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Chapter 7

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University of Toronto Scarborough
Zachariah Campbell

Chapter 7:The Influence on Drugs and Hormones on Behaviour • Psychopharmacology=study of how drugs affect the nervous system and behaviour. Principles of Psychopharmacology • Adrug is a chemical compound that is administered to bring about some desired change in the body. Usually drugs are used to diagnose, treat, or prevent illness, to relieve pain and suffering, or to improve an adverse physiological condition. -On the other hand, throughout human history, drugs have also been used as food substances, for recreation, and even as poisons. -Today, they are also used as research tools. • Psychoactive drugs—substances that act to alter mood, thought, or behavior and are used to manage neuropsychological illness. Many psychoactive drugs are also substances of abuse. -That is, people take them for nonmedical reasons or recreationally to the point that their functioning becomes impaired. Many psychoactive drugs promote craving and can produce addiction. -Some can also act as toxins, producing sickness, brain damage, or death. Routes of Drug Administration • To be effective, a psychoactive drug has to reach its target in the nervous system. • The way in which a drug enters and passes through the body to reach that target is called its route of administration. • Many drugs are taken orally—the most natural and generally the safest way to consume a substance. Drugs can also be inhaled, administered through rectal suppositories, absorbed from patches applied to the skin, or injected into the bloodstream, into a muscle, or even into the brain. • Taking a drug by mouth is convenient, but not all drugs can withstand the acidity of gastric secretions or are able to penetrate the digestive-tract walls. • Generally, there are fewer barriers between a drug and its target if the drug is inhaled rather than swallowed, and fewer still if it is injected into the blood. The fewest obstacles are encountered if a drug is injected directly into the brain. • To reach the bloodstream, an ingested drug must first be absorbed through the lining of the stomach or small intestine. If the drug is liquid, it is absorbed more readily than if it is a solid. Drugs taken in solid form are not absorbed unless they can be dissolved by the stomach’s gastric juices. • Absorption is also affected by other chemical properties of the drug. If a drug is a weak acid, such as alcohol, it is readily absorbed across the stomach lining. If it is a weak base, it cannot be absorbed until it passes through the stomach and into the intestine, by which time the digestive juices may have destroyed it. • The drug must next enter the bloodstream. This part of the journey presents a different set of barriers. Blood has a high water concentration, and so a drug must be hydrophilic to mix with it. Ahydrophobic substance will be blocked from entering the bloodstream.  If a drug does make its way into the circulatory system, it becomes diluted by the blood’s 6-liter volume. • To reach a neurological target, a drug must also travel from the blood into the extracellular fluid. This part of the journey requires that molecules of the drug be small enough to pass through the pores of capillaries, the tiny vessels that carry blood to the body’s cells. Even if the drug makes this passage, it encounters other obstacles. • The extracellular fluid’s volume of roughly 35 liters of water dilutes the drug even further, and, if it passes through cell membranes, the drug is at risk of being modified or destroyed by various metabolic processes taking place in the cells. Routes of Drug Removal • Soon after a drug is taken, the body begins to remove it. • Drugs are metabolized throughout the body, but particularly in the kidneys, liver, and bile. They are excreted in urine, feces, sweat, breast milk, and exhaled air. • Drugs manufactured for therapeutic purposes are usually designed to optimize their chances of reaching their targets and to prolong their survival in the body. • The body has trouble removing some substances, however, and these substances are potentially dangerous because, with repeated exposure, they can build up in the body and become poisonous. Many metals, such as mercury, are not easily eliminated from the body and, when they accumulate there, they can cause severe neurological problems. • In 1956 in Minamata, Japan, many people suffered physical and psychiatric effects from eating fish caught near a factory that released mercury into the sea. This case gave rise to improved rights for Japanese citizens affected by industrial • by-products and to a new term for mercury poisoning—Minamata disease. Because mercury can accumulate in the food chain, especially in fish, pregnant women are advised not to eat tuna, a fish that accumulates mercury by eating other fish. Mercury can produce neurological damage in the fetus as well as in young children. Revisiting the Blood–Brain Barrier • You know that many substances that can affect the body are prevented from entering the brain by the blood–brain barrier. The brain has a rich capillary network. -In fact, none of its neurons is farther than about 50 lm away from a capillary. • Many drugs cannot enter the brain through the blood– brain barrier, whereas other drugs can. • The single layer of endothelial cells that compose brain capillaries is surrounded by the end feet of astrocyte glial cells, covering about 80% of a capillary’s outer surface. • The glial end feet play only minor roles in the blood–brain barrier. The glial cells’main function is to provide a route for the exchange of food and waste between the capillaries and the brain’s extracellular fluid and from there to other cells. • But astrocytes may also play a role in maintaining the tight junctions between endothelial cells and in making capillaries dilate to increase blood flow to areas of the brain in which neurons are very active. Thus, substances that can pass through the endothelial cells’junctions in the body cannot do so in the brain. • Many substances—for instance, oxygen, glucose, and amino acids (the building blocks of proteins)—must routinely travel from the blood to brain cells, just as carbon dioxide and other waste products must routinely be excreted from brain cells into the blood. molecules of these substances cross the blood–brain barrier in two ways: 1. Small molecules such as oxygen and carbon dioxide, which are not ionized and so are fat soluble, can pass through the capillary wall. 2. Molecules of glucose, amino acids, and other nutrients can be carried across the capillary by active- transport systems, which are pumps, such as the sodium–potassium pump described in Chapter 4, that are specialized for the transport of a particular substance. • Afew brain regions lack tight junctions between the cells of capillary walls and so lack a blood–brain barrier. • The pituitary gland of the hypothalamus is a source of many hormones that are secreted into the blood, and their release is triggered in part by other hormones carried to the pituitary gland by the blood. The absence of a blood–brain barrier at the area postrema of the lower brainstem allows toxic substances in the blood to trigger a vomiting response. • The pineal gland also lacks a blood–brain barrier and is therefore open to the hormones that modulate the day–night cycles controlled by this structure. Drug Routes and Dosage • Drugs that can make the entire trip from the mouth to the brain have certain chemical properties. • The most effective consist of molecules that are small in size, weakly acidic, water or fat soluble, potent in small amounts, and not easily degraded. • Given the many obstacles that psychoactive drugs encounter on their journey from mouth to brain, it is clear why inhaling a drug or injecting it into the bloodstream has advantages: these routes of administration bypass the obstacle of the stomach. In fact, with each obstacle eliminated on the route to the brain, the dosage of a drug can be reduced by a factor of 10 and the drug will still have the same effects. For example, 1 milligram (1000 lg) of amphetamine, a psychomotor stimulant, produces a noticeable behavioral change when ingested orally. -If inhaled into the lungs or injected into the blood, thereby circumventing the stomach, 100 lg of the drug (1000 lg 10) produces the same results. - Similarly, if amphetamine is injected into the cerebrospinal fluid, thereby bypassing the stomach and the blood, 10 lg is enough to produce an identical outcome, as is 1 lg if dilution in the CSF also is skirted and the drug is injected directly onto target neurons. • Drugs that can be inhaled or injected intravenously are much cheaper to use because the doses required are a fraction of those needed for drugs taken by mouth. DrugActions in Synapses • Most psychoactive drugs work by influencing the chemical reactions at synapses. • Scientists and pharmaceutical companies continue to develop many forms of each drug in attempts to increase penetration to the brain, increase effectiveness, and reduce side effects. • As an understanding of synaptic activity in the brain advances, drugs that have a more selective action in their therapeutic effects can be designed. At the same time, this research helps explain the psychoactive effects of drugs and their potential benefits and harm. Thus, to understand the psychoactive effects of drugs, we must explore the ways in which they modify synaptic activity. Steps in Synaptic Transmission • Synthesis of the neurotransmitter (1) can take place in the cell body, axon, or terminal. The neurotransmitter may then be (2) stored in storage granules or in vesicles until it is (3) released from the terminal’s presynaptic membrane to (4) act on a receptor embedded in the postsynaptic membrane. Excess neurotransmitter in the synapse is either (5) deactivated or (6) taken back into the presynaptic terminal for (7) reuse. The synapse also has mechanisms for degrading excess neurotransmitter and removing unneeded by-products from the synapse. • Each component of neurotransmission entails one or more chemical reactions that drugs can potentially influence. • Drugs that increase the effectiveness of neurotransmission are called agonists, whereas those that decrease its effectiveness are called antagonists. Agonists and antagonists can work in a variety of ways, but their end results are always the same. -For example, all drugs that stimulate the release of the neurotransmitter dopamine or block the reuptake preventing acetylcholine from acting. -block dopamine’s inactivations are considered dopamine agonists b/c they increase the amount of dopamine available in the synapse. Conversely, all drugs that block the synthesis of dopamine or its release from the presynaptic membrane or that block dopamine receptors or speed up dopamine’s inactivation are considered dopamine antagonists b/c they decrease the biochemical effect of this transmitter in the synapse. Examples of DrugAction: An Acetylcholine Synapse • Black-widow spider venom: agonist b/c it promotes the release of acetylcholine.  In the insects on which the black widow preys, the excitation caused by excess acetylcholine is sufficient to causes paralysis and death. -Ablack widow spider bite does not contain enough toxins to similarly affect a human. • Botulinium toxin: poisonous agent produced by a bacterium that sometimes grows in improperly processed canned foods. act as an antagonist b/c it blocks the release of acetylcholine.  the effects of botulinium poisoning can last up from weeks to months -severe case: result in paralysis of movement and breathing, leading to death. -if injected into a muscle, it paralyzes that muscle, blocking unwanted muscular twitches or contractions in conditions such as cerebral palsy. sold under the trade name Botox for use in cosmetic surgery to reduce wrinkles by relaxing muscles, and , b/c it can also activate pain fibers, it is injected into muscles and joints to reduce pain. • Nicotine: acts as an agonist to stimulate cholinergic receptors.  the cholinergic receptor at the neuromuscular junction is called a nicotinic receptor b/c of this action in nicotine. • Curare: a poison extracted from the seeds of South American plant act as an antagonist in cholinergic receptors, blocking them and acts quickly and is cleared from the body in minutes. Large doses, however, arrest movement and breathing long enough to result in death. • Early European explorers encountered Indians along theAmazon River who killed small animals by using arrows coated with curare. The hunters themselves were not poisoned when eating the animals, because ingested curare cannot pass from the gut into the body. • Many curare-like drugs have been synthesized. Some are used to briefly paralyze large animals for identification tagging or examination. Skeletal muscles are more sensitive to curare-like drugs than respiratory muscles are; so an appropriate dose will paralyze an animal but still allow it to breathe. • The final drug action is that of physostigmine, which inhibits acetylcholinesterase, the enzyme that breaks downACh. It therefore acts as an agonist to increase the amount ofACh available in the synapse. It is obtained from a species ofAfrican bean, was used as a poison by tribes inAfrica. -Large doses can be toxic because they produce excessive excitation of the neuromuscular synapse and so disrupt movement and breathing. -Small doses of physostigmine, however, are used to treat a condition called myasthenia gravis (the name means “muscular weakness”) in which muscle receptors are less than normally responsive to acetylcholine. • Myasthenia gravis, once called “tired housewife’s syndrome” because of its symptoms of fatigue and its tendency to affect women, was formerly viewed as a psychological condition until an understanding of the ACh synapse provided the correct explanation and treatment. • The action of physostigmine is short-lived, lasting from only a few minutes to at most half an hour, but another class of compounds, called organophosphates, bind irreversibly to acetylcholinesterase and consequently are extremely toxic. Many insecticides are organophosphates, and they are also used in chemical warfare. • Some drugs that act onACh synapses at muscles—physostigmine and nicotine, for example—do cross the blood–brain barrier and act on ACh synapses in the brain. Curare, on the other hand, cannot cross the barrier and therefore has no psychoactive effects. Classification of Psychoactive Drugs • Devising a classification system for the many thousands of psychoactive drugs has proved difficult. Classification based on a drug’s chemical structure is not successful, because drugs with similar structures can have different effects, whereas drugs with different structures can have effects that are similar. Classification schemes based on receptors in the brain also are problematic, because a single drug can act on many different receptors. The same problem exists for classification systems based on the neurotransmitter affected by a drug, because a drug can act on more than one transmitter. Class I. Sedative-Hypnotics and Antianxiety Agents • The effects of sedative-hypnotics (“sedative,” to calm or moderate nervousness or excitement, and “hypnotic,” sleep inducing) and antianxiety agents depend on the dose. At low doses, they reduce anxiety; at medium doses, they have a tranquilizing effect; and, at successively higher doses, they anesthetize, induce coma, and kill. • The most common members of this diverse class of drugs are alcohol, barbiturates, and benzodiazepines. ■Alcohol is well known to most people as a beverage and an intoxicant. It is potentially devastating to fetuses because it harms brain development, producing a syndrome of retardation called fetal alcohol syndrome (FAS). ■Barbiturates are sometimes prescribed as a sleeping medication, but they are mainly used to induce anesthesia before surgery. ■Benzodiazepines, also known as minor tranquilizers or antianxiety agents, are used to treat stress.An example is the widely prescribed drug Valium. • Whereas both alcohol and barbiturates can produce sleep, anesthesia, and coma at doses only slightly higher than those that produce sedation, the dose of benzodiazepines that produces sleep and anesthesia is substantially higher than that needed to relieve anxiety. • All sedative-hypnotic drugs may act by influencing a receptor of the neurotransmitter gamma-aminobutyric acid, the GABA A receptor. Continuum of Behavioral Sedation Increasing doses of sedative-hypnotic and antianxiety reduce anxiety and very high doses result in death. • Remember that an influx of Cl _ions increases the concentration of negative charges inside the cell membrane, hyperpolarizing the membrane and thus making it less likely to propagate an action potential. GABA, therefore, produces its inhibitory effect by decreasing a neuron’s rate of firing. -GABAis the inhibitory workhorse of the nervous system with widely distributed receptors, thus allowing drugs that affect the receptor to have widespread effects. -The GABA A receptor possesses not only a binding site for GABAbut two other binding sites. -The binding site where alcohol and barbiturates work, the sedative-hypnotic site, increases the influx of chloride ions and so produces the same effect as that of GABA. Consequently, the higher the dose of these drugs, the greater their inhibitory effect on neurons. • The antianxiety site accepts benzodiazepines and enhances the binding of GABAto its receptors, which means that the availability of GABAdetermines the potency of an anti-anxiety drug. Because GABAis very quickly reabsorbed by the neurons that secrete it and by surrounding glial cells, GABAconcentrations are never excessive; as a result, people are generally unlikely to overdose on anti- anxiety drugs. • Because of their different actions on the GABA Areceptor, sedative-hypnotic and anti-anxiety drugs should not be taken together. Asedative-hypnotic act like GABAbut, unlike GABA, is not quickly absorbed by surrounding cells. -Instead, it remains on the site, allowing its effects to be enhanced by an anti-anxiety drug. • The cumulative action of the two drugs will therefore exceed the individual action of either one. Even small combined doses of anti-anxiety and sedative-hypnotic drugs can produce coma or death. • One group of sedative-hypnotics, called dissociative anesthetics, was developed as anesthetic agents but receive restricted use as such because they also produce altered states of consciousness and hallucinations. They include GHB (gamma-hydroxybutyric acid), flunitrazepam, and ketamine. They have gained notoriety as “date rape” drugs or, more properly, “drug-assisted sexual assault” drugs. They are soluble in alcohol, act quickly, and, like other sedative-hypnotics, impair memory for recent events. • Because a dissociative anesthetic drug can be placed in a drink, party goers are advised not to accept drinks from strangers, drink out of punch bowls, or leave drinks unattended. Class II:Anti-psychotic Drugs • Psychosis refers to various neuropsychological conditions, such as schizophrenia that are characterized by hallucinations (false sensory perceptions) or delusions (false certainty) • Drugs used to treat psychosis are the antipsychotic agents also known as major tranquilizers and neuroleptics. include the phenothiazines (ex. Chlorpromazine) and butyrophenones (ex. Haloperidol) • One effect that all have in common is an immediate reduction of motor activity , which helpsto alleviate the progressive agitation of some patients.  Unfortunately, one (-) side effect of their prolonged use can be to produce symptoms reminiscent of Parkinson’s disease and dyskinesia (involuntary movements), involving rhythmical movements of the mouth, hands, and other body parts that are reversible if the person was taking the drug. • D 2eceptor= one kind of dopamine site this action of antipsychotic drugs led to the dopamine hypothesis of schizophrenia -it holds the same form of schizophrenia may be related to excessive dopamine activity. -also comes from the schizophrenia-like symptoms of chronic signs of amphetamine(a type of stimulant drug) • Amphetamine is a dopamine agonist that fosters the release of dopamine from the presynaptic membrane of dopamine synapses and blocks its reuptake from the synaptic cleft.  If amphetamine causes schizophrenia-like symptoms by increasing dopamine activity, perhaps naturally occurring schizophrenia is related to excessive dopamine action, too. Class III:Antidepressants • Major depression: mood disorder characterized by prolonged feelings of worthlessness and guilt, disruption of normal eating habits, sleep disturbances, a general slowing of behaviour and frequent thought of suicide  occurs twice as frequently in women as men one of the most treatable psychological disorders • Most people recover from depression within a year of its onset; but if the condition is left untreated, the incidence of suicide is high. • 3 different types of drugs have antidepressant effects: monoamine oxidase inhibitors (MAO inhibitors), tricyclic depressants and second –generation antidepressants, sometimes called atypical antidepressants which include and fluoxetine (Prozac) and are similar to the tricyclics. • Monoamine oxidase is an enzyme that breaks down serotonin within an axon terminal  the inhibition of MAO by MAO inhibitors therefore provides more serotonin for release with each action potential • The tricyclic antidepressants block the transporter that takes serotoninback into the axon terminal • The second-generation antidepressants are thought to be especially selective in blocking serotonin reuptake, and consequently some are called Selective Serotonin Reuptake Inhibition (SSRIs)  b/c the transporter is blocked, serotonin remains in the synaptic cleft for a longer period, thus prolonging its action on postsynaptic receptors. • The drugs begin to affect the synapses very quickly and yet their antidepressant effects take weeks to develop.  In addition, 20% of patients with depression fail to respond to antidepressant drugs • There is also controversy over whether some or all tricyclic antidepressants increase the risk of suicide. • Brains of suicide victim features smaller orbital frontal cortex and amygdala. They suggest that these brain regions contribute to executive decisions, which, when impaired, could lead to impulsivity and suicide. • Antidepressant side effects include increased anxiety, sexual dysfunction, sedation, dry mouth, blurred vision, and memory impairments. Many people hoped that the second-generation antidepressants would produce fewer side effects than the tricyclic antidepressants, but that hope has not been realized. -In fact, most antidepressants do not appear to be particularly selective in their action on the brain. Even Prozac, one of the more selective antidepressant compounds, is advertised as a treatment not only for depression but also for obsessive–compulsive disorder, bulimia, and panic disorder. • The major symptoms of obsessive–compulsive disorder (OCD) are obsessive thoughts and compulsive behaviors—ideas that people cannot get out of their heads and ritual-like actions that they perform endlessly. Although OCD, like depression, is associated with guilt and anxiety, most experts consider it a separate disorder. Class IV. Mood Stabilizers • Bipolar disorder, once referred to as manic–depressive illness, is a disorder of mood in which a person might undergo periods of depression alternating with normal periods and periods of intense excitation. According to the National Institute of Mental Health, bipolar disorder can affect as much as 2.6% of the adult population. • Bipolar disorder is frequently treated with drugs called mood stabilizers, which include the salt lithium and a variety of other drugs including valproate, which is also used to treat epilepsy. The mechanism of action of mood stabilizers is not well understood, but lithium may increase the synaptic release of serotonin, and valproate may stimulate GABAactivity. Typically, mood stabilizers mute the intensity of one pole of the disorder, thus making the other pole less likely to reoccur. Class V. NarcoticAnalgesics The narcotic analgesic drugs have both sleep-inducing (narcotic) and pain-relieving (analgesic) properties. Many are derived from opium, an extract of the seeds of the opium poppy, Papaver somniferum. -Opium has been used for thousands of years to produce euphoria, analgesia, sleep, and relief from diarrhea and coughing. - Opium is obtained from the seeds of the opium poppy. • In 1805, German chemist Friedrich Serturner synthesized two pure substances from the poppy plant— codeine and morphine—that demonstrate narcotic properties. Codeine is included in cough medicine and in pain relievers such as aspirin, although not in the United States. Morphine, which was named after Morpheus, the Greek god of dreams, is a very powerful pain reliever. - extracted from opium -Despite decades of research, no other drug has been found that exceeds morphine’s effectiveness as an analgesic. • Heroin, another opiate drug, is synthesized from morphine. It is fatter soluble than is morphine and so penetrates the blood–brain barrier more quickly, thus producing very rapid relief from pain. -heroin is a powder synthesized from morphine. • Another is methadone, a drug widely used to treat addiction by acting as a substitute for heroin or other abused opiod drugs. • Endorphin-containing neurons exist in many brain regions, and morphine is similar enough to these endogenous substances to mimic their action in the brain.  Endorphins are peptides and can be ingested to relieve pain, but they do not easily cross the blood–brain barrier. • Opium antagonists such as nalorphine and naloxone block the action of morphine by blocking endorphin receptors and so are useful in quickly reversing opioid overdoses. • Consequently, morphine, which obviously does, remains a preferred pain treatment. Class VI. Psychomotor Stimulants Stimulants, a diverse class of drugs, increase the activity of neurons in several ways. They are divided into two groups: behavioral stimulants and general stimulants. Behavioral Stimulants • Behavioral stimulants such as cocaine and amphetamine increase motor behavior as well as elevating a person’s mood and level of alertness. • Cocaine is extracted from the Peruvian coca shrub. Indigenous Peruvians originally discovered it in coca leaves, which they chewed to increase their stamina in the harsh environment of the high elevations at which they live. -Purified cocaine can be taken either by sniffing (snorting) or by injection. Many cocaine users do not like to inject cocaine intravenously, and so they sniff a highly concentrated form of it called crack. -Crack is chemically altered so that it vaporizes at low temperatures, and the vapors are inhaled. • Amphetamine is a synthetic compound that was discovered in attempts to synthesize the neurotransmitter epinephrine. Amphetamine also stimulates the release of dopamine from presynaptic membranes. • Both amphetamine and cocaine are dopamine agonists that act by blocking dopamine transport back into the presynaptic terminal, leaving more dopamine available in the synaptic cleft. • Both mechanisms increase the amount of dopamine available in synapses to stimulate dopamine receptors. • Cocaine was popularized as an antidepressant by Viennese psychoanalyst Sigmund Freud. In an 1884 paper titled “Uber Coca,” Freud concluded: The main use of coca will undoubtedly remain that which the Indians have made of it for centuries: it is of value in all cases where the primary aim is to increase the physical capacity of the body for a given short period of time and to hold strength in reserve to meet further demands— especially when outward circumstances exclude the possibility of obtaining the rest and nourishment normally necessary for great exertion. Later, as Freud became aware of its addictive properties, he withdrew his endorsement of cocaine. There is also evidence that cocaine can produce circulatory disturbances, some of which can result in sudden death. Freud also recommended that cocaine be used as a local anesthetic and many of its derivatives, such as Novocaine, are used for this purpose. • Cocaine was once used in soft drinks and wine mixtures, which were promoted as invigorating tonics. It is responsible for the origin of the trade name Coca-Cola. • Amphetamine was first used as a treatment for asthma. Aform of amphetamine, Benzedrine, was sold in inhalers as a non-prescription drug through the 1940s. Soon people discovered that they could open the container and swallow its contents to obtain a sudden energizing effect. • In 1937, an article in the Journal of the American Medical Association reported that Benzedrine tablets improved performance on mental- efficiency tests. This information was quickly disseminated among students, who began to use “bennies” when studying for exams. • Amphetamine has been widely used since World War II to keep tired troops and pilots alert and to improve the productivity of wartime workers. It has also been used as a diet aid. In the 1960s, drug users discovered that they could obtain an immediate pleasurable “rush,” often described as a whole-body orgasm, by intravenous injection of amphetamine. -People who took amphetamine in this way, called “speed freaks,” would inject the drug every few hours for days, remaining in a wide-awake, excited state without eating. -They would then crash in exhaustion and hunger a
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