Lect. 9 Brain Reward Circuit and Drugs of Abuse

DRUGS USED IN DISORDERS OF THE
CENTRAL NERVOUS SYSTEM AND
TREATMENT OF PAIN
Lecture 9:
Brain Reward Circuit and Drugs of Abuse
Marc Imhotep Cray, M.D.

CNS Pharmacology
Lecture 9
Learning Objectives:
2
DRUGS OF ABUSE AND DRUG DEPENDENCY
1. The underlying biological basis of addiction as a disease.
2. The differential diagnostic criteria for drug abuse vs dependence and
the difference between them
3. The MOA within the central nervous system of the major drugs of
abuse
4. The signs and symptoms of overdose caused by the major drugs of
abuse including alcohol, heroin and cocaine.
5. The signs and symptoms of opioid withdrawal
6. The pharmacotherapeutic options for the treatment of opioid abuse
and dependence and their relative benefits and side effects.
7. The signs and symptoms of alcohol withdrawal
8. The pharmacotherapeutic options for the treatment of alcohol abuse
and their relative benefits and side effects.

CNS Pharmacology
Lecture 9
Drugs of Abuse (select): Topical Outline
3
I. Brain Reward Circuit
II. General Features of Substance Abuse
 Drug abuse (addiction) terms and concepts
III. Sedative-Hypnotics
 Ethanol: Deleterious Effects
 Ethanol Abuse: Treatment
 Withdrawal: Opioids, Benzodiazepines, and Barbiturates
IV. Cigarettes
V. CNS Stimulants (sympathomimetics)
 Cocaine
 Khat & Synthetic Cathinones
VI. Hallucinogens (psychotomimetics)
 marijuana (cannabis)
 dronabinol (marinol)

CNS Pharmacology
Lecture 9
I. Brain Reward Circuit
4
Drug abuse involves 2 components:
 psychosocial (e.g., family situation, peer pressure) and
 endogenous (e.g., genetics, enzyme levels)
 Pharmacologic mechanisms of drug abuse involve CNS
neurotransmitter systems that operate for therapeutic drug effects
 An endogenous pleasure or reward pathway in the brain is important
for motivation and learning (survival) and is thought to be excessively
active—because of genetics, overuse, or other factors—in drug abuse

CNS Pharmacology
Lecture 9
I. Brain Reward Circuit (2)
5
 Brain reward circuit consists of neuronal pathways, cortical sites, and
subcortical nuclei, especially within limbic region
 Primary among these are dopaminergic neurons in the ventral
tegmentum that project to the nucleus accumbens and then to the
cortex and other centers
 Also, norepinephrine-containing neurons from the locus ceruleus
project to the ventral tegmentum
 Stimulation or disinhibition of dopaminergic neurons within the
ventral tegmentum may be common to abuse of different substances

CNS Pharmacology
Lecture 9
6
Brain reward circuits

7
Potential sites of
drug action

CNS Pharmacology
Lecture 9
II. General Features of Substance Abuse
8
 Drug abuse (addiction) is a multifaceted problem, involving a
complex combination of biological and psychosocial contributing
factors
 Hereditary predisposition is also suspected to play a role in some
cases
 Many, perhaps most, drug addicts abuse more than 1 drug
 Hence, list of abused drugs is extensive and includes some
substances that are thought of primarily as mood or physique
enhancers or as “recreational” drugs (e.g., anabolic steroids,
mushrooms, designer drugs, hallucinogens, inhalants,
marijuana, nicotine)
 This presentation focuses on some of the major classes of
therapeutic and non-therapeutic drugs that are abused

CNS Pharmacology
Lecture 9
Drug abuse (dependence and addiction)
9
 Abuse is misuse of a drug (e.g., taking it in ways not medically
approved)
 Abuse of a drug is often, but not always, associated with
kinetic, dynamic, homeostatic or learned tolerance
o An acute tolerance (with first dose) has been described for ethanol
o Cross-tolerance occurs between drugs with same mechanism of action
Drugs are abused for a variety of reasons:
 To induce a feeling of euphoria
 To alter perception
 As a means of escape
 Due to peer pressure in young people
Abusers of drugs usually derive more pleasure from a drug with a
rapid onset of action than from a drug with a slow onset of action
within same class

CNS Pharmacology
Lecture 9
Drug abuse (2)
10
 Inappropriate and usually excessive, self-administration of a drug for
non-medical purposes
 Almost all abused drugs exert their effects in CNS
 Drugs with high abuse potential have a tendency to induce
compulsive drug-seeking behavior
 Preoccupation with procurement and use of drug may be so
demanding as to decrease users productivity
 Prolonged abuse may cause chronic toxicity

CNS Pharmacology
Lecture 9
Physical Dependence:
11
Dependence is physical requirement for a drug due to
adaptive physiologic changes (tolerance) after multiple
exposures
 If drug is not available, abstinent withdrawal syndrome
will occur
o Symptoms during withdrawal tend to be opposite of
effects due to drug administration
o Withdrawal from a drug of abuse is usually less severe
with long-acting drugs than, with short-acting drugs
within same class
 This is theoretical basis for replacement therapy
(e.g., methadone for heroin addicts)

CNS Pharmacology
Lecture 9
Addiction:
12
Addiction is psychological requirement for a drug
 It is characterized by compulsive drug use in spite of
associated negative social and biological consequences
 An addicted person can crave a drug even in absence of
physical dependence
 Addiction is thought to be caused by an increase in
CNS dopamine release and/or a decrease in dopamine
reuptake that occurs with use of drug

CNS Pharmacology
Lecture 9
Drug tolerance
13
After chronic use, same amount of drug
is insufficient to cause desired effect and
thus, more drug is used
 A compensatory response
Acquired Tolerance
 Pharmacokinetic or metabolic
 Pharmacodynamic or functional
 Learned or behavioral
Drug Dose
Normal
Tolerance

CNS Pharmacology
Lecture 9
Drug tolerance(2)
14
 Metabolic tolerance (pharmacokinetic tolerance):
 rate of drug elimination increases with long-term use because of
stimulation of its own metabolism (autometabolism)
 Cellular tolerance (pharmacodynamic tolerance):
 Biochemical adaptation or homeostatic adjustment of cells to
continued presence of a drug
o development of cellular tolerance may be due to a
compensatory change in activity of specific neurotransmitters
in CNS caused by a change in their levels, storage, or release
o or to changes in number or activity of their receptors

CNS Pharmacology
Lecture 9
Cross-tolerance
15
When an individual has become tolerant to a drug and
requires higher than normal doses of a second drug to
have its effects
i.e.
Barbiturates  BDZ
Amphetamine  Cocaine
BARBs  Anesthetics

CNS Pharmacology
Lecture 9
Cross-tolerance(2)
16
In general there is cross-dependence and cross-tolerance
between drugs of same class, but not between drugs in
different classes
There is some cross-tolerance btw sedative-hypnotics and
volatile intoxicants;
 thus a person tolerant to barbiturates will require more
anesthesia than a non-tolerant person
LSD type drugs (tryptamine group) and phenylethylamines
have cross-tolerance for each other but not with other
hallucinogens

CNS Pharmacology
Lecture 9
Cross-dependence
17
When a drug is administered to achieve same outcome as
that of another drug
i.e. heroin  methadone
 In a heroin user, methadone can be
substituted for heroin in preventing
withdrawal syndrome

CNS Pharmacology
Lecture 9
Co-administration/Co-abuse
18
Drugs of abuse are used in combination with other drugs
from one or more categories
 Alcohol is used, for example, with almost everything else
 Smoking (nicotine intake) is prevalent in patients using
other drugs
Be aware of possibility of combination of drugs when
treating intoxication, withdrawal or overdose, each drug will
require a specific treatment

CNS Pharmacology
Lecture 9
Important Point:
19
Because of the diverse character of these drugs,
there is no “single reason” for their use, nor is there
an “addictive personality"
 IT IS NOT NECESSARY TO HAVE A PREEXISTING EMOTIONAL
OR PSYCHIATRIC PROBLEM TO BECOME DRUG DEPENDENT!!!

CNS Pharmacology
Lecture 9
Toxicology of Drugs of Abuse:
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A) Tissue and organ toxicity
 Usual dose vs overdose
 Acute use (respiratory depression - narcotics, coma-
barbiturates; cardiovascular effects and seizures-cocaine;
arrhythmias-volatile intoxicants)
 Chronic use (alcohol, tobacco)

CNS Pharmacology
Lecture 9
Toxicology of Drugs of Abuse (2)
21
B) Psychic toxicity
 Acute use (bad trips, flashbacks - hallucinogens; CNS
stimulants)
 Chronic use (alcohol, hallucinogens, stimulants =>
reality distortion)

CNS Pharmacology
Lecture 9
22
C) Behavioral toxicity
 Amotivational syndrome, loss of productivity loss of
psychomotor control, accidents, violence
 Acute use (alcohol, stimulants, PCP)
 Chronic use (alcohol, CNS depressants, stimulants,
hallucinogens, PCP)

D) Associated Diseases
 Infections, AIDS, venereal diseases, tobacco-
related fires, toxicity due to bad batches of drug
(MPTP, PCP congeners), car accidents, big
machinery accidents, other accidents, violent
death
23

CNS Pharmacology
Lecture 9
Controlled substances:
24
 A drug deemed to have abuse liability that is listed on
governmental Schedules of Controlled Substances*
 Such schedules categorize illicit drugs, control prescribing
practices, and mandate penalties for illegal possession,
manufacture, and sale of listed drugs (next slide)
 Controlled substance schedules are presumed to reflect current
attitudes toward substance abuse; therefore, which drugs are
regulated depends on a social judgment
*An example of such a schedule by US Drug Enforcement Agency (DEA)
is shown in next slide. Note that criteria given by an agency do not always
reflect actual pharmacologic properties of the drugs.

CNS Pharmacology
Lecture 9
Schedule for controlled substances*
25
Schedule Criteria Examples
I No medical use; high
addiction potential
Flunitrazepam, heroin, LSD, mescaline, PCP, MDA,
MDMA, STP
II Medical use; high addiction
potential barbiturates, strong
opioids
Amphetamines, cocaine, methylphenidate, short
acting
III Medical use; moderate abuse
potential moderate
opioid agonists
Anabolic steroids, barbiturates, dronabinol,
ketamine
IV Medical use; low abuse
potential
Benzodiazepines, chloral hydrate, mild stimulants
(e.g., Ritalin), most hypnotics (eg, zaleplon,
zolpidem), weak opioids
*See http://www.usdoj.gov/dea/pubs/scheduling.html for additional details

CNS Pharmacology
Lecture 9
III: Sedative-Hypnotics: ETHANOL
26
ETHANOL is a commonly abused legal substance
1. Due to high lipid solubility and high water solubility, ethanol distributes
in total body water
2. Clearance from the body occurs in liver
a. Metabolism by alcohol and aldehyde dehydrogenases follows zero-
order kinetics
i. Products are acetaldehyde and acetic acid, respectively
ii. Two molecules of nicotinamide adenine dinucleotide hydrogenase
(NADH) are produced for each molecule of ethanol
b. An insignificant amount of ethanol is metabolized by mixed-function
oxidases (MFOs), but this can induce the MFOs, particularly in
alcoholics

CNS Pharmacology
Lecture 9
Sedative-Hypnotics: ETHANOL (2)
27
3. Effects of ethanol are related to blood ethanol
concentration
a. Legal limit for driving in most states is a 0.08% (80 mg
EtOH/100 ml blood) blood alcohol concentration
(BAC)
b. Death due to respiratory depression occurs in the
range of 0.4–0.5% BAC, although this is quite variable
c. Treatment of an overdose of ethanol is symptomatic
 Support ABCs/vital signs

CNS Pharmacology
Lecture 9
28
4. Acute adverse effects develop after a single exposure to ethanol
a. Behavior is changed due to a loss of inhibitions
b. Effects of other CNS depressants are enhanced
c. Hypothermia results from peripheral vasodilation, which makes person feel
warm even though body heat is being lost
d. Hangovers are common after drinking ethanol and may represent symptoms of
an acute withdrawal
e. Acute use of alcohol decreases metabolism of other CNS depressants
f. Panic attacks may occur day after alcohol is abused as blood alcohol levels drop
5. A low intake of ethanol (one drink per day) is associated with
increased high-density lipoprotein and decreased low-density
lipoprotein cholesterol. This may reduce the risk of heart disease

CNS Pharmacology
Lecture 9
29
6. Adverse effects from chronic (repeated) use occur on almost every
tissue in body and include:
a. Physical and psychological dependence
b. Activation of MFOs, which increases metabolism of many other drugs (e.g.,
phenytoin, warfarin)
c. Edema and ascites
d. Hypertension
e. Cardiomyopathy and arrhythmias
f. Liver damage (e.g., cirrhosis, fatty liver)
g. Acetaminophen combined with ethanol can cause severe acute liver
damage due to production of hepatotoxic metabolites
h. Changes in blood glucose due to impaired gluconeogenesis
i. Damage to the gastrointestinal tract
j. Megaloblastic anemias due to folate or vitamin B12 deficiency, or anemia
due to iron deficiency caused by GI bleeding

CNS Pharmacology
Lecture 9
30
Adverse effects cont.
k. Malnutrition, especially thiamine deficiency, which leads to Wernicke–
l. Korsakoff syndrome (paralysis of extraocular muscles, ataxia, and
confusion)
m. Psychological sequelae
 Depression and Korsakoff’s psychosis (long-term memory loss)
n. Fetal alcohol syndrome
 Ethanol is a common cause of birth defects and neurologic disorders.
o. Impaired visual acuity (blurry vision)
p. Immune system effects
 Increased inflammation of liver and pancreas and increased risk for
oropharynx and liver cancers

CNS Pharmacology
Lecture 9
Vitamin B1 (thiamine) and alcoholics
31
 Wernicke-Korsakoff syndrome—confusion, ophthalmoplegia, ataxia (classic triad)
+ confabulation, personality change, memory loss (permanent)
 Damage to medial dorsal nucleus of thalamus, mammillary bodies
 Dry beriberi —polyneuritis, symmetrical muscle wasting
 Wet beriberi —high-output cardiac failure (dilated cardiomyopathy), edema
 DEFICIENCY Impaired glucose breakdown ATP depletion worsened by
glucose infusion; highly aerobic tissues (e.g., brain, heart) are affected
first.
 Wernicke-Korsakoff syndrome and beriberi
 Seen in malnutrition and alcoholism (2° to malnutrition and
malabsorption)
 Diagnosis made by in RBC transketolase activity following vitamin B1
administration

CNS Pharmacology
Lecture 9
Ethanol: Deleterious Effects
32
Short- and long-term excess ethanol consumption leads to
widespread problems for the individual and for society
Lifetime prevalence of ethanol dependence is estimated at
10% to 15%, and as many as 30% of male and 10% of female
admissions to general hospitals are related to ethanol-
associated disorders
Ethanol is rapidly absorbed from the GI tract and distributes
to all cells in the body
 It readily passes into fetal circulation

CNS Pharmacology
Lecture 9
Ethanol: Deleterious Effects (2)
33
 Low concentrations of ethanol are safely
metabolized in a 2-step process: first by alcohol
dehydrogenase to acetaldehyde and then by
aldehyde dehydrogenase to acetate
 High concentrations saturate this pathway and
give rise to toxic byproducts of alternative
pathways
 Because ethanol is so widely distributed
throughout body, toxic consequences of excess
ethanol consumption involve essentially every
organ
Modifiedfrom:LippincottIllustratedReviews-PharmacologySixthEdition.2015
The pathway of ethanol metabolism.
ADH = alcohol dehydrogenase;
ALDH = acetaldehyde dehydrogenase.

34
Effects of Alcohol
on End Organs:

CNS Pharmacology
Lecture 9
Organ damage Caused by alcohol
35

36
Alcoholic Liver Disease:
CirrhosisoftheLiver

CNS Pharmacology
Lecture 9
Normal vs Cirrhotic Liver:
37
Normal liver, gross Cirrhosis, gross
Klatt EC. Robbins and Cotran Atlas of Pathology, 2nd Ed. 2010

CNS Pharmacology
Lecture 9
Fetal alcohol spectrum disorder
38
 Fetal alcohol spectrum disorder results from
maternal abuse of ethanol.
 Fetal alcohol syndrome is characterized by
retarded growth, microencephaly,
poorly developed coordination, mental
retardation, and congenital heart
abnormalities.
 Severe behavioral abnormalities can occur in
the absence of dysmorphology.
There is also an increased rate of spontaneous
abortions.

CNS Pharmacology
Lecture 9
Ethanol Abuse: Treatment
39
 Abrupt withdrawal from ethanol (in persons with physical
dependency) is accompanied by excitatory CNS signs such as
delirium tremens and potentially lethal seizures
 Medication management in the past was limited to disulfiram, which inhibits
aldehyde dehydrogenase
 Buildup of acetaldehyde produces an unpleasant reaction when ethanol is
consumed and thereby provides a deterrent to excess ethanol use
 Naltrexone and acamprosate (in Europe) are newer alternative
choices
 Naltrexone is an opioid receptor antagonist that seems to have additional
(perhaps independent) property of reducing chance of relapse when used in
conjunction with psychosocial treatment
 Acamprosate seems to enhance abstinence by a modulatory effect on NMDA
subtype of glutamate receptor

40
Alcohol
Withdrawal
Syndrome:

41
Alcohol
Withdrawal
Syndrome(2)

CNS Pharmacology
Lecture 9
Methanol (wood alcohol) poisoning
42
 Methanol is metabolized by ADH to formaldehyde, which is then oxidized to
formic acid, which is toxic
 Methanol produces blurred vision and other visual disturbances (“snowstorm”)
when poisoning has occurred
 In severe poisoning, bradycardia, acidosis, coma, and seizures are common
o Treatment of methanol toxicity includes the administration of ethanol
to slow the conversion of methanol to formaldehyde (ethanol has a
higher affinity for ADH)
o In addition to other supportive measures, dialysis is used to remove
methanol, and bicarbonate is administered to correct acidosis
o Fomepizole, an inhibitor of ADH that reduces the rate of
accumulation of formaldehyde, is also used to treat methanol (and
ethylene glycol) toxicity

CNS Pharmacology
Lecture 9
Withdrawal: Opioids
43
Abrupt discontinuation of drugs used for long-term abuse results
in withdrawal signs
 In general, these signs are opposite of those induced by drug:
o withdrawal from CNS excitatory drugs is inhibitory, and
o withdrawal from CNS depressants is excitatory
Rate and severity of withdrawal are lessened by tapered
cessation of drug use rather than abrupt cessation
 Withdrawal that is too rapid, particularly from CNS depressant
drugs, such as ethanol and barbiturates, can be life-threatening

CNS Pharmacology
Lecture 9
Opioid Withdrawal(3)
45

CNS Pharmacology
Lecture 9
Withdrawal: Benzodiazepines, and
Barbiturates
46

CNS Pharmacology
Lecture 9
IV: Cigarettes:
47
A. NICOTINE is active substance and is responsible for addictive nature
of cigarettes
1. Nicotine binds to nicotinic acetylcholine receptors, causing
dopamine release in ventral tegmental area of brain
2. Stimulation of CNS induces arousal, relaxation, and mild euphoria
3. Activation of sympathetic nervous system induces
vasoconstriction and
4. increase blood pressure
B. TARS AND CARBON MONOXIDE inhaled in cigarette smoke increase
risk of:
1. Chronic obstructive pulmonary disease (COPD)
2. Cancer
3. Heart disease

CNS Pharmacology
Lecture 9
Cigarettes(2)
48
C. PHYSICAL AND PSYCHOLOGICAL DEPENDENCE occurs. Abstinence
leads to anxiety, insomnia, and enhanced appetite that can last for
several months
D. Many approaches are available that increase the probability of
successfully abstaining from cigarettes
1. Physicians should follow the five As when counseling smokers
a. Ask patients if they smoke
b. Advise patients to quit smoking
c. Assess patients’ readiness to quit
d. Assist patients who would like to quit
e. Arrange for follow-up
.

CNS Pharmacology
Lecture 9
Cigarettes(3)
49
2. Nicotine is available in a patch, in gum, and in an inhaler
 These devices release nicotine more slowly compared
with smoking
3. Other aids are available for smoking cessation
a. Bupropion (Zyban) is an antidepressant
b. Varenicline (Chantix) is a nicotinic receptor partial
agonist
4. Behavioral modification programs and telephone quit lines
are also helpful

CNS Pharmacology
Lecture 9
V: CNS Stimulants: Sympathomimetics
50
A. COCAINE AND AMPHETAMINES are most commonly abused CNS
stimulants in Western society
B. Magnitude of euphoria depends on speed of onset:
1. Amphetamines can be taken orally, which results in a slow onset
 Can also be injected or crushed and snorted, which results in
a much faster onset
2. Cocaine can be ingested, chewed, snorted, injected, or smoked
a. Crack is free-base form of cocaine HCl
 It is formed by heating cocaine HCl in an alkaline solution
b. Smoked crack has most rapid onset and the most pleasurable
effects

CNS Pharmacology
Lecture 9
CNS Stimulants Mechanism of action
51
1. Cocaine blocks the DA transporter (DAT) also norepinephrine and
serotonin transporters(NET and SERT) at higher doses in CNS to
inhibit uptake of DA into nerve terminals in mesolimbic pathway
that includes “brain reward” center
 Blockade of NET also leads to increased sympathomimetic
activity
2. Amphetamine increases release of prejunctional neuronal
catecholamines, including DA and norepinephrine
 Amphetamine also exhibits some direct sympathomimetic
action and weakly inhibits MAO

CNS Pharmacology
Lecture 9
CNS Stimulants (3)
52
C. Stimulants produce euphoria with:
1. Enhanced self-confidence and alertness
2. Increased motor activity
3. Little physical dependence
 Fatigue is primary physical symptom during withdrawal
4. Strong psychological dependence
D. Period of euphoria varies depending on half-life of drug in body
1. Cocaine induces a very short euphoria (approximately 15
minutes), which is followed by a period of marked dysphoria
2. Euphoria from amphetamines has a much longer duration
E. Chronic abusers develop paranoid, psychotic-like symptoms

CNS Pharmacology
Lecture 9
CNS Stimulants (4)
53
F. OVERDOSES can be dangerous
1. Sympathomimetic actions can lead to tachycardia and
arrhythmias
2. Abusers can become aggressive and experience
hallucinations Other dangerous effects include
hypertension, hyperthermia, coma, and death.
3. Cocaine can also induce:
a. Gangrene, due to peripheral vasoconstriction
b. Perforation of nasal septum, due to
vasoconstriction in nasal mucosa
c. Convulsions, due to local anesthetic effects on
brain

CNS Pharmacology
Lecture 9
CNS Stimulants (5) Khat and Synthetic
Cathinones
54
 Cathinone is the psychoactive component in an evergreen shrub called
Khat native to East Africa and the Arabian Peninsula
 Synthetic cathinones, also known as “bath salts,” have become
increasingly popular products are packaged and labeled in such a way as to
circumvent detection, prosecution, and enforcement
 These are substances that are sold as something else at large profits
with an unstated understanding by seller and buyer that they will
produce intoxication
 Synthetic cathinones are not easily detected on urine toxicology
screens

CNS Pharmacology
Lecture 9
CNS Stimulants (5) Khat and Synthetic
Cathinones
55
 Methcathinone, butylone, methylene dioxypyrovalerone, and
naphyrone are just a few examples of synthetic cathinones
 These drugs increase the release and inhibit the reuptake of
catecholamines (norepinephrine, epinephrine, and dopamine) in a
manner very similar to cocaine and amphetamines
 A rapid onset of amphetamine-like stimulation with
psychotomimetic effects of variable duration is common with
synthetic cathinones

56
See: Kebede Y. Editorial. Should the Silence on Khat Be Allowed to
Continue in Ethiopia? Ethiop. J. Health Biomed Sci., 2009. Vol.2, No.1

CNS Pharmacology
Lecture 9
VI: Hallucinogens (psychotomimetics)
Marijuana (cannabis) and dronabinol (marinol)
57
 Active ingredient in marijuana is Δ-9 tetrahydrocannabinol (THC)
 MOA: it acts prejunctionally as an agonist to inhibit adenylyl cyclase
through G-protein-linked cannabinoid receptors
 Through disinhibition of DA neurons it inhibits activity of GABA
neurons in the ventral tegmentum area (VTA)
a. Cannabinol CB1 receptors, which account for most CNS
effects, are localized to cognitive and motor areas of the
brain
b. Cannabinol CB2-receptors are found in immune system
among other peripheral organs

CNS Pharmacology
Lecture 9
Cannabinoids
58
 Cannabinoids are effective antiemetics and appetite stimulants and
have some analgesic actions
 Dronabinol is a synthetic, orally active cannabinoid approved for
treatment of cachexia in patients with cancer or acquired
immunodeficiency syndrome (AIDS) and to treat emesis caused by
cancer chemotherapy in patients who do not respond to conventional
antiemetics
 Many also argue for use of smoked marijuana in treating chronic
pain, improving appetite in AIDS patients, and suppressing spasticity
in multiple sclerosis and spinal injury

CNS Pharmacology
Lecture 9
THE END
59

CNS Pharmacology
Lecture 9
60
Further study (SDL):
MedPharm Digital Guidebook: Unit 3-Drugs Used for CNS Disorders
Companion eNotes: CNS- Central Nervous System Pharmacology
Textbook Reading: Lüscher C. Drugs of Abuse Ch. 32
In: Katzung BG, ed. Basic & Clinical Pharmacology. 12th ed. Pgs. 565-79
Online resource center: Medical Pharmacology Cloud Folder

Lect. 9 Brain Reward Circuit and Drugs of Abuse

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Lect. 9 Brain Reward Circuit and Drugs of Abuse