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PSYC 336 - Drugs and Behavior > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

pharmacology

A

uses, effects, and modes of actions of drugs

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2
Q

psychopharmacology

A

Influence of drugs on behavior and psychological function

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3
Q

neuropharmacology

A

Influence of drugs on brain function

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4
Q

neuropsychopharmacology

A

Influence of drugs on brain, behavior and psychological function

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5
Q

psychoactive drug

A

chemical substance that alters perception, mood, or consciousness

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6
Q

purposes of psychoactive drugs

A

recreational, ritual/spiritual, therapeutic

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7
Q

classification by source

A

natural, synthetic, semisynthetic

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8
Q

classification by behavioral/psychological effects (5)

A

stimulants, depressants, analgesics, hallucinogens, psychotherapeutics

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9
Q

classification by pharmacological action

A

often drugs have multiple pharmacological actions, so it’s difficult to classify

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10
Q

other ways to classify drugs

A

chemical structure, legal status

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11
Q

what terms have been synonymous with addiction?

A

dependence and drug abuse

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12
Q

physical dependence

A

body relies on drug to prevent withdrawal

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13
Q

addiction

A
  • uncontrollable cravings
  • inability to control drug use
  • compulsive drug use
  • use despite doing harm to oneself or others
  • classified as a disease
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14
Q

in the last month, __% of the U.S. population has used illicit drugs

A

13

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15
Q

most common illicit drug used in the U.S.

A

marijuana

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16
Q

age group in which drug use is most common

A

young adults (18-20)

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17
Q

percentage of people with substance use disorder

A

14.5% (40.3 million people)

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18
Q

most common substance abused & diagnosed

A

alcohol

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19
Q

binge drinking

A

at least 5 drinks in one session for men; at least 4 drinks in one session for women

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20
Q

heavy drinking

A

at least 5 binge days out of last 30 days

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21
Q

daily marijuana use has ___ among college students

A

increased

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22
Q

binge alcohol use is ___ in college students than in non-college peers

A

greater

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23
Q

marijuana and nicotine vaping are ___ among college students

A

increasing

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24
Q

illicit drug use in high school students

A
  • steady in 12th graders over the years

- decreased alcohol use across all grades over the last decade

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25
Q

cigarette use in high-school students has ___ over the last 10 years

A

decreased

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26
Q

nicotine and THC vaping have ____ in high-school students

A

increased

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27
Q

psychoactive substances used throughout history (5)

A

nicotine, caffeine, morphine, cocaine, and THC

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28
Q

alcohol temperance movement’s effects on attitudes towards drugs/alcohol

A

did not outlaw alcohol, but drug use in general was socially unacceptable

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29
Q

prohibition

A

alcohol is outlawed and seen as criminal behavior

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30
Q

scientific advancements that led to greater drug use

A

increased addictive potential of drugs and development of hypodermic syringes

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31
Q

approach to drug control that led to increased drug use

A

increased drug availability and lack of drug control laws

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32
Q

changes in treatment of addiction

A

medicalization led to categorizing addiction as a disease

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33
Q

effects of Nixon’s War on Drugs in 1971

A

expanded incarceration, drug crimes more severely punished and policed

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34
Q

targets of the War on Drugs

A

Black population, anti-war left

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35
Q

effects of the War on Drugs in the 80s

A

mandatory minimum prison sentences, increased penalties for posession

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36
Q

Anti Drug-Abuse Act of 1986

A

created a big sentencing disparity between crack and powder cocaine, which further fueled racial disparities in incarceration

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37
Q

top consumer of illicit drugs in the world

A

USA

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38
Q

race typically subjected to higher rates of arrests and incarceration

A

Black population

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39
Q

past approach to the war on drugs

A
  • viewed drugs as a criminal justice problem
  • law enforcement
  • penalization
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40
Q

science’s influence on drug policy

A

little to none

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41
Q

what method is effective when tackling a drug problem

A

treatment programs

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42
Q

future of war on drugs

A
  • drugs are a public health problem
  • increased treatment availability
  • focus on education, prevention
  • reduced drug sentences
  • legalization of marijuana
  • harm reduction (syringe programs)
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43
Q

DSM-5 definition of substance use disorder

A

significant impairment in at least 2 categories in a 12-month period: impaired control, social impairment, risky use, pharmacological properties

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44
Q

changes from DSM-I to DSM-V when discussing addiction

A

gradual transition from stigmatizing to biological basis

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45
Q

addiction is NOT

A

physical dependence and withdrawals

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46
Q

addiction IS

A

craving and relapse

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47
Q

definition of addiction

A

chronic, relapsing brain disease characterized by compulsive drug seeking/use, despite harmful consequences, major impairment to self-control

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48
Q

bioavailability

A

amount of drug available to bind to target sites and elicit drug action

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49
Q

absorption

A

movement from site of administration to blood circulation

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50
Q

oral route of administration

A
  • aka preoral, PO
  • absorption in the GI tract
  • slow, variable
  • undergoes first-pass metabolism in the liver before entering the bloodstream
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51
Q

first-pass metabolism

A

aids in drug degradation and sometimes drug design

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52
Q

routes of administration that typically avoid first-pass metabolism

A

intranasal (bypasses BBB), inhalation, sublingual, rectal, transdermal

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53
Q

injection routes of administration

A

subcutaneous, intramuscular, intravenous (IV)

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54
Q

factors affected by route of administration

A

onset, peak concentration, and duration

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55
Q

slow route of administration

A

typically for medical use, longer duration

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56
Q

fast route of administration

A

typically associated with drug use/abuse, used to achieve highest peak concentration with rapid onset

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57
Q

oral and transdermal administration

A

slow absorption

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58
Q

intravenous injection or inhalation/smoking (route of administration)

A

rapid drug entry, fast onset

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59
Q

increased addictiveness is associated with…

A

fast onset and short duration

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60
Q

how route of administration affects absorption rate

A
  • blood circulation and surface area
  • amount of drug destroyed by digestive or metabolic processes
  • transport across membranes
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61
Q

drug properties that affect absorption rate

A

solubility, ionization

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62
Q

most drugs easily diffuse across membranes when they are

A

lipid-soluble, non-ionized

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63
Q

lipid solubility of heroin vs morphine

A

heroin reaches the brain much faster than morphine because of increased lipid solubility

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64
Q

drug ionization

A

occurs when drugs are dissolved in water (neutral pH) due to them being a weak acid or base

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65
Q

lipid solubility of ionized drugs

A

not readily lipid soluble, making diffusion difficult

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66
Q

factors affecting drug ionization

A

different bodily fluids (different pH)

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67
Q

ion trapping

A

concentration of drug in one compartment

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68
Q

distribution (ADME)

A

movement from blood to target site

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69
Q

factors affecting distribution

A

depot binding and the blood-brain barrier (BBB)

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70
Q

blood-brain barrier

A

selectively permeable (lipophilic) to keep a stable brain environment

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71
Q

weak BBB areas

A

area postrema, median eminence

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72
Q

depot binding

A

can occur in albumin (plasma), fat, and muscle, where the drug remains in an inactive state in the system and is protected from metabolism

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73
Q

factors affected by depot binding

A

peak concentration and duration of drug concentration

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74
Q

example of depot binding

A

THC: depot binding in fat leads to slow release, making THC detectable in urine days after the initial dose

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75
Q

metabolism and excretion (ADME)

A

movement out of the system

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76
Q

drug inactivation (biotransformation)

A

usually by metabolism, occurs in the liver by microsomal enzymes

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77
Q

phase I metabolism

A

oxidation, reduction, or hydrolysis (non-synthetic)

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78
Q

phase II metabolism

A
  • addition of small molecules (glucuronide, sulfate, methyl groups (synthetic)
  • products ionized and less lipid soluble so they become inactive metabolites
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79
Q

active metabolites

A
  • have biological activity of their own

- need further metabolism to become inactive metabolites

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80
Q

drug clearance: first order kinetics

A
  • drugs cleared at exponential rate
  • based on half-life
  • most common
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81
Q

drug clearance: zero-order kinetics

A
  • drugs cleared at constant rate (linear)

- example: alcohol

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82
Q

individual variation in drug metabolism

A
  • sex differences
  • individual adaptation (tolerance)
  • age effects
  • genetic differences
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83
Q

drug therapy for alcoholics (Disulfram/Antabuse)

A

blocks ALDH

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84
Q

pharmacokintetics

A

how drugs move throughout the body

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85
Q

pharmacodynamics

A
  • how drugs affect the body

- actions of drugs at receptor sites

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86
Q

ligand

A

neurotransmitter or drug that fits a given receptor

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87
Q

receptor

A

protein a ligand interacts with to initiate biological effects

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88
Q

drug + receptor =

A

drug effects

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89
Q

agonists

A

ligands that bind to a receptor to initiate a cellular response

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90
Q

antagonists

A
  • ligands that bind to a receptor to block the action of an agonist or endogenous ligand at the same receptor
  • do NOT reverse the effects of an agonist or cause an opposite reaction
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91
Q

receptors are bound at the ___ of the cell

A

membrane

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92
Q

a drug can be ___ specific for the receptor than the endogenous neurotransmitter

A

more

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93
Q

T/F: drugs can show agonist or antagonist actions

A

T

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94
Q

drug-receptor interaction

A

modulate normal neuronal functioning by mimicking, increasing, or inhibiting normal physiological/biochemical processes

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95
Q

characteristics of drug-receptor binding

A

temporary and reversible

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96
Q

binding affinity

A

determines speed of dissociation

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97
Q

law of mass action

A
  • more drug molecules = increased receptor occupancy
  • maximum drug effect = all receptors occupied
  • cellular response proportional to degree of receptor occupancy
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98
Q

dose-response curve

A

relationship between cellular response and receptor occupancy

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99
Q

reversibility of drug-receptor interactions

A
  • most are reversible

- some form long lasting, irreversible bonds

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100
Q

ED100

A
  • effective dose that gives maximum response
  • all receptors occupied
  • giving more of the drug does not increase observed drug effect
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101
Q

ED50

A

dose that produces half the maximum effect

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102
Q

dose-response curve shape

A

sigmoid

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103
Q

therapeutic index

A

evaluates all desirable and undesirable drug effects

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104
Q

TD50

A

dose that produces a given toxic effect in 50% of all subjects

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105
Q

LD50

A

dose that kills 50% of subjects (lethal dose)

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106
Q

therapeutic index (TI, margin of safety)

A

LD50 / ED50

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107
Q

potency

A

amount of drug needed to produce an effect

108
Q

efficacy

A

maximum effect that can be produced

109
Q

factors that affect potency

A
  • pharmacokinetics

- binding affinity for certain receptors (does not determine maximum possible effect however)

110
Q

factors that affect efficacy

A
  • act by different mechanisms (different receptors)

- different activity at the same receptor

111
Q

competitive antagonists

A
  • bind to the same receptor binding site as agonist
  • shifts DRC for agonist to the right
  • antagonist effect can be overcome by adding more agonist
112
Q

non-competitive antagonists

A
  • do not compete with agonists for receptor binding site
  • shifts DRC to the right for agonist, but also changes shape
  • cannot be overcome by adding more agonists, there is a decrease in maximum effect
113
Q

partial agonists

A
  • efficacy is lower than full agonist, higher than antagonist
  • in the presence of a full agonist, they act as antagonists
114
Q

inverse agonists

A
  • bind to receptors and initiate a cellular response that is opposite to the agonist
  • descending DRC
115
Q

allosteric modulators

A

ligands/drugs that indirectly influence the effects of a primary ligand

116
Q

positive allosteric modulators (PAMs)

A

amplify primary ligand effects

117
Q

negative allosteric modulators (NAMs)

A

reduce primary ligand effects

118
Q

tolerance

A
  • drug effect gets smaller
  • more drug required for same effect
  • DRC shifts to the right
119
Q

sensitization

A
  • drug effect gets bigger
  • less drug required for same effect
  • DRC shifts left
120
Q

acute tolerance

A
  • aka tachyphylaxis

- drug effect decreases rapidly within a single session

121
Q

example of acute tolerance

A

when blood-alcohol level is rising vs falling

122
Q

cross-tolerance

A

drug effect decreases due to repeated administration of another drug

123
Q

cross-sensitization

A

drug effect increases due to repeated administration of another drug

124
Q

pharmacokinetic (metabolic) mechanism of tolerance/sensitization

A
  • changes in metabolism

- enzyme induction

125
Q

pharmacodynamic mechanism of tolerance/sensitization

A
  • changes in receptors and corresponding signaling pathways

- change in receptor number/sensitivity

126
Q

behavioral mechanism of tolerance/sensitization

A
  • changes due to learning factors

- can be context-specific

127
Q

pavlovian/classical conditioning

A

conditioned stimulus (CS) training can contribute to sensitization or tolerance effects depending on conditioned reactions (CR)

128
Q

context-specific tolerance/sensitization

A

tolerance/sensitization effects only expressed in a specific environment that was previously paired with the drug

129
Q

context-specific tolerance related to heroin

A

this type of tolerance contributes to fatal heroin overdoses

130
Q

signals sent within a neuron

A

electrical local and action potentials

131
Q

signals send between neurons

A

chemical signals transported via neurotransmitters

132
Q

post-synaptic potentials

A

local changes in electrical activity at the dendrites/input zone

133
Q

action potentials

A

generated down the axon if a post-synaptic potential is large enough to reach the soma, all-or-nothing

134
Q

resting membrane potential

A

difference in electrical charge inside vs. outside the cell (polarized)

135
Q

ions

A

electrically charged molecules

136
Q

ions

A

electrically charged molecules

137
Q

anions

A

negatively charged

138
Q

cations

A

positively charged

139
Q

movement of potassium (K+) in a neuron at resting membrane potential

A

electrical pressure to enter the cell, but chemical pressure to leave the cell

140
Q

movement of sodium (Na+) in a neuron at resting membrane potential

A

electrochemical pressure to enter the cell

141
Q

movement of calcium (Ca2+) in a neuron at resting membrane potential

A

electrochemical pressure to enter the cell

142
Q

movement of chloride (Cl-) in a neuron at resting membrane potential

A

chemical pressure to move out of the cell

143
Q

triggers that can open an ion channel (4)

A
  • ligand binding
  • change in membrane potential
  • phosphorylation
  • G proteins
144
Q

inhibitory post-synaptic potential (IPSP)

A

Cl- or K+ ion channels open, making the cell more negative

145
Q

excitatory post-synaptic potential (EPSP)

A

Na+ ion channels open, making the cell more positive

146
Q

threshold for an action potential

A

around -40 mV

147
Q

what happens during an action potential?

A

membrane potential reverses (inside of cell becomes positive)

148
Q

an action potential is caused by a rush of ___ ions into the axon

A

Na+

149
Q

hyperpolarization is the same as…

A

IPSP

150
Q

depolarization is the same as…

A

EPSP

151
Q

function of voltage-gated Na+ channels

A

conduct the action potential down the axon

152
Q

synapse

A

site of action for most psychoactive drugs

153
Q

axoaxonic synapse (pre-synaptic facilitation/inhibition)

A
  • open ion channels → affect NT release

- signaling cascade → protein function

154
Q

axodendritic and axosomatic synapse

A
  • open ion channels → EPSP, IPSPs

- signaling cascade → protein expression or function

155
Q

presynaptic side of synapse

A

axon terminal contains synaptic vesicles that contain neurotransmitter

156
Q

postsynaptic side of the synapse

A

Receptors respond to the neurotransmitters

157
Q

classical neurotransmitters (4)

A
  • amino acids
  • monoamines
  • acetylcholine
  • purines
158
Q

non-classical neurotransmitters (3)

A
  • neuropeptides (opioids)
  • lipids (endocannabinoids)
  • gases
159
Q

retrograde neurotransmitters

A

lipids and gases

160
Q

examples of amino acid neurotransmitters (2)

A

glutamate and GABA

161
Q

examples of monoamine neurotransmitters

A

DA (dopamine), NE (norepinephrine), 5-HT (serotonin)

162
Q

steps in chemical synaptic transmittion

A
  • synthesis
  • release
  • inactivation
163
Q

synthesis of classical neurotransmitters

A
  • synthesized from dietary precursors
  • enzymes in axon terminals synthesize NTs
  • then transported into small vesicles (~40 nm radius)
164
Q

synthesis of neuropeptides

A

synthesized in cell body → packaged into large vesicles → transported down the axon

165
Q

neuropeptide synthesis is dependent on ___

A

protein-synthesis

166
Q

neurons that release neuropeptides can also release ___

A

classical neurotransmitters

167
Q

classical NTs require ___ transport

A

active

168
Q

vesicular transporters

A

move transmitters into vesicles

169
Q

steps for NT release

A
  • action potential reaches terminal
  • activation of voltage-gated calcium channels
  • influx of calcium
  • calcium mediates fusion of vesicle
  • NT is released via exocytosis
170
Q

SNARE proteins

A

mediates vesicle fusion with the cell membrane

171
Q

Botulinum toxin (Botox)

A

cleaves proteins involved in vesicle fusion

172
Q

endocytosis

A

Vesicle membrane is retrieved from the terminal membrane

173
Q

vesicle recycling

A

New (empty) vesicles can be refilled with NT rapidly

174
Q

NTs rapidly diffuse across narrow synaptic cleft and bind to receptors in vicinity, including on:

A

post-synaptic neuron

175
Q

There is also significant “spillover” at most synapses, or diffusion out of the cleft to reach receptors (3) on:

A
  • presynaptic neuron (autoreceptors)
  • astrocytes (glia)
  • nearby synapses
176
Q

autoreceptors

A

receptors on the same neuron releasing the NT and provide feedback (usually negative feedback)

177
Q

terminal autoreceptors

A

modulate NT release

178
Q

somatodendritic autoreceptors

A

modulate NT synthesis or firing

179
Q

inactivation of NT via:

A
  • enzymatic degradation (metabolism via enzymes)

- Plasma membrane transporters present in nerve terminal (2, reuptake) or glia

180
Q

retrograde transmission

A
  • Signaling from post-synaptic to pre-synaptic cell

- different than anterograde transmission used in most signaling

181
Q

drug-receptor interactions

A

Drugs primarily act outside the cell on targets (receptors) on the cell membrane

182
Q

receptor activation

A

activated by the binding of ligand (neurotransmitter, drug)

183
Q

categories of neurotransmitter receptors

A

ionotropic and metabotropic

184
Q

ionotropic receptors

A
  • ligand-gated ion channels
  • 4-5 subunits (separately encoded proteins) bound together to form an ion channel
  • fast, rapidly reversible
185
Q

metabotropic receptors

A
  • G-protein coupled receptors
  • use second messengers to open an ion channel or trigger cellular changes
  • 1 subunit with 7 transmembrane domains coupled to intracellular G protein
  • slower, long lasting
186
Q

nAChR

A
  • aka nicotinic acetylcholine receptor

- gates a cation channel

187
Q

GABAa

A

gates a chloride ion channel

188
Q

second messenger system - sequence

A
  • activation of G protein
  • change in activity of effector enzyme
  • change in second messenger levels
  • activation of protein kinase
  • phosphorylation of of a substrate protein
189
Q

families of G proteins

A
  • α subunit

- βγ subunit complex

190
Q

α subunit

A

Gs (stimulatory), Gi (inhibitory), Gq (quirky?)

191
Q

all neurotransmitters have _____ receptors, but only some utilize _____ receptors

A

metabotropic, ionotropic

192
Q

receptors that utilize ionotropic receptors

A

glutamate, GABA, acetylcholine, and serotonin (only one)

193
Q

receptors determine whether effects are ____ or ____

A

excitatory, inhibitory

194
Q

calcium regulation

A

tightly regulated due to playing a large part in neuronal function

195
Q

protein kinase

A

modify other proteins by adding phosphate groups to them (phosphorylation).

196
Q

protein kinase targets

A

ion channels, receptors, cytoskeletal proteins, transcription factors, etc.

197
Q

protein phosphatastes

A

dephosphorylate proteins

198
Q

phosphorylation

A

changes the structure/function of a protein to activate or inhibit

199
Q

transcription factors

A
  • family of proteins that bind to regulatory sites on genes to promote or suppress transcription of DNA to mRNA.
  • activation can cause second messengers to alter gene regulation
200
Q

immediate early genes (IEGs)

A
  • first genes to be transcribed into mRNA and then translated into protein quickly
  • include transcription factors
201
Q

c-Fos

A
  • a transcription factor and immediate-early gene

- marker of neuronal activation

202
Q

epigenetics

A

can potentially change gene expression for a lifetime

203
Q

unconditioned animal behavior

A
  • simple behavior observation
  • motor activity
  • analgesia
  • anxiety
204
Q

locomotor activity chamber

A

measures horizontal and vertical movement using infrared beam breaks

205
Q

analgesia tests

A

tail flick and hot plate tests measure reduced pain sensation (analgesia)

206
Q

elevated plus maze test

A

used to measure anxiety

207
Q

light-dark box and open field

A

both measure anxiety

208
Q

classical conditioning examples

A

fear conditioning, conditioned place preference

209
Q

instrumental conditioning examples

A

operant chamber learning

210
Q

fear conditioning

A

test of learning and remembering emotionally aversive events

211
Q

drug discrimination

A

used to assess stimulus properties, “what does the drug feel like?”

212
Q

drug discrimination test findings

A
  • animals classify drugs just like humans

- predictions have been highly sensitive and accurate

213
Q

reward

A

something that is “wanted” or “liked,” drives appetite behavior

214
Q

positive reinforcement

A

when adding something increases the probability of a behavior

215
Q

negative reinforcement

A

when removing something increases the probability of the behavior

216
Q

conditioned place preference

A
  • used to assess rewarding properties

- do you “like” the drug?

217
Q

conditioned place aversion

A

occurs when the drug is aversive and causes the animal to avoid the context they were in when given the drug

218
Q

drug self-administration

A
  • measures whether subject wants the drug and whether they will work for it
219
Q

drugs that do not maintain self-administration

A

most hallucinogens (aspirin, LSD, mescaline, etc)

220
Q

fixed ratio schedule

A

reinforced after every nth response

221
Q

variable ratio schedule

A

reinforced on average after every nth response

222
Q

progressive ratio schedule

A

each reinforcement requires more responses

223
Q

cocaine self-administration in rats

A

rats will adjust rate of cocaine self-administration according to dose

224
Q

dose-response curve of fixed-ratio schedule

A

inverted U shape

225
Q

drug satiety

A

may explain why replacement therapy works

226
Q

breakpoint (progressive ratio schedule)

A
  • highest ratio attained before the animal “gives up.”
  • measure of drug motivation.
  • “How hard are you willing to work for the drug?”
227
Q

rate of responding changes with dopamine antagonist

A

DA antagonist will increase FR responding and decrease PR responding

228
Q

dose-response curve for progressive ratio schedule

A

just increases (not inverted U shape)

229
Q

ligand binding

A

used to visualize receptors

230
Q

antibody binding

A

used to visualize proteins

231
Q

hybridization

A

used to visualize mRNA

232
Q

tissue extract

A

provides quantification; in vitro

233
Q

tissue slice

A

provides localization; in situ

234
Q

living organism

A

in vitro

235
Q

autoradiography

A

radioligand (radioactive ligand) shows location and density of receptors

236
Q

autoradiography with PET

A

used to visualize receptors in live human brains (in vivo), injected intravenously

237
Q

striatum

A

high concentration of dopamine receptors

238
Q

immunohistochemistry

A

binding of specific antibodies to visualize location of proteins

239
Q

primary antibody

A

binds to protein of interest

240
Q

secondary antibody

A

binds to primary antibody

241
Q

label (immunohistochemistry)

A

colored product from enzyme reaction

242
Q

CLARITY

A
  • ‘dissolves’ fats/lipids

- no sectioning of the brain, whole cellular brain architecture

243
Q

in situ hybridization (ISH)

A

complementary RNA/DNA probes bind to mRNA

244
Q

advantages of static visualization techniques

A

high specificity, full brain coverage, high spatial resolution

245
Q

electroencephalogram (EEG)

A

non-invasive, good time resolution, poor spatial resolution

246
Q

functional magnetic resonance imagine (fMRI)

A

non-invasive, detects blood flow changes

247
Q

techniques requiring intracranial surgery

A

electrophysiology, neurotransmitter detection, lesions, and local drug delivery

248
Q

another term for intracranial surgery

A

stereotaxic

249
Q

stereotaxic surgery

A

allows for accurate targeting of specific brain structures

250
Q

intracranial electrophysiology

A

record activity from (and stimulate) neurons in specific brain areas

251
Q

microdialysis / voltammetry

A

can be used in freely moving animals to measure neurotransmitter levels and see how they change over time

252
Q

common property in addictive drugs

A

evoke dopamine release in the ventral striatum (nucleus accumbens, NAc)

253
Q

why do we need manipulation of variables in an experiment?

A
  • to determine causation
  • determine whether a specific brain area is necessary for a certain behavior
  • is it necessary or sufficient for a drug effect?
  • where in the brain is the drug rewarding?
  • can we block the effects?
254
Q

general neurotoxin lesion example

A

NDMA, toxic to all neurons

255
Q

specific neurotoxin lesion example

A

6-OHDA toxic only to catecholamine neurons

256
Q

local drug delivery (intracranial manipulation)

A

drug gets microinjected into a specific brain area of an awake animal

257
Q

genetic manipulation techniques

A
  • mutations
  • gene silencing
  • gene editing
  • viral vectors
258
Q

3 different kinds of mutants (usually mice)

A
  • knockout
  • knockin
  • transgenic
259
Q

knockout (genetic mutation)

A

removal of a gene, loss of function

260
Q

knockin (genetic mutation)

A

replace gene, gain of function

261
Q

transgenic (genetic mutation)

A

introduce new gene

262
Q

gene silencing

A

performed via injection of RNA interference

263
Q

gene editing

A

performed via CRISPR-Cas9; can remove, replace, or add DNA

264
Q

viral vectors

A
  • used for gene therapy in humans
  • replication-disabled viruses that can infect cells, integrate into the host genome and cause stable expression of introduced genes
265
Q

optogenetics

A
  • incorporate light-gated ion channels and pumps into neurons
  • allows depolarization/hyperpolarization of cells using light

PSYC 336 - Drugs and Behavior (2 decks)

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