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PSY 245 Final Exam Study Guide (SHORT VERSION)

by: Kristi Dorsey

PSY 245 Final Exam Study Guide (SHORT VERSION) PSY 245

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Kristi Dorsey
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This version of my study guide includes only the questions in Unit III and the exam questions Galizio mentioned in class.
Drugs and Behavior
Mark Galizio
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PSY245, DrugsAndBehavior, MarkGalizio, uncw
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This 30 page Study Guide was uploaded by Kristi Dorsey on Thursday April 28, 2016. The Study Guide belongs to PSY 245 at University of North Carolina - Wilmington taught by Mark Galizio in Spring 2016. Since its upload, it has received 108 views. For similar materials see Drugs and Behavior in Psychlogy at University of North Carolina - Wilmington.


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Date Created: 04/28/16
Exam Study Q’s Mentioned in Class: Drug laws, neurotransmitters and drug action, basic principles of pharmacology (tolerance and dependence), synergy (there’s synergy among opiate drugs; methadone is synergistic with heroin; synergy within depressant drugs; valium is synergistic with alcohol; there’s synergy that crosses over between opiates and depressant drugs like alcohol)  1914 Harrison Act: Banned all of the naturally occurring opiates (except for medical use) and cocaine.  Looking into someone’s eyes to determine what drug they are on o Pupils normal but eyes are blood shot – cannabinoids o Pupils widely dilated – sympathomimetic drugs (ecstasy, LSD, psilocybin, cocaine, amphetamine, caffeine) o Pinpoint pupils – opiates  Rebound Effect: withdrawal symptoms of drugs show effects exactly opposite the effects of taking the drug  Alcohol and depressants can cause seizures which cause death  Cross-Dependence (and tolerance) between all opiate drugs (but not alcohol/depressants) o Tolerance to drugs never taken that results from protracted tolerance to another drug CHAPTER 10: OPIATES 1. What is opium? Comes from the papaver somniferum, one of the many species of the poppy plant; native to the Mediterranean Sea; now cultivated extensively throughout Asia and the Middle East; petals fall after the poppy blooms, leaving a round seedpod the size of an egg; If the seedpod is scored lightly with a knife, it secretes a milky white sap; after drying, this sap forms a thick, gummy, brown substance that is called opium; a person experiences the effects of opium by consuming the substance orally or by smoking it 2. Consider its early history. Sumerian and Assyrian civilizations cultivated and used opium 6,000 years; Egyptians had discovered medical uses for opiates 3,500 years ago; use of opium for medical and recreational purposes became widespread among the Islamic peoples of the Middle East [because the Koran’s explicit prohibition of the use of alcohol and other drugs; holds true today]; By the 9th century, Arab traders spread the use of opium to India and China, where the practice of smoking opium developed; dependence on opium was first recognized as a problem in China, which led to the Opium Wars between Britain and China [British ships continued to trade opium gown in India for Chinese tea; Great Britain won the conflict] 3. What is analgesia? Pain relief produced without a loss of consciousness. 4. What is the relation between opium, morphine, heroin and codeine? German pharmacists F.W. Serturner [1803] developed a process that separated morphine from opium; morphine is the major active chemical in opium and is 10 times more potent than crude opium; codeine is another opiate drug found in opium; German pharmacologist Heinrich Dreser [1898] rediscovered diacetylmorphine, an alteration of morphine [twice as potent as morphine; so powerful that he viewed it as a new treatment with “heroic” possibilities and it was named heroin]; immediately used as a cough suppressant and pain reliever 5. What was soldier's disease? Opiate addiction among soldiers on both sides during the Civil War in America 6. How did opiate drug use change from the 19th to the 20th century? After the legitimate channels for obtaining drugs were blocked for many addicts, they turned to a growing black market to maintain their addiction [as a result of the 1914 Harrison Narcotics Act]; when opiates became illegal, they began to be used mainly in large cities where organized crime provided a supply [heroin quickly emerged as the addict’s drug of choice]; addicts tended more and more to be young, poorly educated men of lower socioeconomic status 7. Where is opium grown today? Poppies grown in Southwest Asia [EX: Afghanistan has produced nearly 80% of the world’s opium]; the opium is processed to heroin and transported to Europe or Mexico before being smuggled into the United States; most of the heroin entering the United States today comes from poppies grown in Latin America [Mexico and Colombia] 8. How are opiate drugs administered? Most are readily absorbed from the gastrointestinal tract, although a given dose has a greater effect if it is injected intravenously; most opioids are also absorbed through the nasal mucosa and lungs [opium and pure forms of heroin are often smoked, and heroin is frequently taken intranasally]; also absorbed after intramuscular or subcutaneous administration. 9. How are they distributed? Opioids are distributed throughout the body and accumulate in the kidneys, lungs, liver, spleen, digestive tract, muscles, and the brain; with some opiates [such as morphine] only a small amount penetrates the blood-brain barrier; main difference between morphine and heroin is that heroin is more lipid-soluble so it more readily penetrates the blood- brain barrier; once in the brain, heroin is converted to morphine. 10. How are they metabolized? Most opiate drugs are rapidly metabolized in the liver and excreted by the kidneys; excretion of opiates is fairly rapid, with 90% excretion within a day after taking the drug; traces of morphine may remain in urine for two to four days after use 11. What are the major risks associated with heroin addiction? Addicts are at great risk for disease and death from AIDS, hepatitis, and other diseases spread by sharing contaminated needles; overdose deaths most commonly occur when heroin or another opiate drug is combined with alcohol or another depressant drug due to synergy, but another factor is that different concoctions of street heroin can vary enormously in potency. 12. What is the relationship between IV drug use and AIDS? Drug-related cases account for 25% of all AIDS cases; drug users are at risk for HIV infection because they are likely to engage in both risky sex and the common practice of sharing needles; using a needle contaminated with the blood of someone who has HIV leads to direct blood-to-blood transmission; “shooting galleries” [places where people gather to inject and enjoy the effects of the drug; a single needle may be used to deliver dozens of injections in such a place] 13. What is naloxone (Narcane)? Short-acting opiate antagonist that blocks or reverses the effects of opiate drugs [when given to a patient who is overdosing on heroin or morphine, it completely reverses the effects of those drugs] 14. What are endorphins? It is now believed that heroin, morphine, and other opiate drugs produce their effects by triggering activity in the brain’s endorphin systems; Candace Pert and Solomon Snyder [early 1970s] discovered “opiate receptors” that responded selectively to opiate drugs; Neurochemists found the “brain’s own opiates” in 1975; Although several morphine-like sub- stances (e.g., beta-endorphin, enkephain, and dynorphin) are found in the brain, these complex peptide molecules are referred to collectively as endorphins, a contraction of endogenous morphine. 15. Consider their normal role in the brain. One idea is that endorphins are part of a natural pain- relief system; it has been argued that endorphins are released and produce analgesia or pain relief after certain kinds of pain or stress; may explain why under certain circumstances [such as on the battlefield or in an athletic event], a person may sustain severe injury but not feel pain; pain relief produced by acupuncture may be related to endorphin release because naloxone can reverse acupuncture-induced analgesia 16. What opiate drugs are used medically, and for what are they employed? The major medical use of opiate drugs is for their analgesic or pain-relieving effects [relieve pain without causing unconsciousness]; primarily used for severe pain [very few patients who use the drugs as directed develop problems]; constipating effect that can treat diarrhea; still used to treat coughs [EX: dextromethorphan: synthetic opiate that has no analgesic or addictive properties but is a cough suppressant]; treatment of heroin addicts in withdrawal and in maintenance programs designed to help addicts stay off heroin [EX: Methadone] 17. Consider the issue of abuse of medical opiates such as Oxycontin. Prescription opiate drug use has more than tripled since the 1990s to present; there has been an increased number of drug treatment admissions and ER room admissions involving these drugs; rate of overdose deaths has been higher than rates associated with heroin and cocaine in recent years 18. OxyContin. Introduced by Purdue Pharma in the mid-1990s [designed to treat severe chronic pain, so it contained a higher dose of oxycodone; duration of action ~ 12 hours; illicit users discovered they could crush the tablet to produce a powder the could inject or snort; large doses in a single tablet are dangerous]; in September 2007, Purdue Pharma paid $20 million in civil penalties to 26 states and the District of Columbia, and $600 million in fines for misrepresenting the abuse liability of OxyContin; in 2010, OxyContin was reformulated to prevent injection (if crushed, it becomes gluey and cannot be dissolved); illicit use quickly shifted to another prescription opioid, called Opana (oxymorphone); By 2011, Opana abuse overtook OxyContin and it too was reformulated; former users of these prescription opiate drugs may be switching away from the reformulated compounds to injectable heroin 19. What is designer heroin? Produced illicitly by chemists who design or develop chemical analogues to heroin; these new compounds are untested but usually produce effects similar to those of heroin or other opiates; most are derivatives of the power opioid fentanyl [often sold on the street as “China White”; 10 to 1000 times more potent than heroin so risk of overdose is much greater] 20. MPTP? Underground chemist in San Francisco Bay produced a designer heroin called MPPP in the 1980s; due to poor lab technique, some portion of his product was a closely related but highly toxic compound called MPTP; the error was discovered when a number of young drug users were hospitalized with complete paralysis; William Langston tried to use L-dopa with these “frozen” addicts and the L-dopa was successful enough that the paralyzed patients were able to talk a little; eventually identified as heroin addicts who had tried MPTP; we now know that MPTP selectively attacks and rapidly destroys the substantia nigra, which leads to symptoms of advanced Parkinson’s disease 21. Psychological effects of opiate drugs. Euphoria [drowsiness, body warmth, and a heavy feeling of the limbs]; interfere with cognitive functions; some research suggests cognitive impairment; 22. Physiological effects of opiate drugs. Reduce sexual drive of interest and often produce impotence in men; like depressant drugs, opiates cause respiratory depression and lowered body temperature; nausea and vomiting often occur immediately after taking opiates; constriction of the pupils [“pinpoint pupils” are a sign of opiate poisoning]; when a high dose of heroin is fatal, the immediate cause is usually respiratory failure; typically a lethal drug interaction or synergy between heroin and alcohol or another depressant] 23. Tolerance. Tolerance develops to opiates, so their effects are generally diminished unless users escalate the dose, which often occurs; Experiment: volunteer with a history of extensive drug abuse was studied under lab conditions in which he could regulate his daily intravenous morphine dose; his dose gradually increased over time from 500mg to > 1000 mg within four months; there is a similar pattern of heroin self-administration by monkeys that could obtain heroin by pressing a lever 24. Withdrawal. The withdrawal symptoms associated with opiate dependence may appear after only one to two weeks of chronic use of heroin, morphine, or a synthetic opiate drug. The symptoms become more severe with longer-term use of higher doses. Early indications of withdrawal begin 8 to 12 hours after the last dose 25. How does the motivation to use opiates change with chronic use? Although repeated use is initially motivated by a desire to re-experience the pleasant rush associated with taking the drug, addicts report that continued use of a drug does not make them nearly as high as before. They continue to use the drug to avoid the unpleasant symptoms of abstinence; the processes that maintain heroin use change from positive to negative reinforcement 26. Opiate abstinence syndrome? Flu-like symptoms such as runny nose, tearing, sweating, irritability, and tremor; as time passes, these symptoms become more severe and others appear, including pupil dilation, anorexia, and piloerection (goose bumps); these symptoms continue to worsen and reach a peak after 48 to 72 hours; at this time, heart rate and blood pressure are elevated, and addicts experience severe flu-like symptoms such as nausea, diarrhea, sneezing, excessive sweating, and pain in the bones; addicts may show spastic movements of the arms and legs that may appear similar to kicking; other symptoms, which indicate a rebound of an addict’s sexual system, include spontaneous erection and ejaculation in men and orgasm in women; the loss of fluids and failure of addicts to eat or drink much during withdrawal can leave them physically and emotionally drained and occasionally can be fatal 27. How do partial opiate agonists like buprenorphine (Suboxone) differ from full agonist like morphine? Full opiate agonists bind to endorphin/opiate receptors and produce strong physiological activity; partial agonists also bind to these same receptors, but produce lower levels of activity; partial agonists are often still capable of producing analgesia, but generally with lower abuse liability; these partial agonists are providing safer ways of relieving pain and new directions in the treatment of addiction 28. How are these being used medically? Buprenorphine is a popular alternative to methadone treatment for opiate addiction [it can relieve withdrawal symptoms and cravings in opiate addicts]; Suboxone is a combination of buprenorphine and the opiate antagonist naloxone; designed to be taken sublingually (under the tongue) and the naloxone is inactivated when taken as recommended; if addicts inject the Suboxone, the naloxone will block the effects of the buprenorphine and the addict will experience little or no effect 29. What is the significance of the heroin addiction epidemic that failed to occur in the 1970's? Near the end of the Vietnam War in the early 1970s, heroin addiction rates among returning US soldiers were reaching 21%; soldiers were required to go through detox before their return to the US; given the 90% relapse rate, one would have expected most would return to use heroin at home; follow-up studies showed that few soldiers did relapse (less than 15%); clearly illustrates that environmental and psychosocial factors associated with Vietnam were apparently responsible for the development of dependence; upon returning to the US, Vietnam veterans found heroin far less available; the changes in lifestyle and social environment in the US eased the pressures that led to their initial dependence; the radical change in environment from Vietnam to the United States cannot be duplicated in the typical treatment setting; this is one reason that treating heroin addiction is so difficult, CHAPTER 11: MARIJUANA 30. What is Cannabis sativa? The term marijuana is thought to be based on the Portuguese word mariguango, which translates as “intoxicant.”; marijuana is not the same as hashish, although both are derived from the Cannabis sativa plant; marijuana is the leafy top portion of the plant, whereas hashish is made from the dust of the resin that the hemp plant produces for protection from the sun and heat and for maintaining hydration; plants that grow in warmer climates produce greater amounts of the resin, which generally has stronger psychoactive effects 31. Early history of marijuana. Earliest known evidence of use of cannabis occurred during the Stone Age over 10,000 years ago; earliest references to the use of cannabis for its pharmacological properties are attributed to Shen Nung in 2800 BC [mythical Chinese emperor and pharmacist who shared knowledge of the medicinal uses of cannabis with his subjects; speculated that cannabis was used in this period in China for sedating, treating pain and illness, and countering the influences of evil spirits, and gaining its general psychoactive effects]; gradually spread from China to surrounding Asian countries; adopted in India where cannabis served a religious function [included as one of the five sacred plants in Hinduism literature]; use spread to the Middle East and then to north Africa; during this expansion, hashish was first identified 32. How was it introduced in the Americas? The presence of cannabis in the New World dates to 1545, when the Spaniards brought it to Chile; in the North American colonies, the Jamestown settlers in Virginia raised the cannabis plant for fiber in 1611; this hemp product became a staple crop and was cultivated by George Washington, among many others; cannabis was harvested in New England starting in 1629; it remained a core U.S. crop until after the Civil War; the center of hemp production was Kentucky, where it was a major crop product for decades; following the lead of European doctors, American physicians used cannabis in the 1800s, as a general, all-purpose medication; by the 1850s, marijuana was listed in the United States Pharmacopeia, a listing of legitimate therapeutics; it remained there until 1942; cannabis was consumed for recreational purposes only to a limited extent during this period, and descriptions of its psychoactive effects were not common. 33. What is the Marijuana Tax Act? Harry J. Anslinger became director of the Federal Bureau of Narcotics in 1932 and was convinced that marijuana represented a major threat to the safety and well-being of the country; successfully encouraged many states to restrict the trafficking and use of Marijuana; The Tax Act did not officially ban marijuana; acknowledged the medicinal uses of marijuana and permitted the prescription of marijuana following payment of a license fee of $1 per year; any other possession or sale of marijuana was strictly outlawed; punishments for violation were a $2,000 fine, five years of imprisonment, or both; Anslinger’s efforts overall were successful in reducing the legal spread of marijuana 34. LaGuardia commission on marijuana. Mayor LaGuardia’s Committee on Marihuana was created by the New York Academy of Medicine at the request of New York City Mayor Fiorello LaGuardia; coordinated input by physicians, psychologists, pharmacologists, and sociologists; Data were gathered on marijuana use and effects in tea-pads as well as in laboratory settings; the general finding of the study was that marijuana use was not particularly harmful to users or to society at large; the report failed to find evidence for the claim that aggression, violence, and belligerence were common consequences of marijuana smoking; however, a number of individual changes were noted, including in more extreme form “mental confusion and excitement of a delirious nature with periods of laughter and of anxiety”; these report findings were consistent with those of commission reports published earlier. 35. What about more recent commission? Two influential documents recommended the approval of smoking marijuana for treating certain categories of medical disorders; the first report was prepared by Britain’s House of Lords (1988) and the second by the United States National Academy of Sciences [concluded that there was scientific foundation for studying marijuana as a treatment in such areas as pain relief, control of nausea and vomiting, and appetite stimulation]; A more recent report, entitled Cannabis: Our Position for a Canadian Public Policy (Senate Special Committee on Illegal Drugs recommended amendments to existing law to allow compassionate medical access to cannabis and its derivatives; a system through which licensed individuals would produce and sell cannabis; that the government of Canada declare an amnesty for any person convicted of possession of cannabis under current or past legislation 36. Marijuana use surveys. Marijuana is the most widely used illicit drug in the Western world and the third most commonly used recreational drug after alcohol and tobacco; WHO [illicit substance most widely cultivated, trafficked, and abused]; annual and current rates decreased significantly from 1979 to 1988, decreased more gradually for several more years, and were generally stable from around 1993 until the increases noted in 2001 and 2002; rates have been relatively stable through the latest survey; prevalence rates of lifetime use have been gradually rising since the mid- 1990s, with a larger increase apparent from 2000 to 2002; men were more likely than women to be current users of marijuana (9.3% versus 4.9%).; the reasons for the overall decline in marijuana use since the late 1970s probably reflect broad cultural factors, growing concerns about health and fitness, and concerns over possible negative effects of drug use in general; High School Seniors Survey: percentages of seniors ever using, using in the past month or year, and using daily for the past month all dropped around 1979 until 1992; in 1993, marijuana was making a comeback among high school students; increased significantly in 1993, and continued to rise through 1997; remained relatively constant for the following years 37. Is marijuana a "gateway" drug? “Stepping-stone” theory of drug use posits that use of licit and illicit substances follows a predictable pattern; research has shown that the vast majority of marijuana users do NOT go on to become heroin addicts; BUT substance use does appear to follow a uniform sequence of drugs; High school students tend to use drugs in the same sequence [alcohol, marijuana, and then “hard drugs” such as cocaine, crack, hallucinogens, and heroin]; Interpretation: not everyone who uses marijuana will subsequently se other illicit drugs; people who start using marijuana after previously using alcohol typically do not stop using alcohol 38. “Correlated Vulnerabilities” Theory: alternative to “stepping-stone” theory; suggests that the “stepping-stone’ pattern of substance use is explained by the common characteristics [i.e. general predisposition to use of drugs] of those who use cannabis and other drugs 39. What are the active ingredients in marijuana? delta-9-tetrahydrocannabinol [known as D-9- THC or THC]; research since 1964 has shown that the D-9-THC cannabinoid accounts for the vast majority of the known specific pharmacological actions of marijuana; although THC is the prime psychoactive agent in cannabis, other cannabinoids, such as cannabidiol and cannabinol, can be biologically active and can modify THC effects, but they tend not to be psychoactive in and of themselves 40. What are some of the factors that determine the absorption of THC? Potency of the cannabis being smoked [only half of the THC available in a joint is in the smoke, and the amount ultimately absorbed into the bloodstream is probably less]; amount of time the inhaled smoke is held in the lungs [the longer it is held, the more time for absorption of THC]; number of people who share the marijuana cigarette [more smokers may decrease the amount of marijuana available to any one user]; the amount of THC in a marijuana cigarette that is actually absorbed by smoking averages around 20%, with the other 80% lost primarily through combustion, sidestream smoke, and incomplete absorption in the lungs 41. How long do metabolites of THC remain detectible? THC is carried through the bloodstream and deposited within various organs; then metabolized to less active products over time; process occurs primarily in the liver, but can occur in other organs; the THC metabolites are excreted slowly through feces and urine; approximately half of the THC is excreted over several days and the remainder by the end of about a week; however, some metabolites of the THC, a number of which may still be active in the system, can be detected in the body at least 30 days following ingestion of a single dose and in the urine for several weeks following chronic use 42. What is anandamide? Two types of cannabinoid receptors [CB1 and CB2] have been identified; they are uniquely stimulated by THC; CB1 receptors are located predominantly in brain areas that control memory, cognition, the motor system, and mood; CB2 receptors are most prevalent in the immune system; anandamide is a chemical that binds to the same receptors on brain cells as do cannabinoids; researchers are now using the compound anandamide to study how the cannabinoid receptors affect functions such as memory, movement, hunger, and pain, which are affected by marijuana use 43. What is Spice? K2? Synthetic/designer marijuana that is sprayed onto herbal or plant material and advertised for sale as a herbal preparation; most commonly sold as dried leaves in a small bag, generally labeled as incense, potpourri, or a herbal smoking blend; these substances have often been found to contact potent CB1 agonists, so that smoking these plant materials is very likely to mimic a powerful marijuana-like “high” 44. What effects do they produce? Acute effects: elevated HR and BP, drowsiness, agitation, vomiting, paranoia, and loss of physical control; its use has resulted in various stages of kidney failure; longer-term use effects have not been identified 45. What about tolerance and dependence to THC? The evidence for tolerance to cannabis in humans is less clear, with many studies indicating tolerance but a number of others not; more likely to occur with higher doses used over longer periods of time; mechanisms by which tolerance occurs are still unknown; ongoing debate as to whether physical dependence can occur in the context of marijuana use; some have argued that there is no significant withdrawal syndrome identifiable, but there is some evidence for aspects of dependence associated with sustained heavy use of marijuana [sleep disturbance, nausea, irritability, and restlessness]; although debate continues as to whether these symptoms are more indicative of a psychological as op- posed to physical dependence on marijuana; at present, it appears that aspects of physical dependence, when they occur, are most likely to be associated with sustained heavy use of marijuana 46. Medical uses for marijuana? Nausea and Vomiting [frequently associated with chemotherapies and some radiation treatments for cancer; there are indications that children undergoing cancer chemotherapy may particularly benefit from orally administrated high doses of cannabinoids]; Cachexia is a disorder in which an individual physiologically “wastes away” often due to HIV infection or cancer [has been proposed that patients with cachexia use marijuana to stimulate appetite and thus gain weight; these reports have had some empirical support]; Glaucoma is a generic term used to denote ocular disease that involve increases in intraocular pressure [shown to decrease intraocular pressure, but marijuana may also reduce blood flow to the optic nerve and possible exacerbate loss of vision; mechanisms through which cannabis reduces intraocular pressure have not been determined; most experts believe that existing non-THC medications have equal or greater benefit in the treatment of glaucoma]; 47. Note the political developments involving medical marijuana (e.g., the Cannabis Buyer's Club). Cannabis Buyers Club in San Francisco (1992) was founded by Denis Peron, following the death of a friend from AIDS; Peron was instrumental in getting a proposition to make marijuana available to sick people placed on the 1991 San Francisco citywide ballot (approved despite being in violation of California state law); California became the first state [Proposition 15] to legalize medical marijuana; still legal in 18 states (number fluctuates as a function of ballot initiates and changes in state laws); there has been progressive decriminalization and even legalization of marijuana sale and possession [marijuana possession, at least in small amounts, should not entail the same criminal penalties as “harder drugs” and costs associated with enforcing many existing laws regarding marijuana 48. In what states is recreational use of marijuana now legal? The 2012 approval of Colorado and Washington to regulate, tax, and control marijuana was surprising to many 49. What are the acute physiological effects of marijuana? Although cannabis produces physiological effects, most of these actions are different for different users, not only in strength or intensity of the effect but also in duration; most commonly experienced effects are cardiovascular [bloodshot eyes which is dose related; increase in HR and pulse rate; both of these effects last about an hour and each appears to be dose related]; peak heart rate occurs around 20 minutes after smoking; BP slightly elevated]; no evidence indicates that these effects create any permanent damage within the normal cardiovascular system; generalized decrease in motor activity; decreases the total REM sleep achieved [typically occurs with higher doses]; minor or infrequent effects include dry mouth, thirst, fluctuations in respiration and body temperature, hunger or “the munchies” (peaking two to three hours after smoking), nausea, and headache or dizziness. 50. What are the long-term effects? Data on the longer-term effects of marijuana unfortunately are sparse and difficult to interpret; the research that has been conducted has focused on four central systems: respiratory [proper lung functioning appears to be altered but much of this impairment is reversed following abstinence; cannabis tar contains greater amounts of cancerous agents than does tobacco tar; cannabis smokers frequently smoke cigarettes too so separating the effects of the two substances is difficult], cardiovascular [no evidence that smoking marijuana produces deleterious cardiovascular effects in healthy individuals; potentially dangerous among people who have existing cardiovascular problems], immune [no significant long-term threat to the immune system; acts as an immunosuppressant and decrease resistance to some viruses and bacteria; mechanism by which immune dysfunction occurs has not yet been identified], and reproductive [chronic marijuana use has been associated with decreases in the number of sperm and sperm motility among men; may produce nonovulatory menstrual cycles in which menstruation is not preceded by the release of an ovum]; Summary: appears the majority of effects associated with marijuana use are more acute than chronic and that longer-term effects tend to be reversible with the termination of drug use; however, smoking marijuana may be found to be linked to various respiratory disorders, including cancer; most of the negative effects found are correlated with higher doses and frequency of use than those described by most cannabis smokers in this country 51. What are the behavioral effects of marijuana? The most common behavioral effect is a generalized decrease in psychomotor activity and decrements in some domains of psychomotor performance; these effects appear to be dose related, with more pronounced changes associated with greater amounts of marijuana taken in; the general decrease in motor activity appears to be pervasive, and the state is described as associated with feelings of relaxation and tranquility; some users first experience a stage in which they feel excited and restless [fairly soon, however, these users virtually always experience a transition to the relaxation stage]; decreased sensitivity to pain during marijuana intoxication; there appear to be dose-related dysfunctions in motor coordination, signal detection, and the ability to monitor a moving object; appears that cannabis can cause psychomotor impairment and that this impairment becomes more apparent in tasks that require thinking and concentration; long-term or heavy use of marijuana has been associated with temporary impotence among men and temporary decreases in sex drive among women 52. What are the cognitive effects of marijuana? Two primary cognitive consequences of cannabis intoxication have been documented; the first is impaired short-term memory and the second is the perception that time passes more slowly; decreased ability to attend and concentrate so that users are easily distracted (may produce “racing thoughts”); describe occasional feelings of “unreality” and attachment of increased meaning to events or objects not previously perceived as important; most of the effects are short-term; no consensus on long-term cognitive effects 53. Marijuana and violence? Typical emotional response to cannabis is a carefree and relaxed state; users may fluctuate between experiencing these negative feelings and the more positive states; the overwhelming conclusion drawn from data, including surveys, laboratory investigations, and field studies, is that cannabis use is not causally related to increased aggression; when aggression is observed, it probably is more a function of the beliefs and characteristics of the individual drug users; levels of aggression actually decrease following cannabis use 54. Amotivational syndrome? Loss of effectiveness and reduced capacity to accomplish conventional goals as a result of chronic marijuana use; what seems to occur is that users either are more relaxed in the situation and thus perceive less anxiety or interpret their behavior differently while under the influence of marijuana; the list of behaviors proposed as part of the syndrome includes apathy, decreased effectiveness, lost ambition, decreased sense of goals, and difficulty in attending and concentrating. 55. What is AMP? Marijuana soaked in embalming fluid or formaldehyde (the fluid’s main ingredient) and dried before being smoked; psychiatric effects [slowed sense of time, memory impairment, disorientation, paranoid thoughts, anxiety, confusion, disordered thought and difficulties in reality testing, and tremor]; physiological effects [elevated BP, hypersalivation, tachycardia, and psychomotor excitement] CHAPTER 12: HALLUCINOGENS 56. What properties do the various hallucinogens have in common? Hallucinations and other alterations in perception; most of the drugs in hallucinogens generally do produce sensory disturbances or alterations that can be considered hallucinogenic; certainly not the only effect these drugs produce; hallucinogens exert profound effects on mood, and thinking and physiological processes; hallucinogens alter nearly all aspects of psychological functioning, and the phrase “altered stated of consciousness” describes these drugs well 57. What are the serotonergic hallucinogens? A class of drugs that include the synthetic compound LSD (lysergic and diethylamide) and related drugs, such as mescaline (from the peyote cactus) and psilocybin (from certain mushrooms), along with many other less well-known compounds; all produce vivid visual hallucinations and a variety of other effects on consciousness; despite differing chemical structures, these drugs also have in common the action of influencing serotonergic transmission in the brain [drugs in this group all seem to bind to a particular subtype of serotonin receptor referred as the 5-HT2A receptor, and activation of these receptors is thought to be the key factor in producing visual hallucinations] 58. Mescaline? Comes from the peyote cactus [referred to as peytol]; peyote may have been the most widespread hallucinogenic drug in the New World; Aztecs used peyote in their rituals; [southwestern tribes gathered peyote by cutting the cactus at the soil line, leaving the root intact; cactus was sliced and dried into hard “buttons,” which could be transported great distances without losing their potency]; the ritual itself is almost identical regardless of the tribe studied [the all- night ceremony takes place in a large tepee where the participants sit in a circle around a fire, eating peyote buttons and drinking peyote tea; they smoke tobacco in cigarettes or a pipe; the night is spent chanting, singing, praying, and later on discussing and interpreting the peyote-induced visions]; some Native American people still conduct these ceremonies today, much as they did many centuries ago; mescaline’s chemical structure is different from the others; in fact, mescaline is far more similar to amphetamine than to LSD; for this reason, it has often been classified as having a different mechanism from LSD; unlike amphetamine (and the methylated amphetamines like MDMA), mescaline produces vivid visual hallucinations virtually identical in form to those of LSD 59. Psilocbyin? Comes from certain mushrooms [called teonanacatl] by the Aztec and Mayan peoples, which means “flesh of the gods”]; mushrooms were viewed as sacred; mushroom icons found in Mayan ruins dating back to before 1000 BC suggest that the use of the sacred mushroom was an ancient practice; One Spanish writer, de Sahagun in the 1500s, described the use of mushrooms by Aztecs as follows: “These mushrooms caused them to become intoxicated, to see visions and also to be provoked to lust. . . . They ate the mushrooms with honey and when they began to feel excited due to the effect of the mushrooms, the Indians started dancing, while some were singing and others weeping. . . . Some Indians who did not care to sing, sat down in their rooms, remaining there as if to think. Others, however, saw in a vision that they died and thus cried; others saw themselves eaten by a wild beast; others imagined that they were capturing prisoners of war; others that they were rich or that they possessed many slaves; others that they had committed adultery and had their heads crushed for this offense. . . . (Schlieffer, 1973, p. 19)”; People normally take psilocybin orally by either eating the mushrooms or drinking a brew containing them; difficult to specify doses because the amount of psilocybin varies depending on the species of mushroom, among other things 60. DMT (Ayahuasca)? Used by indigenous people of the western Amazon area of Brazil, Columbia, Peru, Ecuador, and Bolivia; several different plants may be used to produce ayahuasca tea, but generally it includes at least one plant that contains the serotonergic hallucinogen, dimethyltryptamine (DMT); DMT is normally not effective when taken orally because it is broken down by enzymes (MAO) before reaching the brain [Ayahuasca tea usually contains a second plant, usually a woody vine (Banisteriopsis caapi or B. inebrians) that contains an MAO inhibitor that prevents the breakdown of the DMT and is thought to allow it to reach the brain]; Ayahuasca produces a brief (1- to 2-hour) experience characterized by intense visual hallucinations and is traditionally used in healing ceremonies, initiation rites, and other rituals; the effects are similar to those of the other serotonergic hallucinogens; the altered state of consciousness and visual hallucinations are seen as a means of communication with a spirit world and of obtaining divine guidance; shamans use ayahuasca in healing ceremonies to improve physical health and to exorcise evil spirits 61. Where do these hallucinogens come from? The hallucinogenic properties of these plants were primarily discovered and used by the Indian peoples of Central and South America; an exception is ibogaine, which tribal peoples of Africa discovered and used 62. Consider their early history. When the Spanish conquistadores began to explore and colonize Mexico and other parts of Central and South America, they encountered new civilizations with customs and religious practices unfamiliar to Europeans; among these practices was the use of hallucinogenic plants in religious ceremonies; although each of these plants contains a different drug, all produce vivid visual hallucinations, and the Indians took the visions as oracles that could reveal the future and solve other mysteries, help in decision making, and aid the medicine man or shaman in healing the sick 63. How were the hallucinogenic properties of LSD discovered? Albert Hofmann, a chemist working in Sandoz Laboratories, discovered LSD in 1938; Hofmann was studying derivatives of ergot [a fungus that infests grain and occasionally caused outbreaks of disease in medieval Europe when infected bread was eaten; ergot derivatives have medical use in the treatment of migraine headache and to induce uterine contractions during pregnancy]; Hofmann eventually synthesized compounds involving lysergic acid, the 25th of which was lysergic acid diethylamide [abbreviated LSD- 25 on the bottle]; LSD underwent several preliminary animal tests, but it showed no commercially interesting properties and was shelved; stayed unknown until 1943, when Hofmann decided to reexamine its properties; during a lab experiment, Hofmann apparently spilled a small amount of LSD on his hand, where it was absorbed; he began to trip on LSD; Hofmann decided the bizarre experience must have been due to contact with LSD, so he decided to test that hypothesis with an experiment [he reasoned that LSD must be very potent to have produced such effects through an accidental exposure, and he measured out for oral administration 250 micrograms—a minute amount by the standards of drugs known at that time]; what Hofmann could not have known is that LSD is so potent that this dose was at least twice as potent as the normal effective dose (25 to 125 micrograms); as the intensity of the drug effects began to subside, Hofmann reported enjoying the hallucinations and altered thought processes; after he recovered and made his report to Sandoz, many other experiments followed 64. How was LSD popularized by Leary and Kesey, etc.? Leary and his Harvard associate Richard Alpert (who later became known as religious writer Baba Ram Dass) had taken LSD and other hallucinogens and become convinced of their psychological and spiritual value; what began as legitimate experiments, including work on the possible beneficial effects of hallucinogens on prison inmates, began to look suspiciously like LSD parties involving Harvard faculty, students, and an assortment of celebrities and intellectuals. At some point, Leary had become the leader of a social and religious movement; harassment by law enforcement officials continued to increase Leary’s eminence, and he became viewed as something of a martyr; On the West Coast, LSD was popularized by Ken Kesey [author of One Flew over the Cuckoo’s Nest]; Kesey’s “acid tests” were large parties where hundreds of people were “turned on to LSD” in a single night; LSD began to make an impact on the emerging hippie subculture, 65. How do LSD and similar hallucinogens act on the brain? Similar chemical structures that resemble that of the naturally occurring serotonin transmitter; the structural similarity led to the notion that LSD and related compounds might act by mimicking serotonin and thus activate serotonin receptors in the brain; this hypothesis has now received considerable support; EX: it has been shown that LSD and the related hallucinogens bind to certain subtypes of serotonin receptors (5-HT2A receptors), and that this effect correlates strongly with the potency of the drug as a hallucinogen; mescaline, like LSD, is an agonist at the specialized group of serotonin receptor subtypes called 5-HT2A receptors, providing further support that these receptors play an important role in mediating the visual hallucinations common to all the drugs in this class 66. What about tolerance and cross-tolerance? Tolerance to all the effects of LSD develops fairly rapidly, and the same is true for mescaline; there is cross-tolerance between LSD, mescaline, and other drugs of this class 67. How does LSD differ from other serotonergic hallucinogens? LSD is the most potent of the class, with oral doses as small as 25 micrograms producing effects [street doses range from about 12 to 350 micrograms and are prepared by placing a small amount of LSD solution in a gel (windowpane), in a tablet, or, most commonly, on paper (blotter) with colorful cartoon designs]; LSD is rapidly absorbed, and subjective effects are usually noted within 20 to 60 minutes after consumption; distributed throughout the body and readily penetrates the blood-brain barrier; effects persist for 8 to 12 hours, and the drug is rapidly metabolized and eliminated from the body; even the most sensitive techniques can detect LSD or its metabolites in urine for no longer than 72 hours after use 68. How is the LSD experience similar or different to schizophrenia? It is true that hallucinations, unusual affective reactions, and loss of reality contact are characteristics of both schizophrenia and hallucinogenic experiences; the hallucinations experienced under the influence of LSD are primarily visual, whereas those of schizophrenics are usually auditory [the subjective experiences of the psychotic are certainly not identical to those of hallucinogen users]; an intriguing similarity is that chlorpromazine and the other antipsychotics used in the treatment of schizophrenia are effective antagonists of LSD effects; thus serotonergic hallucinogens may yet provide clues about the biochemistry of mental disorders 69. What about LSD and psychotherapy? The general idea was that therapists would be able to learn important information when their patients were using LSD and that the patients would be better able to gain insight into their condition because LSD could break down ego defenses; many extravagant claims were made about the benefits of LSD for mental health and spiritual development in the 1960s, but interest in the use of LSD in psychotherapy declined in the wake of Timothy Leary; most therapists thought the potential risks of LSD outweighed the benefits; there has been, a renewed interest in the therapeutic value of these drugs has surfaced; EX: Grob et al. (2011) found that a moderate dose of psilocybin administered to patients with advanced stage cancer reduced their anxiety and depression; there is also interest in potential psychotherapeutic benefits of MDMA and ketamine 70. What are the physiological effects of serotonergic hallucinogens? Similar to those of amphetamine and cocaine; sympathomimetic – include pupil dilation, and increased heart rate, blood pressure, body temperature, and sweating; effects more potent than amphetamines 71. What are the major psychological effects? Common to all the serotonergic hallucinogens are profound changes in visual perception, and there is some consistency in the types of visual changes that occur; form constants and synesthesia 72. Form constants [R.K. Seagull]. Vortex patterns [2-dimensional objects become 3-dimensional; EX: you might look at a wall and report that you see a hole or tunnel opening in the wall], spiral explosions [most often seen in migraine sufferers before they get a migraine; the perception of this 3-dimensional object might be moving/spinning], and the lattice pattern [a checkerboard pattern that appears in an otherwise plain surface; designed to represent experiences during the peyote ritual; pattern is very vivid/colorful] 73. Synesthesia. An effect sometimes produced by hallucinogens that is characterized by the perception of a stimulus in a modality other than the one in which it was presented (EX: a subject may report “seeing” music). 74. What about LSD and chromosome damage? Claim that those who used the drug, male or female, would stand a high risk of having deformed children; this concern was based on a study that found that LSD produced chromosome breaks in white blood cells artificially cultured in the laboratory; however, breaking chromosomes in white cells in a test tube under high doses of LSD has not been shown to generalize to in vivo conditions; after considerable research into this question, there is no convincing evidence that LSD (or any other serotonergic hallucinogen) increases birth defects in offspring when taken in normal doses [as with most drugs, however, there is risk of fetal damage if taken by pregnant women] 75. Flashbacks? Re-experience of some aspect of a hallucinogenic trip that may have occurred months or even years before; the nature of the experience usually involves visual disturbances such as flashes of color, trails in the visual field, or fleeting perceptions in the peripheral field of view; often brought on by stress, fatigue, entering a dark environment, or marijuana use; it is difficult to estimate the frequency of flashbacks; it appears that users do not find their flashbacks to be problematic, so many go unreported; in unusual cases, flashbacks can be frequent and severe and may disrupt an individual’s life; the diagnosis of hallucinogen persisting perception disorder is applied to such cases [very rarely, the visual distortions are nearly constant and may reflect permanent loss of serotonergic neurons]; treatment with antipsychotics or benzodiazepines may relieve the symptoms of such cases 76. Bad trips? Acute panic or paranoid reactions to the drug; can leave individuals in an acute psychotic state during which they may harm themselves or others; the frequency of bad trips is difficult to estimate, but it was high enough in the 1960s to lead to the widespread development of walk-in crisis centers where victims could be brought for reassurance (talking the subject down) and, if necessary, hospital referral; appear to be less frequent today [perhaps because more is known about how to prevent them]; the psychological state of the user and the environmental setting are important [EX: one of the few documented LSD suicides took place after a man was administered LSD without his knowledge in an experiment conducted by the CIA in the 1950s]; a calm and comfortable setting and low doses of the hallucinogen are thought to reduce the frequency of bad trips, although bad trips may occur even under the best of circumstances 77. Long-term psychiatric disorder? LSD also has been linked to long-term psychiatric disorders; EX: Charles Manson and his “family”; when one is confronted with a psychotic individual who has used LSD, it is difficult to determine whether LSD caused the psychosis or the person was psychotic to begin with and LSD made the symptoms more flagrant; most users of LSD who are diagnosed as psychotic have extensive histories with other drugs as well, and the role these other drugs may have played is rarely certain; it generally is agreed that hallucinogens may precipitate or exacerbate psychosis or emotional disturbance in certain vulnerable individuals; the controversy focuses on the precise role of LSD and related hallucinogens; the general consensus seems to be that, when chronic psychiatric problems occur following serotonergic hallucinogen use, it generally involves individuals who had already been diagnosed with or have manifested psychotic or pre-psychotic symptoms before the drug use 78. What is ibogaine and how is it being used? Tabernanthe iboga is a shrub native to West Africa; several tribal groups in the region made up of Cameroon, Congo, and Gabon have used this plant for many centuries for its hallucinogenic properties; the bark of the iboga root is eaten in ceremonies by members of the Bwiti religion who believe that the plant produces divine visions and permits them to commune with their ancestors; contains a number of psychoactive chemicals, but the critical component isolated from the bark preparation seems to be the chemical ibogaine; generally classified as a serotonergic hallucinogen, but recent studies have suggested that its neurochemical actions may be more complex, including effects on glutamate, endorphin, norepinephrine, and dopamine pathways; has become quite controversial because of claims that it may be of value in the treatment of addiction [anecdotes from ex-addicts who believe that ibogaine visions helped in their recovery from dependency on alcohol, cocaine, and heroin have circulated since the 1960s; there has been very little research] 79. What are the methylated amphetamines? How are they similar to and different from the serotonergic hallucinogens? Include MDA and MDMA (Ecstasy); these drugs are structurally related to amphetamine (as is mescaline); MDA and MDMA [methylenedioxymethamphetamine] produce alterations in mood and consciousness [mild euphoria accompanied by openness, feelings of warmth and empathy, and lack of defensiveness] with little or no sensory change [produce few or no visual hallucinations]; like amphetamine and cocaine, these drugs act on dopamine, norepinephrine, and serotonin synapses; although their effects are most potent on the serotonergic system, they do not bind selectively to the 5-HT2A receptor; this is thought to be the basis of their difference from the LSD-like hallucinogens; these properties led some psychotherapists to advocate the use of these drugs, particularly MDMA, as an adjunct to therapy; some scientists classify MDMA with the hallucinogens, others with the amphetamines, and still others consider these drugs as belonging to a unique category, entactogens or empathogens 80. Consider recent trends in MDMA use. MDMA has become perhaps the most controversial illegal drug in our society today; rapid increase in popularity in the late 1990s; prior to 1996, the annual high school senior survey did not even have a specific category for MDMA; in 1996, 4.6% of U.S. high school seniors reported having used it during the past year; that number doubled by 2001, when 9.2% reported using it; after that peak, use declined and has leveled off in recent years; one important reason for this decline is the publicity about the many adverse effects of MDMA, including claims that it may produce brain damage and death; these claims have generated considerable controversy and a tremendous amount of research on MDMA in the past few years 81. What are some possible adverse effects associated with ecstasy? There is an initial overall increase in serotonin and dopamine activity after taking the drug, but this is followed after several hours by a marked decrease in serotonin activity; produce clear sympathomimetic effects [increased HR, BP, and pupil dilation]; additional physical effects include muscle tension, teeth grinding (bruxism), increased body temperature, appetite suppression, and insomnia, which are remarkably similar to amphetamine; psychological effects include euphoria, increased emotional warmth and empathy, lowered defensiveness, and increases in verbal behavior; Although MDMA is not associated with dramatic physical withdrawal symptoms, commonly reported aftereffects include drowsiness, muscle pain, depression, paranoia, and anxiety [these effects typically dissipate within a few days but can be more persistent in some cases]; in recent years, researchers have seen a renewed interest in the possibility of MDMA therapy, and controlled trials have provided some support for the value of using MDMA as an adjunct to cognitive behavior therapy in the treatment of post-traumatic stress syndrome and other psychological disorders 82. Residual Effects of MDMA. One of the major controversies about MDMA and other methylated amphetamines concerns the possibility that they may produce long-term damage of certain brain structures; some users report commonly taking 15 or more tablets in a night, and this would likely produce doses well above those shown to produce long-term serotonin deficits in nonhumans; human users may take lower doses of MDMA but take them many times, intermittently, over many years, and we do not yet know what neural consequences may occur following this pattern of use; how rapidly neurons recover from the toxic effects of the drugs is also open to debate, but one study showed effects that persisted for as long as seven years after drug administration in primates; serotonin is a neurotransmitter that modulates sleep, mood, and many other functions, so depletion of serotonin could lead to serious problems; numerous studies have used brain imaging technology such as PET techniques and consistently have found reductions in serotonergic functioning between heavy MDMA users and controls; however, there is also evidence that the serotonin system recovers from these effects after a period of abstinence; MDMA and related drugs pose risks of acute toxic effects and possible deficits in neuropsychological functioning, particularly among heavy users 83. What are synthetic phenethylamines and what issues are associated with them? A group of new synthetic compounds includes a host of hallucinogens with MDMA or LSD-like effects; many of these are drugs with the phenethylamine structure like 2C-B and 2C-I NBOMe, but a bewildering array of similar compounds have turned up in recent years, often sold over the Internet; very little is known about their effects including the range of safe doses; in March 2011, a group of teenagers in the Minneapolis area attended a rave and took a drug purchased over the Internet called 2C-E(2,5-dimethoxy-4-ethylphenethyl- amine), or Europa, resulting in a mass overdose [11 were hospitalized, some in critical condition, and one died]; in the wake of this episode and numerous other overdose deaths in recent years, many of the “2-C” phenethylamine compounds, including 2C-E, 2C-C, 2C-D, 2C-I, and 2C-T-2, were explicitly banned by the 2012 Synthetic Drug Abuse Prevention Act; Alexander Shulgin, the chemist who initially synthesized many of these compounds, lists 179 psychoactive phenethylamine drugs alone, most of which are not explicitly scheduled (although some may be illegal based on the Analog Act) 84. What are the anticholinergic hallucinogens? Less familiar to most people and includes drugs such as atropine and scopolamine found in plants such as mandrake, henbane, belladonna, and jimsonweed; these drugs produce a dreamlike trance in users from which they awaken with little or no memory of the experience; users seem delirious and confused but may be able to describe visions if asked; the drugs in this class are antagonists of a subtype of acetylcholine receptors called muscarinic receptors; found in a number of plants known throughout the world and have a long history of use; anticholinergic hallucinogens produce a variety of physiological effects, including dry mouth, blurred vision, loss of motor control, and increased heart rate and body temperature; can be fatal as they cause respiratory failure at doses only slightly higher than the effective dose; these drugs are rarely seen on the street today 85. What are some examples of them? Atropine and scopolamine are drugs that block acetylcholine receptors in the brain; in low doses, these drugs are used for a variety of medical purposes, and atropine in particular has been in the news recently because it is standard issue to troops in the Middle East where there is risk of nerve gas attack; deadly nerve gases (sarin and soman) are toxic because they inhibit the enzyme that breaks down acetylcholine, and as an acetylcholine antagonist, atropine is an antidote if administered rapidly after exposure; however, drugs like atropine and scopolamine also can produce hallucinogenic effects 86. Fly Agaric Mushroom (Amanita Muscaria): Contains several different hallucinogenic chemicals, including muscarine, which is a cholinergic agonist, and muscimole, a hallucinogen that may be similar to the LSD-like drugs; although rarely used today, the mushroom represents one of the earliest forms of hallucinogen use; grows throughout much of Europe and Asia, and it may have been the mysterious “Soma” de- scribed in the Hindu Rig- Veda more than 2,000 years ago, which describes the rather bizarre practice of recycling the drug effect by drinking the urine of an intoxicated individual [muscimole is the only hallucinogen known that passes unchanged through the system into the urine]; the effects of the mushroom are unique among hallucinogens, because users typically fall into a stupor for several hours during; which they experience visions, and later they experience intense euphoria and energy accompanied by visual hallucinations 87. What are the dissociative anesthetic hallucinogens? Includes phencyclidine (PCP or angel dust) and the related compound ketamine; often referred to as the dissociative anesthetics because of their ability to produce surgical anesthesia while an individual remains at least semiconscious; dissociative anesthetics are thought to act through a receptor that influences activity of the excitatory amino acid neurotransmitter, glutamate; in clinical trials of PCP and ketamine with humans, some patients experienced hyper excitability, delirium, and visual disturbances; these drugs were largely abandoned for human use, although both were marketed for use as anesthetics and tranquilizers in veterinary medicine; PCP is no longer extensively used in veterinary medicine; ketamine remains quite popular in this regard; ketamine abuse is an issue as it is often included among the “club” drugs; recently, several small-scale clinical trials have found that ketamine can reduce symptoms of depression (within a few hours as opposed to weeks with current medications); although ketamine treatment for depression may be of value, the search is on for less dangerous drugs with action at the NMDA receptor in the hope that safe, rapid-acting treatments for depression can be developed 88. How are they similar to and different from the other hallucinogens? A moderate dose (1 to 10 mg) of the dissociative anesthetics produces feelings of euphoria and numbness resembling alcohol intoxication; speech may be slurred, and generally there is motor discoordination; users may be catatonic and rigid with a blank stare or may be aggressive and hyperactive; effects include profuse sweating, increased HR and BP, and rapid jerky eye movements called nystagmus; subjects often report blurred vision or double vision but rarely visual hallucinations; rather, there are changes in perception of body


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