DRUGS, BRAIN & BEHAVIOR
STUDY GUIDE
Unit I: Principles of Psychopharmacology
Lesson 1-1: Pharmacology: The Science of Drug Action (CH.1, pp. 4-7)
Objectives:
a) Distinguish among the three specialty areas within pharmacology.
b) Identify the different types of effects a drug can have.
Key Terms:
pharmacology
neuropharmacology
neuropsychopharmacology
psychopharmacology
drug action
drug effect
therapeutic effect
side effect
placebo
double-blind experiment
Lesson I-2:
Pharmacokinetic Factors Determining Drug Action, part 1 (CH. 1, pp.7-10)
Objectives:
a) Identify the pharmacokinetic components of drug action..
b) Describe the hazards associated with the intravenous use of street drugs.
c) Compare the selected routes of administration shown in Table 1.1
Key terms:
bioavailability
pharmacokinetic
depot binding
biotransformation
oral administration
absorption
first-pass effect
intravenous (IV)
intramuscular (IM)
intraperitoneal (IP)
subcutaneous (SC)
topical
transdermal
epidural
intracranial
intracerebroventricular
Lesson I-3:
Pharmacokinetic Factors Determining Drug Action, part 2 (CH. 1, pp.11-16)
a) Identify the factors that contribute to drug absorption.
b) Describe the structure of cell membranes.
c) Name the two factors that contribute to ionization.
d) Discuss the effect of ionization on absorption.
e) Explain why medication is often prescribed to be taken before meals.
f) Describe the effects of size and sex on blood plasma levels.
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g) List the organs where drugs are found in the highest concentrations.
h) Explain how the blood-brain barrier works.
i) Give examples of substances that can pass through the placental barrier.
Key terms:
psychoactive drug
phospholipid
passive diffusion
concentration gradient
ionization
teratogen
Lesson I-4:
Pharmacokinetic Factors Determining Drug Action, part 3 (CH.1, pp. 16-21)
Objectives
a) Identify four significant effects of depot binding.
b) Distinguish between first-order and zero-order kinetics.
c) Distinguish between Type I and Type II biotransformation.
d) Discuss the four main factors influencing drug metabolism.
e) Determine the most important route of elimination of drugs from the body.
Key terms:
drug depot
depot binding
first-order kinetics
half-life
zero-order kinetics
biotransformation
microsomal enzyme
cytochrome P450
enzyme induction
enzyme inhibition
drug competition
genetic polymorphism
Lesson I-5:
Pharmacodynamics: Drug-Receptor Interactions (CH.1, pp.21-26)
Objectives:
a) Compare the two types of receptors (Figure 1.10).
b) Identify five characteristics of receptors.
c) Describe the information conveyed in a dose- response curve.
d) Explain how one computes the therapeutic index of a drug.
e) Distinguish between the two types of antagonists.
Key Terms:
pharmacodynamics
receptor
ligand
affinity
efficacy
up-regulation
down-regulation
receptor subtype
potency
therapeutic index
competitive antagonist
noncompetitive antagonist
physiological antagonism
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additive effect
potentiation
Lesson I-6:
Behavioral Effects of Chronic Drug Use (CH.1, pp. 27- 31)
Objectives:
a) Identify the characteristics of drug tolerance.
b) Compare metabolic, pharmacodynamic, and behavioral tolerance.
c) Discuss the role of classical conditioning, operant conditioning, and state-dependent learning in
drug tolerance.
Key Terms:
tolerance
cross-tolerance
acute tolerance
habituation
sensitization
Lesson I-7:
Cells of the Nervous System (CH.2, pp. 34-40)
Objectives:
a) Distinguish among the three types of neurons.
b) Describe the components of the dendrite, axon, and soma.
c) Identify the characteristics of ion channels.
d) Distinguish between the ligand-gated and voltage-gated channels.
e) Discuss the function of the four main types of glial cells.
Key terms:
neuron
glial cell
cytoplasm
extracellular fluid
mitochondria
synapse
convergence
divergence
dendritic spines
axon hillock
collaterals
terminal button
synaptic vesicle
neurotransmitter
myelin
nodes of Ranvier
chromosome
gene
coding region
transcription factor
promotion region
transcription
translation
axoplasmic transport
cytoskeleton
receptor
enzyme
transporter protein
Schwann cell
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olgodendroglia
astrocyte
microglia
Lesson I-8:
Electrical Transmission within a Neuron (CH.2, pp. 40-47)
Objectives:
a) Identify the forces responsible for the resting potential.
b) Describe the effects of depolarization and hyperpolarization.
c) Identify the characteristics of local potentials.
d) Summarize the events that take place in an action potential.
e) Compare the speed of conduction in myelinated and unmyelinated axons.
f) Explain how local anesthetics such as Novocaine work.
Key terms:
polarized
electrostatic pressure
concentration gradient
equilibrium potential
sodium-potassium (Na+ - K+) pump
action potential
threshold
local potential
excitatory postsynaptic potential (EPSP)
inhibitory postsynaptic potential (IPSP)
summation
integration
absolute refractory period
relative refractory period
saltatory conduction
Lesson I-9:
Organization of the Nervous System, part 1 (CH.2, pp. 47-54)
Objectives:
a) Describe the function of each part of the nervous system shown in Figure 2.15.
b) Explain the purpose of the 12 pairs of cranial nerves.
c) Describe the function of CSF.
Key terms:
sensory afferent
motor efferent
meninges
dura matter
arachnoid
pia mater
cerebral ventricle
central canal
Lesson I-10:
Organization of the Nervous System, part 2 (CH.2, pp. 54-60)
a) Identify the brain areas that make up the six anatomical divisions of the adult CNS and describe
the function of each one.
Key terms:
nuclei
tract
ganglia
nerve
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brain stem
area postrema
reticular formation
locus coeruleus
dorsal
median raphe nuclei
cerebellum
cerebellar peduncle
periaqueductal gray (PAG)
substantia nigra
ventral tegmental area (VTA)
basal ganglia
limbic system
cingulate
hippocampus
amygdala
nucleus accumbens
fissure
sulci
gyri
corpus callosum
primary cortex
secondary cortex
tertiary association area
Lesson I-11:
Chemical Signaling between Nerve Cells (CH. 3 pp. 64-65)
Objectives:
a) Compare axodendritic, axosomatics, and axoaxonic synapses.
Key terms:
presynaptice cell
postsynaptic cell
synaptic cleft
synaptic vesicle
mitochondrion
presynaptic inhibition
presynaptic facilitation
neuromuscular junction
Lesson I-12:
Neurotransmitter Synthesis, Release, & Inactivation (CH.3, pp.65-72)
Objectives:
a) List the six criteria for verifying a chemical’s status as a neurotransmitter.
b) Distinguish among the major categories of neurotransmitters (Table 3.1).
c) Identify members of each category of neurotransmitters (Table 3.1).
d) Explain how neuropeptides differ from other neurotransmitters.
e) Summarize each of the steps shown in Figure 3.5 and Figure 3.6.
f) Identify the mechanisms that regulate neurotransmitter.
g) Describe the ways that neurotransmitter molecules can be inactivated.
Key terms:
amino acid
monoamine
precursor
neuropeptide
lipid
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gaseous transmitter
neuromodulator
exocytosis
active zone
endocytosis
vesicle recycling
autoreceptor
terminal autoreceptor
somatodendritic autoreceptor
heteroreceptor
transporter
reuptake
Lesson I-13:
Neurotransmitter Receptors and Second-Messenger Systems (CH.3, pp.72-77)
Objectives:
a) Identify the two key concepts necessary for understanding neurotransmitter receptors.
b) Compare ionotropic and metabotropic receptors (Table 3.2).
c) Discuss the role of G proteins and protein kinases in neurotransmission.
d) Describe the mechanism of action of second messengers.
e) Discuss the significance of tyrosine kinase in the nervous system.
f) Explain what makes NO unique as a neurotransmitter.
Key terms:
receptor subtype
subunit
second messenger
transmembrane domain
G protein
effector enzyme
protein kinase
phosphorylation
cyclic adenosine monophosphate (cAMP)
tyrosine kinase receptor
neurotrophic factor
nerve growth factor (NGF)
Lesson I-14:
Pharmacology of Synaptic Transmission (CH.3, pp.78-80)
Objectives:
a) Summarize the mechanisms by which drugs can alter synaptic transmission (Figure 3.14).
Lesson I-15:
The Endocrine System (CH. 3, pp.80-87)
Objectives:
a) Identify the major endocrine glands and their location in the body.
b) Explain the function of glucocorticoids such as cortisol.
c) Describe two important roles of testosterone.
d) Distinguish between the effects of an underactive and overactive thyroid.
e) Identify the function of each hormone secreted by the pituitary.
f) Compare the function of peptide hormones with that of steroid and thyroid hormones.
Key terms:
hormone
endocrine gland
adrenal gland
adrenal medulla
epinephrine (EPI)
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norepinepherine (NE)
adrenal cortex
glucocorticoid
cortisol
steroid
gonads
ovaries
testes
estrogen
progesterone
androgen
islets of Langerhans
insulin
glucagon
thyroid gland
thyroxine (T4)
triiodothyronine (T3)
pineal gland
melatonin
pituitary gland
anterior pituitary
thyroid-stimulating hormone (TSH)
adrenocorticotropic hormone (ACTH)
follicle-stimulating hormone (FSH)
leutinizing hormone (LH)
growth hormone (GH)
prolactin (PRL)
hypothalamic-releasing hormone
thyrotropin-releasing hormone (TRH)
corticotropin-releasing hormone (CRH)
gonadotropin-releasing hormone (GnRH)
vasopressin
oxytocin
Lesson I-16:
Catecholamine Synthesis, Release, and Inactivation (CH.5, pp.120-124)
Objectives:
a) Summarize the steps in the synthesis of catecholamine neurotransmitters.
b) Discuss the therapeutic benefit of L-DOPA and AMPT.
c) Explain why vesicular packaging is important.
d) Describe the effects of reserpine, amphetamine, and methamphetamine.
e) Explain how autoreceptors inhibit catecholamine release.
f) Specify the two processes that inactivate catecholamines.
g) Compare the effects of tricyclic antidepressants, reboxetine, and cocaine.
h) Explain how MAO and COMT inhibitors work.
Key Terms:
dopamine (DA)
norepinephrine (NE)
epinephrine (EPI)
catecholamine
monoamine
biogenic amine
adrenergic
noradrenergic
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dopaminergic
tyrosine
tyrosine hydroxylase (TH)
aromatic amino acid decarboxylase (AADC)
dopamine B-hydroxylase (DBH)
rate-limiting enzyme
L-DOPA
a-methyl-para-tyrosine (AMPT)
vesicular monoamine transporter (VMAT)
reserpine
amphetamine
methamphetamine
stereotyped behavior
clonidine
yohimbine
DA transporter
NE transporter
tricyclic antidepressant
reboxetine
cocaine
catechol-O-methyltransferase (COMT)
monoamine oxidase (MAO)
MAO inhibitor
phenelzine
tranylcypromine
entacapone (Comtan)
tolcapone (Tasmar)
volume transmission
Lesson I-17:
Organization and Function of the Dopaminergic System (CH.5, pp.124-132)
Objectives:
a) Distinguish among the three major dopaminergic pathways.
b) Discuss the effects of lesions of the dopaminergic pathways in animals.
c) Compare the effects of the two most common subtypes of dopamine receptors.
d) Describe the typical effects of DA receptor agonists and antagonists.
e) Compare the effects of 6-OHDA and haloperidol.
Key Terms:
substantia nigra
ventral tegmental area (VTA)
nigrostriatal tract
mesolimbic dopamine pathway
mesocorical dopamine pathway
6-hydroxydopamine (6-OHDA)
neurotoxin
Parkinson’s disease (PD)
apomorphine
catalepsy
haloperidol
behavioral supersensitivity
receptor up-regulation
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Lesson I-18:
Organization and Function of the Noradrenergic System (CH.5, pp132-137)
Objectives:
a) Discuss the function of the locus coeruleus.
b) Identify he two routes by which NE can reach the heart.
c) Compare the effects of alpha and beta adrenoreceptors.
d) List the behavioral functions of NE.
e) Discuss the therapeutic benefits of adrenergic agonists and antagonists.
Key Terms:
locus coeruleus (LC)
vigilance
adrenoceptors
phenylephrine
isoproterenol
dexmedetomidine (Precedex)
albuterol
prazosin
propranolol
metoprolol
Unit II: Neurotransmitters, Alcohol and Opiates
Lesson II-1:
Acetylcholine Synthesis, Release, and Inactivation (CH.6, pp.140-144)
Objectives:
a) Explain how ACh is synthesized in the body.
b) Name the factors that affect the rate of ACh synthesis.
c) Describe the effect of vesamicol treatment on ACh levels.
d) List the symptoms of overactivity of the cholinergic system.
e) Identify the location and function of AChE in the body.
f) Discuss the uses of drugs that block AChE.
g) Explain how nerve gas antidotes work.
Key Terms:
choline
acetyl coenzyme A (acetyl CoA)
choline acetyltransferase (ChAT)
vesicular ACh transporter
vesamicol
acetylcholinesterase (AChE)
choline transporter
physostigmine (Eserine)
neostigmine (Prostigmin)
pyridostigmine (Mestinon)
myasthenia gravis
autoimmune disorder
Sarin
Soman
Lesson II-2:
Organization & Function of the Cholinergic System (CH.6, pp.144-151)
Objectives:
a) Describe the role of ACh in the sympathetic and parasympathetic nervous system.
b) Explain why anticholinergic drugs are prescribed instead of L-DOPA in the early stages of
Parkinson’s Disease.
c) Cite evidence that ACh plays a role in cognitive functioning.
d) Identify the two ACh receptor subtypes.
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e) Discuss the location, structure, and function of nicotinic receptors.
f) Give examples and describe the effects of nicotinic receptor agonists and antagonists.
g) Discuss the location and function of muscarinic receptors.
h) Give examples and describe the effects of muscarinic receptor agonists and antagonists.
Key Terms:
orphenadrine (Norflex)
benztropine mesylate (Cogentin)
trihexyphenidyl (Artane)
basal forebrain cholinergic system (BFCS)
nicotinic receptor
muscarinic receptor
nicotine
alkaloid
muscarine
desenstitized
resensitize
depolarization block
succinylcholine
D-tubocurarine
dry-mouth effect
pilocarpine
arecoline
parasympatholytic agents
atropine
scopolamine
Lesson II-3:
Serotonin Synthesis, Release, and Inactivation (CH.6, pp.151-154)
Objectives:
a) Identify the two steps in the synthesis of serotonin (5-HT).
b) Explain why protein-rich diets do not increase 5-HT levels in the brain whereas diets low in
protein and high in carbohydrates do.
c) Discuss the similarities and differences between 5-HT and the catecholamines (DA and NE).
Key Terms:
serotonin (hydroxytryptamine or 5-HT)
tryptophan
tryptophan hydroxylase
5- hydroxytryptophan (5-HTP)
aromatic amino acid decarboxylase (AADC)
serotonergic
insulin
para-chloroamphetamine
fenfluramine
3,4-methylenedioxymethamphetamine (MDMA)
5- HT transporter
fluoxetine (Prozac)
selective serotonin reuptake inhibitor (SSRI)
5-hydroxyindoleacetic acid (5-HIAA)
Lesson II-4:
Organization and Function of the Serotonergic System (CH.6, pp.155-160)
Objectives:
a) Identify the location of most serotonergic neurons.
b) Discuss the function of serotonergic neurons in the dorsal raphe nucleus.
c) List the two major mechanisms by which 5-HT1A receptors work.
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d) Describe the effects of 5-HT1A agonists.
e) Identify the mechanism by which 5-HT2A receptors work.
f) Describe the effects of 5-HT2A agonists in humans.
g) Explain how clozapine and risperidone work.
Key Terms:
raphe nuclei
dorsal raphe nucleus
median raphe nucleus
hyperphagia
buspirone (Buspar)
hypothermia
hallucinogenic
lysergic acid diethylamide (LSD)
clozapine (Clozaril)
risperidone (Risperdal)
Lesson II-5:
Glutamate Synthesis, Release, and Inactivation (CH.7, pp.164-166)
Organization and Function of the Glutamatergic System, part 1 (CH.7, pp.166-169)
Objectives:
a) Indicate how glutamate differs from other neurotransmitters.
b) Briefly describe the synthesis release, and transport of glutamate
c) Discuss the role of glutamate in ALS.
d) Describe the function of glutamate in the nervous system.
e) Compare the three subtypes of ionotropic glutamate receptors.
f) Discuss the role of co-agonists in NMDA receptors.
g) Explain how PCP and ketamine interact with glutamate receptors.
Key Terms:
glutamate
aspartate
excitatory amino acid neurotransmitter
glutamatergic neuron
glutamine
glutaminase
vesicular glutamate transporter (VGLUT)
excitatory amino acid transporter (EEAT)
amyotrophic lateral sclerosis
glutamine synthetase
AMPA receptor
kainite receptor
NMDA receptor
glycine
D-serine
co-agonist
phencyclidine (PCP)
ketamine
Lesson II-6:
Organization and Function of the Glutamatergic System, part 2 (CH.7, pp.169-176)
a) Cite evidence that NMDA receptors play a key role in learning.
b) Identify the effects of monosodium glutamate (MSG) on the brain.
c) Discuss the excitotoxicity hypothesis.
d) Distinguish between apoptosis and necrosis.
e) Describe the effects of domoic acid poisoning.
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f) Discuss methods of treatment for ischemia.
Key terms:
long-term potentiation (LTP)
excitotoxicity hypothesis
necrosis
lysis
apoptosis
domoic acid
ischemia
Lesson II-7:
GABA Synthesis, Release, and Inactivation (CH.7, pp. 176-178)
Organization and Function of the GABAergic System (CH.7, pp.178-182)
Objectives:
a) Identify the two major inhibitory amino acid neurotransmitters.
b) Explain how GABA is synthesized in the body.
c) Discuss the therapeutic use of tiagabine and vigabatrin.
d) Indicate where GABA is found in the brain.
e) Distinguish between the function of GABAA and GABAB receptors.
f) Describe the effects of muscimol and of GABAA antagonists such as bicuculline.
g) Explain how BDZs exert their influence on GABAA receptors.
Key Terms:
GABA
glutamic acid decarboxylase (GAD)
vesicular GABA transporter (VGAT)
tiagabine (Gabitril)
GABA aminotransferase (GABA-T)
vigabatrin (Sabril)
GABAA receptor
GABAB receptor
muscimol
bicuculline
benzodiazepine (BDZ)
barbituate
ethanol
diazepam (Valium)
inverse agonist
neurosteroids
baclofen (Lioresal)
Lesson II-8:
Introduction to Drug Abuse and Addiction (CH.8, pp. 186-190)
Features of Drug Abuse and Dependence (CH.8, pp.190-196)
Objectives:
a) Identify four trends that have influenced modern patterns of drug use and regulation in the U.S.
b) List the two principle aims of the Harrison Act.
c) Describe the regulatory function of the Controlled Substance Act.
d) List three features of recent conceptions of addiction.
e) Distinguish between substance abuse and substance dependence.
f) Summarize the information in Figures 8.4 and 8.5.
g) Distinguish among the five classes of drugs in the Schedule of Controlled Substances and give
examples of each class.
h) List the five different categories for drug abuse potential.
i) Summarize the findings in Table 8.4.
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Key Terms:
craving
remission
relapse
substance dependence
substance abuse
substance-induced disorders
continuum of drug use
Schedule of Controlled Substances
Lesson II-9:
Models of Drug Abuse and Dependence, part 1 (CH.8, pp.196-207)
Objectives:
a) Summarize the basic principles of the physical dependence model of addiction.
b) Identify three criticisms of the physical dependence model.
c) Summarize the basic principles of the positive reinforcement model.
d) Explain how the progressive-ratio procedure is used to measure the relative strength of drug
reinforcement.
e) Give a possible reason why reinforcement may occur (see Box 8.2).
f) Identify the limitation of the positive reinforcement model.
g) Compare the incentive-sensitization and opponent-process models of addiction.
h) Summarize the revisions made by Koob & LeMoal to the opponent-process model.
i) Distinguish between the two different types of disease models.
j) Identify two key benefits and three criticisms of the disease model.
Key Terms:
physical dependence model
abstinence syndrome
drug detoxification
positive reinforcement model
progressive-ratio
breaking point
euphoria
incentive-sensitization model
opponent-process model
incentive salience
neuroadaptation
counteradaptation
dysphoria
disease model (medical model)
susceptibility model
loss of control
exposure model
moral model
Lesson II-10: Toward a Comprehensive Model of Drug Abuse and Dependence (CH.8, pp. 207-213)
Objectives:
a) Summarize the information in Table 8.5.
b) Discuss the reinforcing effects of drugs at the behavioral and neural level.
c) Describe a gender difference with respect to comorbidity.
d) Compare the three personality-related pathways to addiction.
e) List four different functions served by drug abuse.
f) Identify two different ways to think about protective factors in drug addiction.
Key Terms:
biopsychosocial model
primers
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comorbidity
self-medication hypothesis
Lesson II-11: Psychopharmacology of Alcohol, part 1 (CH.9, pp.216-222)
Objectives:
a) Discuss the effects of the Eighteenth Amendment.
b) Indicate how alcohol is produced and how alcohol concentration is increased.
c) Explain the concept of “proof.”
d) Identify the factors that affect alcohol absorption and distribution.
e) Compare the metabolism of alcohol to that of other drugs.
Key Terms:
blood alcohol concentration (BAC)
alcohol dehydrogenase
acetaldehyde dehydrogenase (ALDH)
cytochrome P450
induction
Lesson II-12: Psychopharmacology of Alcohol, part 2 (CH.9, pp.222-231)
Objectives:
a) Identify four mechanisms that contribute to alcohol tolerance.
b) Offer some possible explanations for hangover.
c) Describe the symptoms of alcohol withdrawal.
d) Discuss the effects of alcohol on the CNS.
e) Summarize the causes and symptoms of Wernicke-Korsakoff syndrome.
f) Discuss the effects of alcohol on the cardiovascular, renal-urinary, reproductive and
gastrointestinal systems, as well as the liver.
Key Terms:
tolerance
cross-tolerance
acute tolerance
drug disposition tolerance
pharmacodynamic tolerance
behavioral tolerance
physical dependence
cross dependence
hangover
delirium tremens
blackout
alcohol poisoning
Wernicke-Korsakoff syndrome
fatty liver
alcoholic hepatitis
alcoholic cirrhosis
Lesson II-13: Neurochemical Effects on Alcohol (CH. 9, pp.231-237)
Objectives:
a) Compare the specific and non-specific effects of alcohol.
b) Explain how alcohol affects glutamate, GABA, dopamine, and opioid systems.
Key Terms:
nonspecific action
specific action
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Lesson II-14: Alcoholism (CH.9, pp.237-243)
a) Identify the DSM-IV criteria used in the diagnosis of alcohol dependence and abuse.
b) Discuss the relationship of gender and age with alcohol consumption.
c) Identify the psychological, neurobiological, and sociocultural factors that contribute to
alcoholism.
d) Compare psychosocial and pharmacotherapeutic approaches to alcohol treatment.
Key Terms:
alcoholism
binge drinking
alcohol abuse
alcohol dependence
linkage studies
case-control method
denial
enabler
detoxification
psychosocial rehabilitation
pharmacotherapeutic treatment
Lesson II-15: Narcotic Analgesics (CH.10, pp. 246-249)
Opioid Receptors and Endogenous Neuropeptides (CH.10, pp.249-256)
Objectives:
a) Compare the effects of morphine and heroin.
b) Discuss the effects of opioids on the CNS and the gastrointestinal tract.
c) Distinguish among the three opioid receptor subtypes.
d) Identify endogenous opioids and the brain areas where they are produced.
e) Describe three ways that opioids reduce synaptic transmission.
Key Terms:
narcotic analgesic
anesthetic
partial agonist
pure antagonist
mixed agonist-antagonist
transfection
receptor cloning
endorphin
prodynorphin
pro-opiomelanocortin (POMC)
proenkephalin
endomorphin
Lesson II-16: Opioids and Pain (CH.10, pp. 256-260)
Objectives:
a) Compare the two components of pain.
b) List three ways that opiates regulate pain.
c) Identify two ways that opioids reduce the transmission of pain signals at the spinal cord.
d) Discuss the role of the PAG in pain transmission.
Key Terms:
spinal interneurons
descending modulatory pathways
supraspinal
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Lesson II-17: Opioid Reinforcement, Tolerance, and Dependence (CH.10, pp. 260-266)
Objectives:
a) Describe the effects of opiates on the VTA.
b) Identify three consequences of chronic opioid use.
c) Describe the symptoms of opiate withdrawal.
d) Discuss the addiction potential of opiates in chronic pain sufferers.
e) Indicate which brain areas are implicated in the physiological response to opiate withdrawal.
f) Summarize Himmelsbach’s hypothesis of opioid tolerance and dependence.
g) Identify the acute effects of opioids on µ-receptors.
h) Discuss the role of environmental cues in tolerance, abuse, and relapse.
Key Terms:
cross-tolerance
withdrawal
abstinence syndrome
detoxified
cross dependence
primer
Lesson II-18: Treatment Programs for Opiate Addiction (CH.10, pp.266-272)
Objectives:
a) Identify the three characteristics of biopsychosocial models of therapy.
b) Describe the effects of methadone and clonidine in detoxification.
c) Discuss the effectiveness of methadone maintenance.
d) Give five reasons why methadone is used in opiate drug treatment programs.
e) Explain why LAAM and buprenorphin are used in place of methadone.
f) Explain why the use of narcotic antagonists such as Naltrexone has only limited usefulness.
Key Terms:
methadone
clonidine
LAAM
buprenorphine
multidimensional approach
Units III: Drug Pharmacology, Mechanisms, and Effects
Lesson III-1:
Background and History (CH.11, pp.276-277)
Basic Pharmacology of Cocaine (CH.11, pp.277-279)
Mechanisms of Cocaine Action (CH.11, pp.279-280)
Objectives:
a) Identify the source and method of production of cocaine HCl and crack.
b) Compare the effects of the different routes of consumption of cocaine.
c) Describe what happens to cocaine in the bloodstream.
d) Identify the combined effects of cocaine and alcohol.
e) Compare the effect of cocaine on 5-HT, DA, and NE transporters.
f) Discuss the anesthetic effect of cocaine.
Key Terms:
psychomotor stimulant
freebasing
crack
benzoylecgonine
cocaethylene
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Lesson III-2:
Acute Behavioral and Physiological Effects of Cocaine (CH.11, pp.280-286)
Objectives:
a) Describe the typical aspects of the cocaine “high.”
b) Discuss the physiological consequences of acute cocaine administration and the potential
adverse consequences of heavy cocaine use.
c) Compare the neurochemical effects of cocaine and amphetamine.
d) Identify two factors that determine the rewarding and reinforcing effects of cocaine.
e) Discuss the research of Volkow et al.
f) Compare D1 and D2 receptors.
Key terms:
focused stereotype
sympathomimetic
Lesson III-3: Cocaine Abuse and the Effects of Chronic Cocaine Exposure (CH.11, pp.286-292)
Objectives:
a) Identify the factors that affect the long-term abuse potential of cocaine.
b) Explain how psychostimulants can produce both tolerance and sensitization.
c) Distinguish between the two phases of sensitization.
d) Identify the three phases of the cocaine abstinence syndrome.
e) Explain why the negative mood state and craving associated with cocaine withdrawal occur.
f) Discuss the health consequences of cocaine use.
g) Explain why desipramine is used in the treatment of cocaine addiction.
h) Identify possible cognitive deficits associated with cocaine use (see Box 11.1).
i) Describe psychosocial treatment programs for cocaine addiction.
j) Discuss the approach to treatment developed by Higgins et al.
Key Terms:
cocaine binge
induction
expression
psychosocial treatment program
relapse prevention therapy
Lesson III-4:
The Amphetamines
Background and History (CH.11, pp. 292-294)
Basic Pharmacology of Amphetamine (CH.11, p.294)
Mechanisms of Amphetamine Action (CH.11, pp.294-295)
Behavioral and Neural Effects of Amphetamine (CH.11, pp. 295-296)
Objectives:
a) Identify five common amphetamines and two naturally-occurring plant compounds that are
similar in structure to amphetamines.
b) Describe the health risks associated with ephedra use
c) Compare the effects of amphetamine and methamphetamine.
d) Discuss the mechanisms of amphetamine action.
e) List the physical and psychological symptoms of amphetamine use.
f) Cite evidence of methamphetamine neurotoxicity.
Lesson III-5: MDMA—The Entactogenic Amphetamine (CH.11, pp.296-300)
a) Explain why MDMA is called an “entactogen.”
b) Describe the symptoms of MDMA use.
c) Explain how MDMA differs from other amphetamines.
d) Discuss the use of methylphenidate in the treatment of ADHD (see Box 11.2).
e) Describe the effects of MDMA on serotonergic pathways and on cognitive functions.
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Lesson III-6:
Nicotine:
Background and History (CH.12, p.304)
Basic Pharmacology of Nicotine and Its Relationship to Smoking (CH.12, p.304-306)
Mechanisms of Action (CH.12, p.306)
Behavioral and Physiological Effects (CH.12, pp.307-312)
Objectives:
a) Explain why smoking has such powerful reinforcing effects.
b) Describe the process by which nicotine is metabolized.
c) Discuss the mechanism of action of nicotine in the brain.
d) Describe the effects of nicotine on mood and cognitive function.
e) Explain how the dopamine system mediates nicotine’s reinforcing effects.
f) Identify the effects of nicotine on the sympathetic and parasympathetic nervous system.
g) Describe the symptoms of nicotine poisoning
h) Explain why smokers often find the first cigarette of the day most pleasurable.
i) Summarize the findings of Foulds et al (1997).
j) Discuss the mechanism underlying the nicotine abstinence syndrome.
Key Terms:
tar
cotinine
cytochrome P450 2A6 (CYP2A6)
methoxsalen
nicotinic cholinergic receptors (nAChRs)
Lesson III-7:
Cigarette Smoking (CH.12, pp.313-319)
Objectives:
a) Summarize the findings of the 2002 National Survey on Drug Use and Health.
b) Identify possible reasons why teenagers take up smoking.
c) Cite evidence that nicotine is a key factor in smoking.
d) Describe the symptoms of nicotine abstinence syndrome.
e) Discuss the role of reinforcement and MAO inhibition in smoking.
f) Summarize the adverse health effects of smoking.
g) Compare behavioral and pharmacological interventions to treat tobacco dependence.
Key Terms:
nicotine resource model
deprivation reversal model
chipper
nicotine replacement
Lesson III-8:
Caffeine:
Background (CH.12, p.319)
Basic Pharmacology of Caffeine (CH.12, pp.319-320)
Behavioral and Physiological Effects (CH.12, pp.320-321)
Mechanisms of Action (CH.12, pp.321-324)
Objectives:
a) Indicate how caffeine is absorbed and excreted.
b) Compare the effects of low and high doses of caffeine.
c) Identify the physiological actions of caffeine that may have subjective effects.
d) Name two therapeutic uses of caffeine.
e) Cite evidence of caffeine tolerance.
f) List the symptoms of caffeine withdrawal.
g) Identify possible health risks associated with caffeine.
h) Discuss the mechanisms of action of caffeine.
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i) Describe the function of adenosine in the brain.
Key Terms:
adenosine
caffeinism
Lesson III-9:
Marijuana and the Cannabinoids:
Background and History of Marijuana (CH.13, p.328-329)
Basic Pharmacology of Marijuana (CH.13, p.329-330)
Mechanisms of Action (CH.13, p.331-332)
Objectives:
a) Identify two forms in which cannabis is obtained.
b) Describe the effect of breathhold duration on the subjective effects of THC.
c) Compare the effects of oral THC consumptions versus smoking.
d) List the brain areas in which cannabinoid receptors are found.
e) Discuss the effects of CB1 receptors.
f) Explain how endocannabinoids differ from other neurotransmitters.
g) Indicate how endocannabinoids are released and metabolized.
h) Discuss the mechanism of action of endocannabinoids.
Key Terms:
cannabinoids
Δ9-tetrahydrocannabinol (THC)
sinsemilla
hashish
hash oil
cannabinoid receptor
CB1
CB2
anandamide
endocannabinoids
fatty acid amide hydrolase (FAAH)
retrograde messenger
Lesson III-10:Acute Behavioral and Physiological Effects of Cannabinoids (CH.13, pp.333-340)
Objectives:
a) Describe the four stages of subjective and behavioral effects associated with cannabis.
b) List the physiological effects of cannabis.
c) Identify the adverse effects of cannabis use.
d) Cite evidence that expectancy influences the effects of cannabis.
e) Offer two possible explanations why the maximum level of intoxication occurs when plasma
THC levels are declining.
f) Describe the effects of cannabis on cognitive and psychomotor performance.
g) Cite evidence that THC is reinforcing.
h) Discuss the role of DA and opioid systems in cannabis reinforcement.
i) Explain what is meant by “cross-talk” of endocannabinoid systems.
Key Terms:
hyperalgesia
Lesson III-11:Cannabis Abuse and the Effects of Chronic Cannabis Exposure (CH.13, pp. 340-345)
Objectives:
a) Identify risk factors in the development of heavy cannabis use by teenagers.
b) Indicate whether or not marijuana tolerance occurs.
c) List the symptoms of cannabis dependence and withdrawal.
d) Discuss the neurochemical basis of cannabis abstinence syndrome.
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e) Describe common methods of treatment for cannabis dependence.
f) Identify the adverse psychological and health effects of chronic cannabis use.
Key Terms:
precipitated withdrawal
amotivational syndrome
Lesson III-12:Mescaline (CH.14, p.348)
Psilocybin, DMT, and 5-MeO-DMT (CH.14, pp.348-350)
LSD (CH.14, pp.350-352)
Objectives:
a) Identify the sources and methods of ingestion of: mescaline, psilocybin, and DMT.
b) Highlight the history of LSD (including information in Box 14.1).
Key Terms:
lysergic acid diethylamide (LSD)
mescaline
psilocybin
dimethyltryptamine (DMT)
psychotomimetic
psychedelic
hallucinogenic
peyote cactus
peyote button
psilocin
pscycholytic therapy
psychedelic therapy
Lesson III-13:Pharmacology of Hallucinogenic Drugs (CH.14, pp.352-358)
Objectives:
a) Compare the subjective effects of different hallucinogens.
b) Describe the four phases of an LSD “trip”.
c) Identify two classes of hallucinogens.
d) Describe the mechanism of action of LSD.
e) Summarize the findings of Vollenweider et al (1998).
f) Discuss the mechanism underlying the high rate of tolerance of hallucinogens.
g) Offer two hypotheses concerning the neural mechanisms of hallucinogens.
h) Discuss the addictive potential of hallucinogens.
i) Identify the most common problems associated with hallucinogen use.
Lesson III-14: Therapies for Affective Disorders (CH.16, pp.394-401)
Objectives:
a) List the three major classes of antidepressants
b) Indicate when MAO-I’s are prescribed.
c) Identify the mechanism of action and side effects of MAO-I’s.
d) Identify the mechanism of action and side effects of tricyclic antidepressants.
e) Identify the mechanism of action and side effects of SSRI’s.
f) Identify the mechanism of action and side effects of ECT.
g) Identify the mechanism of action and side effects of lithium.
Key Terms:
MAO inhibitor (MAO-I)
tricyclic antidepressant (TCA)
selective serotonin reuptake inhibitors (SSRI)
serotonin syndrome
dual NE/5- HT modulator
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lithium carbonate
Lesson III-15: Drugs for Treating Anxiety (CH.17, pp.420-430)
Objectives:
a) List the effects of anxiolytics.
b) Compare the pharmacokinetics of the three classes of barbiturates.
c) Identify four side effects of barbiturates.
d) Describe the illicit uses of barbiturates.
e) Describe the therapeutic uses of BDZ’s.
f) Name the advantages of BDZ’s over barbiturates.
g) List the symptoms associated with the abstinence syndrome for BDZ’s.
h) Compare busiprone to BDZ’s.
i) Offer a possible explanation for the use of SSRI’s to treat OCD.
Key Terms:
anxiolytic
sedative- hypnotic
CNS depressant
ultrashort-acting
short/ intermediate-acting
long-acting
hypnotic
muscle relaxant
anticonvulsant
alcohol
barbiturate withdrawal
Lesson III-16: Neurochemical Basis of Anxiety and Anxiolytics (CH.17, pp.430-438)
Objectives:
a) Explain how GABA works.
b) Distinguish between the mechanism of action of BDZs and barbiturates.
c) Describe the role of amygdale and prefrontal cortex in anxiety.
d) Cite evidence that GABA is important in the reduction of anxiety.
e) Cite evidence that multiple brain areas are involved in the response to anxiety.
f) Compare the effects of two types of endogenous ligands for BDZ receptors.
g) Summarize the findings of PET research with panic-disorder patients.
h) Briefly describe the role of the following in anxiety: norepinephrine, CRF, dopamine, and
serotonin.
Lesson III-17: Classic Neuroleptics and Atypical Antipsychotics (CH.18, pp.447-458)
Objectives:
a) Identify the two classes of neuroleptics and give examples of each.
b) Describe the psychokinetics of neuroleptics.
c) Discuss the mechanism of action of neuroleptics.
d) Indicate how neuroleptics affect HVA levels.
e) Identify the four dopamine pathways in the brain.
f) Describe the common side effects of classic neuroleptics.
g) List three differences between the second-generation and classic neuroleptics.
h) Discuss the benefits of each of three classes of second-generation neuroleptics.
Key Terms:
neuroleptic
law of thirds
parkinsonian symptoms
tardive dyskinesia (TD)
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neuroleptic malignant syndrome (NMS)
selective D2 receptor antagonist
broad-spectrum antipsychotic
dopamine system stabilizer
Lesson III-18: Neurochemical Models of Schizophrenia (CH.18, pp.463-467)
Objectives:
a) Cite evidence supporting the dopamine hypothesis, neurodevelopmental model, and glutamatedopamine model.
Key Terms:
dopamine hypothesis
DA imbalance hypothesis
neurodevelopmental model
glutamate-dopamine model
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