Midterm 1 Flashcards

(208 cards)

1
Q

What is the EC50? How do you find it on a graph?

A

The dose that is effective in 50% of the time, assuming everyone is the same. Found at Y=50
Think: effective

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2
Q

What is the KD50?

A

The dose that proves lethal 50% of the time
Think: kill dose

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3
Q

What is the ED50?

A

Similar to the EC50, but considering variability
Think: effective dose

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4
Q

What is the LD50?

A

Similar to KD50, but considering variability
Think: lethal dose

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5
Q

What is the therapeutic index? How is it calulated?

A

The ratio of dose required for a desirable effect to undesirable effect
TI=LD50/ED50
TI=KD50/EC50

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6
Q

What is potency? How can you gauge it on a graph?

A

The extent of the drug’s effects
More potent = leftmost on graph

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7
Q

What is drug efficacy? How can you gauge it on a graph?

A

A drug’s ability to produce a maximum, biologically functional response
Higher curve = more effective

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8
Q

What are primary effects? Secondary effects?

A

Primary: the intended reason for taking the drug
Secondary: side effects, anything else

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9
Q

Give an example of a polar ion

A

Therosine

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10
Q

Name some charged ions

A

Arginine+, Histidine+

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11
Q

Name some hydrophobic ions

A

Valine, Isoleucine, Leucine, Methionine, Tryptophan, phenylalanine

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12
Q

Name some special case ions

A

Cystine, glycine, proline

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13
Q

What type of bond is the strongest? Weakest?

A

Strong: Covalent bond
Weak: Hydrophobic bond

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14
Q

Explain lipid diffusion

A

The migration of lipophilic and non-charged ions through the cell membrane. Guided by concentration gradients

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15
Q

Explain aqueous diffusion

A

Pores allow the passage of specific sized molecules through tight junctions
NOT through blood-brain barrier

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16
Q

Explain the relation between pH and PKA

A

PKA is the pH at which 50% of ions are charged
Charged drugs cannot pass barrier

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17
Q

How can you predict the charge of an ion from pH and PKA?

A

PKA>pH = weak base is neutral
PKA<pH = weak base is ionic (charged)

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18
Q

What is PKA?

A

The pH at which 50% of the molecules are charged

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19
Q

Explain active transport

A

Specific molecules bind to specific carriers to be transported over the barrier

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20
Q

What is saturated active transport? Inhibited?

A

Transport that requires no energy
Blocked transport

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21
Q

Explain endo/exocytosis

A

Passing over (in or out) the membrane, surrounds the molecule in a vesicle

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22
Q

What is ADME?

A

Absorption, Distribution, Metabolism, Excretion

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23
Q

What is bioavailability?

A

how much of the drug ‘makes it in’ or takes effect on the body

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24
Q

What are the different routes of administration?

A

Parenteral: Injection, Inhalation, Transdermal, Nasal, Topical
Enteral: Oral, rectal

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25
What are the types of injections? (6)
Sub-q: under skin Intramuscular: muscle Intraperitoneal: peritoneal cavity Intravenous: vein Intrathecal: between skull and V1 Intracerebroventricular: brain ventricles
26
How do injections get absorbed into the body?
Injection makes its way into bloodstream Makes its way in deoxygenated blood through heart to lungs Oxygenated and sent back through heart to body to brain
27
How are inhaled substances ADME?
Substance inhaled into lungs(A) Gas exchange allows drug to pass into oxygenated blood, pumped through heart to brain and body (D) Slow metabolism throughout body (M) Expelled by breathing out (E)
28
THC ADME when inhaled
Inhaled particles remain in lung and absorb into bloodstream for distribution (A,D) Body metabolizes and expels like solids (M,E)
29
How are oral substances ADM?
Absorption through the walls of the stomach and intestine (A) Into bloodstream via villus, pass throughout body (D) Breakdown in saliva, stomach acid, liver, kidneys (M)
30
What is first pass metabolism?
Any drug absorbed via the digestive system is pre-metabolized in the stomach, gut, and liver
31
How are transdermal substances absorbed?
Lipophilic substances seep in through S.C (top layer of skin)
32
What are distribution compartments? How do they affect distribution
Fat, bone, intracellular fluid, extracellular fluid Fat and bone have reservoirs that hold on to substances (slower release)
33
Where does most of metabolism occur?
Liver and Kidneys
34
Explain phase 1 metabolism Give examples of the enzymes
Enzymes break down the molecule to make them polar CYP1, CYP2, CYP3, CYP3A4
35
Explain phase 2 metabolism
Drugs are transformed into conjugates
36
How do the kidneys aid in metabolism?
Filers certain substances out of blood, sends waste to be eliminated
37
What are first-order kinetics?
The elimination rate of substances dependent on concentration
38
What is half-life when discussing elminination?
Half life is the time it takes for the body to eliminate 50% of the substance
39
What is zero-order kinetics?
When a substance is eliminated at a constant rate, independent of concentration
40
What is the therapeutic window?
the range of a substance's concentration in the blood between maximum and minimum efficacy
41
How can you determine the therapeutic window?
The same as the therapeutic index KD50/EC50 LD50/ED50
42
What factors affect PK/PD?
Genetics, age, sex, state of subject, diet
43
Explain how the state of a subject affects PK/PD
Alcoholics create more of the enzyme (alcohol dehydrogenase) for breakdown, thus it is faster
44
Explain how age can affect PK/PD
Children and fetuses do not produce alcohol dehydrogenase enzyme, cannot break down
45
What is an agonist effect? How does it relate to drugs?
A molecule that activates the receptor it binds to An drug that produces an agonist effect will activate the receptor, but does not stop when overstimulated
46
What is an antagonist effect? How does it relate to drugs?
A molecule that blocks the receptor it binds to A drug that is an antagonist will block a ligand from activating the receptor
47
What is a full agonist effect?
The maximum activation response to molecule binding
48
What is a partial agonist effect?
Activates to mid potential, above average but not full
49
What is a competitive antagonist?
When a molecule will compete for the receptor
50
What is an irreversible antagonist?
A molecule that kicks everything else off the receptor to block it
51
What is an inverse agonist effect? How does this relate to drugs?
When a GPCR spontaneously activates due to an absence of ligands A drug that takes this effect will reverse that spontaneous activation
52
What is an allosteric modulator?
A substance that binds to additional receptors, altering the effect of primary binding
53
What is PAM? What does it mean
Positive allosteric modulator A substance that enhances the primary effect
54
What is NAM? What does it mean
Negative allosteric modulator A substance that inhibits/reduces the primary effect
55
What is a 1+1=0 drug interaction? Give an example
An antagonist effect, drug B cancels/reduces drug A Naloxone for opiods
56
What is a 1+1=2 drug interaction?
An additive effect, drug B adds to the effect of drug A
57
What is a 1+1=3 drug interaction?
A superadditive / synergism effect, the combined effect of A with B are greater than the effect of A and B (A+B) > (a) + (b)
58
What is a 0+1=2 drug interaction?
A potentiation effect, drug A has no effect unless taken with drug B
59
How is resting potential maintained?
Simple diffusion, electrostatic charge, differential permeability, transporter pumps
60
How does simple diffusion maintain resting potential?
Na+, K+, Cl-, A- move along their concentration gradient, in and out of the cell to maintain an inner difference of -70mV
61
How does electrostatic charge maintain resting potential?
K+, Na+ are repelled by the more positive charge outside the cell, inclined to stay internal Cl-, A- are repelled by the more negative charge inside the cell, inclined to stay external
62
How does differential potentiation maintain resting potential?
Non-gated ion channels are open to allow K+ and Na+ to pass as needed
63
How do transporter pumps maintain resting potential?
Active exchange of K+ (in) for Na+ (out) Sodium-potassium pump
64
How is an action potential generated (7 steps)
1. Threshold met 2. Na+ enter 3. K+ leaves 4. Na+ channels close 5. K+ keeps leaving (repolar - hyperpolarization) 6. K+ channels close causing (cell is hyperpolar) 7. Excess external K+ diffuses away
65
What is an EPSP? Explain it
Excitatory Post Synaptic Potential Causes an excitation response, starts a process
66
What is an IPSP? Explain it
Inhibitory Post Synaptic Potential Causes an inhibition response, stops something
67
How does an ionotropic receptor work?
Charged ions (Na+, K+, Cl-) bind to the receptor to activate or inhibit
68
What are the products of ionotropic receptors?
IPSP or EPSP
69
How does a metabotropic receptor work?
G-protein coupled molecules bind to the receptor and initiate a second messenger
70
What are the second messengers associated with metabotropic receptors?
cAMP cGMP
71
What does the second messenger cAMP do? cGMP?
Activates PKA Activates PKG Proteins (enzymes) that alter the functioning of other receptors
72
What is Glutamate? How is it synthesized? Reuptake/Breakdown? Role?
Excitatory amino acid Synthesized from glutamine Reuptake via EAAT Role: cell plasticity, learning + memory
73
What is the AMPA? How does it work?
Glutamate receptor Ionotropic Glutamate/drug binds Na+ IN, K+ OUT Local depolarization and at Mg2 site EPSP
74
What is NMDA? How does it work?
Glutamate receptor Binding Depolarizing opens Mg2 site Glutamate and glycine receptors bind Na+, Ca2+ INTO cell
75
What receptor does PCP affect? How?
NMDA Antagonist effect
76
What is GABA? How is it synthesized? Reuptake/Breakdown? Role?
Inhibitory amino acid Synthesized by GAD from glutamate Reuptake by GAT Role: memory, impulse, decision making
77
What is GABA(A)? How does it work?
GABA receptor Ionotropic Substance binds, Cl- passes into cell IPSP
78
What receptor does Alcohol affect? How?
GABA(A) Binds to receptor, opening flow of Cl- into cell Inhibits actions Affects: memory formation, decision making, impulse control
79
What is Dopamine? How is it synthesized? Reuptake/Breakdown? Role?
Monoamine Synthesized from Tyrosine Reuptake by DAT Breakdown by MAO, COMT Role: reward-related processes, motor behaviour
80
What is the D1? How does it work
Dopamine receptor Metabotropic Binding activates the G protein Stimulate cAMP (second messenger) production Increase excitability
81
What is the D2? How does it work?
Dopamine receptor Metabotropic Binding activates the G protein Inhibit cAMP (second messenger) production Decrease excitability
82
What effect does Cocaine have? How?
Agonist effect on dopamine Blocks DAT reuptake, causing dopamine to keep binding and overstimulate cell
83
What effect do methamphetamines have? How?
Agonist effect on dopamine Reuptake reversal Mimics dopamine and binds to D receptors Excess dopamine binds after Overstimulate cell Affects: euphoria in reward path
84
What is serotonin? How is it synthesized? Reuptake/Breakdown? Role?
Monoamine Synthesized from Tryptophan Reuptake by SERT Breakdown by MAO Role: mood, sleep/wake cycles, aggression
85
What kind of receptors are the 5-HT?
Serotonin receptors 5-HT1,2,4-7 = Metabotropic 5-HT3 = ionotropic
86
What effect does LSD have? How?
Agonist effect on serotonin LSD binds to receptors, inhibiting or exciting them Affects: ability to sleep, mood
87
What effect does Ecstasy have? How?
Agonist effect on serotonin Mimics serotonin to bind first, excess serotonin then binds and over stimulates cell Affects: mood, sleep, perception, appetite
88
What is Acetylcholine? How is it synthesized? Reuptake/Breakdown? Role?
Monoamine Found at neuromuscular junction, PNS, CNS Synthesized from acetate+choline Breakdown by enzyme acetylcholinesterase
89
What is the nAChR? How does it work?
Nicotinic ACh receptor Ionotropic ACh/drug binds to receptor Na+ IN, K+ OUT EPSP
90
What effect does nicotine have? How?
nAChR agonist effect Binds to receptors like ACh
91
What is the mAChR? How does it work?
Muscarinic ACh receptor Metabotropic ACh binding to M1,3,5 = second messenger to open K+ and Cl- channels ACh binding to M2,4 = second messenger to decrease cAMP
92
What effect does muscarine have? Atropine?
mAChR agonist effect mAChR antagonist effect
93
What are endocannabinoids? How is it synthesized? Reuptake/Breakdown? Role?
Neuromodulator Produced from lipid compounds Breakdown by enzymes Role: homeostasis
94
What is the CBR1? How does it work?
Endocannabinoid receptor Metabotropic Inhibits pre-synaptic action by Depolarization induced Suppression of inhibition/excitation Binds to pre-syn. heteroceptors, G-protein inhibits Ca2+ channel
95
What effect does marijuana have? How?
Agonist effect on dopamine THC binds to heteroreceptors, blocking feedback to dopamine production Dopamine continues to bind Affects: wakefulness, pain receptors, appetite, memory + concentration
96
What are some types of opioid peptides? How are they synthesized? Reuptake/Breakdown? Role?
Beta-endorphin, enkephalin, dynorphin Synthesized by polypeptides Breakdown by peptidases enzyme Role: homeostasis, reward-related processes, stress+pain response
97
What are the MOR/KOR/DOR? How do they work?
Opioid peptide receptors Metabotropic G-protein regulates K+, Ca2+, or second messenger Inhibits excitability
98
What effect does morphine have? Naloxone?
Agonist effect on MOR receptor Antagonist effect on MOR receptor
99
What effect does heroin have? How?
Agonist effect on MOR Binding turns off dopamine inhibition Affects: pain receptors, stress response, emotional attachment
100
What is norepinephrine (NE)? Role?
Monoamine Role: attention, sleep/wakefulness. feeding behaviours, emotion, arousal, motivation
101
What are Alpha1, Beta1, Beta2? How do they work
NE receptors Metabotropic Excitatory
102
What is Alpha2? How does it work?
NE receptor Autoreceptor Inhibitory
103
What is the division of the nervous system?
NS 1. Central 2. Peripheral a) Somatic b) Autonomic - Parasympathetic - Sympathetic
104
What does the somatic NS in charge of?
Motor and sensory nerves
105
What is the autonomic NS in charge of?
Stress response
106
What part of the NS is most affected by drugs?
Autonomic NS
107
What is the parasympathetic NS in charge of?
Rest/Digest
108
What is the sympathetic NS in charge of?
Fight/Flight/Freeze
109
What does the Medulla Oblongata play a role in?
Consciousness, heart rate, blood pressure, breathing, muscle tone, reflexes
110
What drugs affect the Medulla Oblongata? In what way?
Barbiturates, opioids, alcohol: depress breathing Opiates, nicotine: cause nausea + vomiting
111
What does the Pons play a role in?
Bridges and refines motor commands conveyed between parts of the cortex and cerebellum
112
What drugs affect the Pons? In what way?
Benzodiazepines: increase the inhibitory effects of GABA, relieving anxiety Amphetamines, cocaine: stimulate adrenergic synapses, causing anxiety
113
What does the cerebellum play a role in?
Receives and processes sensory and motor stimuli Maintains posture, fine-tunes movement, smooths eye movement, procedural memory
114
What drugs affect the cerebellum? In what way?
Alcohol may affect this area and cause motor effects
115
What are the two subsets of the Reticular formation? What differentiates them?
Ascending (RAS) - to brain Descending - to spinal cord / body
116
What does the Descending Reticular Formation play a role in?
Autonomic nervous system, reflexes, posture balance, motor movement
117
What does the Ascending Reticular Formation play a role in?
Cortex activation, cognitive arousal, selective attention, wakefulness
118
What drugs affect the Reticular Formation? In what way?
Barbiturates, alcohol: decrease the ability of the neurons in RAS to fire repeatedly, causing a decrease in arousal
119
What is the PAG? What role does it play a part in?
Periaqueductal Grey Pain sensation, defensive behaviour
120
What drugs affect the PAG? In what way?
Opioids: block pain by stimulating the PAG
121
What is the VTA? What role does it play a part in?
Ventral Tegmental Area Component of the reward pathway, sends dopamine throughout the brain
122
What does the Basal Ganglia play a role in?
Voluntary movement, action selection, switching between motor beh/habits/eye movement, memory for locations in space, classical conditioning
123
What are the components of the Basal Ganglia?
GPe GPi SNr SNc STN
124
What drugs affect the Basal Ganglia? In what way?
L-Dopa: can alleviate parkinson's symptoms Antipsychotics: can cause them
125
What does the limbic system play a role in?
Emotion, memory, alertness, stress response, executive function, motivation
126
What are some of the main parts of the limbic system?
Hippocampus, Amygdala, Thalamus, parts of the Cortex, hypothalamus
127
What is the role of the hippocampus? How does it interact with drugs?
Learning, declarative + spatial memory Mediates place/drug preference
128
What is the role of the amygdala?
Process neg. emotions (FEAR/RAGE), emotional memory, behavioural memory
129
What does the Thalamus play a role in?
Transmit sensory input to cerebral cortex, regulate arousal + excitability of cortex
130
What does the Hypothalamus play a role in?
Homeostasis control: body temp, blood pressure, fluid balance, metabolism, eating/drinking motivation, etc
131
What drugs affect the Hypothalamus? How?
Benzodiazepines reduce aggression and produce a calming effect
132
What parts of the Cortex play a role in integrating sensory information?
Primary Visual/Auditory/Somatosensory cortices
133
What are secondary and association cortices? What are their roles?
Smaller, non-primary Integrate sensory information with other sensory perceptions and store them as memories
134
What does the Primary Motor Cortex play a role in?
Voluntary motor actions
135
What does the Prefrontal Cortex play a role in?
Sending and receiving information from the limbic system Abstract reasoning, insight, planning, motivation, decision making, judgement
136
What drugs affect the Prefrontal cortex? How?
Alcohol inhibits many decision making and impulse control mechanisms
137
What is the Nigrostriatal pathway? What NT travels through it? What path does it take?
Pathway for movement Dopamine Substantia Nigra to Striatum
138
What is the Mesolimbic pathway? What NT travels through it? What path does it take?
Reward pathway Dopamine Ventral Tegmental Area to Nucleus Accumbends
139
What is the Mesocortical pathway? What NT travels through it? What path does it take?
Pathway for motivation and emotion Dopamine Ventral Tegmental Area to Cortex
140
What is the Tuberoinfundibular pathway? What NT travels through it? What path does it take?
Posterior pituitary pathway Dopamine Hypothalamus to Pituitary
141
What is the path of the Norepinephrine pathway? What role does it play a part in? *FUN FACT*
From the Locus Coeruleus throughout the brain Arousal and motivation *Locus Coeruleus is BLUE*
142
What pathway includes the Basal Nucleus of Mynert and Medial Septal Area? In what way?
The Acetylcholine pathway Plays part in learning, memory, and cortical action
143
What disease impacts the Acetylcholine pathway? How?
A loss of ACh transmission results in Alzheimer's Disease
144
What pathway includes the Mesopontine tegmental area? In what way?
The Acetylcholine Pathway Role: REM sleep
145
What role does the VTA play in the Acetylcholine pathway?
Reward system
146
What is the 5-HT pathway? What is its role?
The 7 different Raphe Nuclei project information to the CNS in ascending/descending motion Role: Controls enkephalin release (PAIN)
147
How can teratogens alter development? What defines HOW it will affect a fetus?
Teratogens can interrupt the formation of circuits and prematurely prune connections Time is the most indicative of what effect will occur
148
Explain MRI What is the final outcome?
Magnetic Resonance Imaging Relies on magnets and radio waves to map the movement of hydrogen atoms Results on a high contrast resolution image Used to look at the body
149
Explain fMRI How does it differ from MRI?
Functional MRI Uses blood-oxygen level to measure brain activity Used to look at the brain rather than the body
150
Explain PET scans What are they used for?
PET uses radioactive tracer isotopes to capture metabolic/biochem function Relies on O2, N, C, F- Allows the study of receptor distribution/density, metabolic activity and changes in receptors over time
151
Provide a brief summary of the history of Behavioural Pharmacology
1920s: Psychopharmacology, Macht at Johns Hopkins, still used outside North America 1950s: Beh. Pharma, Dews at Harvard, Operant analysis of drug effects Today: Beh. Pharma, Drug effects tested using Beh. Psych + Beh. Neuroscience
152
In the early 1900s, who's theory changed how Psychology did testing? How? What is the logic?
Watson's behaviourism proposed that Psych needs precise, systematic means of describing, recording, and analyzing beh. Observable behaviour is objective
153
Explain the Forced Swim Test Why is it used? What drug-related research does it aid with? How?
A mouse/rat is placed in a beaker of water, the amount of time spent swimming is recorded Good predictive validity Useful for Antidepressant testing: reduced immobility in non-depressed animals indicates a functional drug
154
Explain the Avoidant-Escape Task What conditioning does it rely on?
Animal learns that the tone indicates an incoming shock, decision to leave is rewarded Operant conditioning
155
What is a controlled experiment?
An experiment in which it would be possible to say, with a degree of certainty, what would happen if a drug is NOT given Use of control group
156
What is experimenter bias? How is it countered?
The unconscious change of outcomes due to the experimenter's beliefs, reactions, wording, etc Countered using blind experiments
157
What are the features of a parallel design experiment?
Between subjects Compares control group to drug group Random selection
158
What are the features of a crossover design experiment?
Within subject and between subject Compares individuals with and without drug Compares Group A to Group B Washout period: time taken to rid body of substance
159
What are the features of a balanced placebo design experiment? When is it used?
G1: expects drug, gets drug (drug effect only) G2: Expects drug, gets placebo (placebo effect) G3: expects placebo, gets drug (placebo+drug) G4: expects placebo, gets placebo (baseline) Mainly used in the mid 1970s
160
What are the features of a 3-group design experiment?
G1: Placebo G2: Drug G3: Control / established drug
161
What are some features of a Longitudinal study? Limitations?
Non experimental Long, expensive, big sample Follows individuals over time Attrition (quitting), 'Survivor bias'
162
What are some features of a cross sectional study?
Quick less expensive Snapshot view in time Compares groups at different stages at one point in time Generalizability Show patterns of change
163
What are some features of a prospective study?
individuals followed over time to see final outcome - not yet known Less risk of spurious correlations Increased cost, time, effort
164
What are some features of a cohort study?
Observe sample over time, looking for the development of a specific response Less risk of spurious correlations
165
What are some features of a case control study?
Compare specific cases to control Increased risk of spurious correlations (case selection bias)
166
What are some features of a retrospective study?
Outcomes already known, working back to find correlations Increased risk of spurious correlations
167
What does direction refer to in a correlation?
If the correlation is positive or negative
168
What scale is used to determine strength? What are the levels?
Schober 0.00 to <0.10 = negligeable 0.10 to <0.40 = weak 0.40 to <0.70 = moderate 0.70 to <0.90 = strong 0.90 to 1.00 = very strong
169
Explain the spontaneous motor activity test How does it relate to drug testing?
Animal placed in open field, movement activity measured electronically or by line-crossing Time spent in middle indicates low anxiety Study effects of benzodiazepines (anti-anxiety)
169
What tests can be used to measure unconditioned behaviour?
Spontaneous motor activity test Elevated Plus Maze
170
Explain the elevated plus maze How does it relate to drug testing?
Cross shape, two closed in arms, two open Time spent in open arms indicates low anxiety Study effects of benzodiazepines (anti-anxiety)
171
What is classical conditioning? Give an example
The continued pairing of a CS and US to produce a reflex (UR) Eventually CS produces UR (now CR) Bell + food = salivate Bell = salivate
172
Explain the conditioned place preference test How does it relate to drug testing?
US: drug UR: reaction to drug CS: coconut smell CR: go to coconut smell Time spent in coconut chamber determines addictiveness / strength of reinforcement
173
What are some features of Drug Discrimination testing How does it work?
Used to test the onset and duration of subjective effects To determine receptors being binded Substitution tests for like-drugs Operant or Classical conditioning
174
What are the features of a Fixed Interval schedule of reinforcement? How does it affect response rate?
"Every so often" Reinforcement is only given after a set amount of time following task Moderate response rate, significant pause after reinforcement
175
What are the features of a Variable Interval schedule of reinforcement? How does it affect response rate?
"Value dependent" Reinforcers are given at different intervals, making it impossible to predict Slower response rate
176
What are the features of a Fixed Ratio schedule of reinforcement? How does it affect response rate?
"Response Quota" Animal must perform the task a given number of times for reinforcer High response rate
177
What are the features of a Variable Ratio schedule of reinforcement? How does it affect response rate?
"Estimated Quota" Animal must perform the task about X many times High response rate
178
What do Self Administration Studies measure? How do drugs impact the rate of responding?
Compares the pressing of a drug-paired and a saline-paired lever Uses a fixed or progressive ratio schedule Preferential increase of pressing drug lever indicates the drug is a strong reinforcer, may press more often even if not getting drug
179
What do ICSS studies measure? How do drugs impact the rate of responding?
Measure of a drug's ability to alter operant responding to electrical stimulation of reward path The addition of a drug lowers the Hz needed to reach the response threshold - facilitates responding (sensitive to)
180
What do Choice Studies measure? How do they work? How do drugs affect the rate of responding?
Measure of choice between a drug and another reinforcer (drug b/food/etc) Animal gets equal exposure to lone-reinforcers, then must choose which they want Choice indicates the stronger reinforcer
181
How are subjective effects measured in people? Explain each test
Introspection: ask how they feel Rating scales + Self-reports: rate their experiences in different factions, ask about specific feelings
182
How are objective effects measured in people?
Drug state discrimination Perception Motor performance Attention + Vigilance Memory Response inhibition Driving ability
183
How do drug state discrimination tests measure objective effects?
Participant is exposed to IDENTIFIED drug and placebo They are then asked to identify an UNIDENTIFIED drug as similar effect to drug or placebo
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How do perception tests measure objective effects? Explain the different tests
Measure the sharpness of senses (sight and hearing) Critical flicker fusion frequency: measure of the ability to detect a flicker in the light Auditory flicker
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How do motor performance tests measure objective effects? Explain the different tests
Measure the reaction time in motor related activities Simple RT test: press button ASAP after cue Complex RT test: multiple responses and cues Pursuit rotor: Hand-eye coordination Finger tapping rate Hand steadiness
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How do attention and vigilance tests measure objective effects? Explain the tests
Measure of response time to visual cues Mackworth clock test: press button when clock moves by 2sec instead of 1sec
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How do memory tests measure objective effects? Explain the tests
Measure of recall Short term N-back test: when cue symbol is shown, must recall the last N# back (previous symbols) Long term Free recall: remember a list of words to be recalled later Cued recall: remember a list of words to pick out from a longer list later
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How do response inhibition tests measure objective effects? Explain the tests
measure the ability to stop or withhold reaction Go-No go: Press on cue 1, don't press on cue 2 Go-Stop: like go-no go but with STOP cue. STOP cue closely follows other cues, must halt initial reaction
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What drugs will affect response inhibition? How?
Alcohol: increase the delay between cue and STOP required for accurate response
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How do driving-ability tests measure objective effects? Explain the tests
Measure of perception, motor control, attention, response In traffic In closed course Simulated
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What is tolerance?
The effect of repeated drug exposure that results in diminished effects or the need to increase doses to reach intoxication
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What is cross-tolerance?
Increased tolerance of one drug will affect all the drugs in the family
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What is acute tolerance? How does it explain tolerance?
Short term tolerance The point at which a higher concentration makes no difference in effect Receptors are desensitized and cannot be re-activated for a given time
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What is Pharmacokinetic tolerance? How does it explain tolerance? Give an example
The increase in the rate/ability of the body to metabolize a drug *ADME Fewer molecules at the site of action change the duration of action Heavy drinkers produce more enzymes to break down alcohol
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What is Pharmacodynamic tolerance? How does it explain tolerance?
Adjustments made by the body to compensate for effects caused by the continued presence of a drug\ *Homeostasis* The body gets better at compensating over time and can handle the drug better
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What are the two ways in which Pharmacodynamic tolerance results in changes
Up-regulation: added receptors increase sensitivity Down-regulation: blocked receptors reduce stimulation and sensitivity
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What is behavioural tolerance?
Learned tolerance Through experience with a drug, an organism can learn to decrease the effect *How to sober up*
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What is the Opponent Process Theory?
The theory that the stimulation of drugs activates two processes that work oppositely to create dependence
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Explain the steps of the Opponent Process Theory
Drug is administered, starting A process A effect is pleasurable As drug wears off, so does A effect, starting B process B effect is dysphoric/negative
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Explain how to classically condition a drug effect using an example
US: drug UR: Nausea CS: cues presented prior to drug CR: person starts to get nauseous after the cues are presented, no drug
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Explain how to classically condition a compensatory effect using an example
US: drug UR: Pain relief CS: cues presented prior to drug CR: person starts feeling pain relief after cues, no drug
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What is conditional tolerance? How can it be dangerous What is another name for it?
Increased tolerance that is tied to the environment the drug is typically administered in If the drug is taken in a novel location, the person is at higher risk for OD Environmental sensitization
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How can operant conditioning lead to behavioural tolerance? Use an example
G1: Amph, task with DRL- low response rate reinforcement (must wait a given time between responses) G2: Task with DRL, Amph If G2 is given the Amph first, they never learned to withhold their responses and do so too early (punished)
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What is sensitization? What part of the cell does it affect?
The increase in drug effects as a result of repeated administrations Can affect the pre and postsynaptic neurons
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What is the nocebo effect?
When you expect negative outcomes and therefor experience negative outcomes
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How does self administration affect drug effects?
The control of self-administration increases dopamine production and amplifies the effect
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How do novel environments affect drug effects?
In novel environments, the locomotion stimulation is increased (hyperlocomotion)