Psychopharmacology

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For the journal, see Psychopharmacology (journal). For the album, see Psychopharmacology (album).
psychoactive
drugs

Psychopharmacology (from

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

The common muscimol-bearing mushroom Amanita muscaria (fly agaric)

Not often mentioned or included in the field of psychopharmacology today are

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
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

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

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

Main articles: Psychiatric medication and Psychoactive drug

Alcohol

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]

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]

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 GABAA 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

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-HT2A 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

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

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

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]

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

Main articles:
Psychoactive substances and Psychiatric medication

In psychopharmacology, researchers are interested in any substance that crosses the

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

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]

See also

References

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Further reading

Peer-reviewed journals

External links

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