|isbn=0-19-261626-9| veditors = Lader M |lccn=87034979}}
+*{{Cite book|url=https://archive.org/details/HandbookOfClinicalPsychopharmacologyForTherapistsSeventhEditionONealJohnH.PrestonJohnD.Talaga|title=Handbook of Clinical Psychopharmacology for Therapists| vauthors = Preston JD, O'Neal JH, Talaga MC |publisher=New Harbinger Publications|year=2013|isbn=978-1626259256|edition=Seventh|location=Oakland, CA|lccn=2012034630}}
+{{refend}}
+===Peer-reviewed journals===
+* ''[[Experimental and Clinical Psychopharmacology]]'', [[American Psychological Association]]
+* ''[[Journal of Clinical Psychopharmacology]]'', Lippincott Williams & Wilkins
+* ''[[Journal of Psychopharmacology]]'', British Association for Psychopharmacology, SAGE Publications
+* ''[[Psychopharmacology (journal)|Psychopharmacology]]'', Springer Berlin/Heidelberg
+== External links ==
+{{Commons category}}
+*[https://web.archive.org/web/20170829074130/https://www.acnp.org/publications/psycho4generation.aspx ''Psychopharmacology: The Fourth Generation of Progress''] — [http://www.acnp.org American College of Neuropsychopharmacology] (ACNP)
+*[http://ahp.yorku.ca/?p=125 Bibliographical history of Psychopharmacology and Pharmacopsychology] — Advances in the History of Psychology, [[York University]]
+*[https://www.ncbi.nlm.nih.gov/pmc/issues/193894 Monograph ''Psychopharmacology Today'']
+*[http://www.bap.org.uk British Association for Psychopharmacology] (BAP)
+*[http://psychopharmacologyinstitute.com Psychopharmacology Institute]: Video lectures and tutorials on psychotropic medications.
+{{Psychology}}
+{{Psychiatry}}
+{{Neuroscience}}
+{{Pharmacology}}
+{{Authority control}}
+[[Category:Psychopharmacology| ]]
+[[Category:Neuropharmacology]]

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