Week 2 - Review of Neurobiology Flashcards

1
Q

What are the Drug Use Models?

A
  • Disease model
  • Physical dependence Model
  • Positive reinforcement model
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2
Q

What is the disease models definition of addictive behaviour?

A

• Compulsive (impaired control over use of the drug) & self-destructive (harmful consequences to user)

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3
Q

What are the related theories of the disease model?

A

Predisposition and exposure theories

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4
Q

What are the strengths of the disease model?

A
  • May make accessing treatment easier
  • Rules that usually govern behavior may not apply to drug taking, since this behavior is abnormal
  • Can account for individual differences in response to drugs
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5
Q

What are the limitations of the disease model?

A
  • “What is the disease?” (by, to what extent do we need to be able to identify the disease?)
  • May reduce individual responsibility for behavior
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6
Q

What factors does the disease model not consider?

A

x. Related to socioeconomic factors – increase in opium use when socially acceptable
x. Addiction follows the same pattern as epidemic (growth and lessening, isolated to areas ect)
x. Other factors other than just the drop – also the do with socioeconomic, culture ect

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7
Q

What is the Physical Dependence Model?

A

“The state in which the discontinuation or reduction of a drug would cause withdrawal symptoms”

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8
Q

What are withdrawal effects?

A

• Repeated drug administration  body learns to adjust to drug-induced changes
• Drug removed  body readjusts again (withdrawal)
• Withdrawal symptoms: usually opposite symptoms incurred by drug
• > Can be stopped by re-administering the drug, or a similar drug (cross-dependence)
o Drug may be re-administered to counteract withdrawal effects

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9
Q

What doesn’t the PDM account for?

A

relapse that happens after the withdrawal effects are over

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10
Q

What are the strengths of the Physical Dependence Model?

A

o Compatible with disease model; plausible explanation for addiction to drugs with withdrawal effects

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11
Q

What are the limitations of the Physical Dependence Model?

A

o Individual differences as well as the disease model can;
o Substances of addiction that show little to no withdrawal sickness;
o Voluntary withdrawal (despite symptoms)
• Attempts to refine model: psychological dependence
o Circular reasoning
o Difficult to assess outward manifestations

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12
Q

What is the Positive Reinforcement Model?

A

• Drugs are self-administered because they act as positive reinforcers (operant conditioning)

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13
Q

What is a positive reinforcer?

A

“any stimulus that increases the frequency of a behavior it is contingent on”

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14
Q

What are two things that support the positive reinforcement model?

A

• Drugs that are self-administered by animals even in the absence of physical dependence/withdrawal
o (Intragastric, intracranial, intraventricular, inhalation & oral routes)
• How the drug is administered has a large impact on how addictive it can be
o E.g. smoke is taken up by body much faster than those taken through the digestive system (e.g. crack cocaine much more addictive as it can be smoked/ opium ect)

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15
Q

What are the limitaitons of the positive reinforcement model?

A

o Can the positive consequences of behavior outweigh the costs (positive reinforcement paradox)?
o Circularity: drug is +ve reinforcer bcs increased drug taking behavior; then positive reinforcement cannot explain drug taking

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16
Q

What are the strengths of the positive reinforcement model?

A

o Accounts for drug-taking behavior in absence of dependence/withdrawal;
o Compatible with disease/physical dependence model;
o Compatible with general models of reinforcement

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17
Q

How does classical and operant conditioning apply to drug taking?

A
  1. Reinforcing effects of drugs can be paired with other stimuli through conditioning
  2. An extinction phase can be demonstrated
  3. Responses to operant reinforcement schedules can be elicited as predicted
  4. Responses can be elicited following priming
  5. Response patterns to substances that act as aversive stimuli are consistent with avoidance behaviours
  6. A conditioned compensatory response can be demonstrated
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18
Q

How does positive reinforcement relate to neurobiology?

A

• Positive reinforcers activate motivational circuits
o May increase likelihood of behavior repeating
• Pleasure centers/motivational circuit (neuroanatomy)
• Motivational circuit relies on activity of neurotransmitters (NTs)
• Incentive salience (natural and acquired)

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19
Q

What is the incentive sensitization theory?

A

• Repeated drug administration
o Increased sensitization of mesolimbic DA response and motivation circuitry
o Increased incentive salience of drug and associated stimuli -> craving

20
Q

What is drug craving?

A

desire/urge to experience the effect (s) f a previously experienced psychoactive substance (‘wanting’)

21
Q

What are the strengths of the Incentive sensitization theory?

A

o Accounts for the development of addiction over time/use

o Explains craving triggers (associated stimuli that have acquired incentive salience) and priming effects

22
Q

What is Hedonic Dysregulation and Adaption?

A

Modern version of physical dependence model

23
Q

What is an allostatic process?

A

o Repeated use and/or cessation of use -> opponent process or functioning and neuroadaptation
o Contrast to homeostasis (changing/lowered set point)
o Increased tolerance to pleasurable (‘liking’) effect of drug and increased insensitivity to pleasure

24
Q

What is dysphoria

A

withdrawal mechanism of psychological dependence

- o Can explain relapse long after physical withdrawal symptoms gone

25
Q

What are the circuits that regulate addiction?

A
  1. “reward/saliency” (e.g. nucleus accumbens and ventral tegmental area)
  2. “motivation/drive” (e.g. orbitofrontal cortex and motor cortex)
  3. “memory/conditioning” (e.g. anygdala and hippocampus)
  4. “inhibitory control/executive function” (e.g. dorsolateral prefrontal cortex and anterior cingulate gyrus)
    - All interconnected circuits; receive input from DA neurons
26
Q

What is a neuron?

A

responsible for receiving sensory information, integrating and storing information and controlling muscles and glands

27
Q

What is a neurotransmitter? What does it do?

A

chemical messengers that operate between synapses
• NTs released at synaptic vesicles into synaptic cleft & occupy reception sites on post-synaptic neuron
• Receptor site may depolarize or hyperpolarize post-synaptic cell

28
Q

What is the process of axon stimulation?

A

o Action Potential (AP)
 The breakdown & restoration of the resting potential
• Firing; all-or-none law
 Depolarization (EPSP)
• Moves toward zero and positive numbers
 Hyperpolarization (IPSP)
• Moves further away (more negative) from zero
 Threshold of excitation
 Voltage gated ion channels
o Stimulation of dendrites and cell body
 Postsynaptic potentials (PSPs): graded; excitatory (EPSP) vs. inhibitory (IPSP); summation across time and space

29
Q

What is the action at a synapse?

A

o NTs (1st messengers”) – effects depend on receptor site binds to
o Receptors – iontropic vs. metabotropic
o Second Messengers
 Special molecule is released into the postsynaptic cell
 Multiple mechanisms and durations of effect

30
Q

What are the two types of receptors?

A

iontropic vs. metabotropic

31
Q

How do most drugs work?

A

interfering with the chemical process that occurs at a synapse

32
Q

How do drugs alter the synaptic process?

A
  1. Mimicking NTs and occupying their receptor sites
  2. Lowers activity of enzymes that create or destroy NTs
  3. Altering NT reuptake
  4. Altering the activity of a second messenger
  5. Interfering with ion channels
  6. Changing the amount of NT released
33
Q

What are the Cholinergic synapses?

A
  • Nicotinic

- Muscarinic

34
Q

What are nicotinic synapses blocked and stimulated by?

A
  • Stimulated by nicotine

- blcoked by curare and botox

35
Q

What are the muscarinic synapses blocked and stimulated by?

A
  • Stimulated by muscarine

- Blocked by atrophine and scopolamine

36
Q

How does the plasticity of Physiology incluence drug taking?

A
  • CNS is not static; changes make take place in the CNS in response to drug taking (e.g. more receptor sites, more sensitivity of receptors etc.)
  • Such plasticity may account for another aspect of drug taking – tolerance
37
Q

What is tolerance?

A

lowers effectiveness (or potency) of drug usually resulting from repeated administrations; necessity of increased dose to maintain its effect

38
Q

What is cross-tolerance?

A

tolerance to one drug diminishes the effect of another drug

39
Q

What is acute tolerance and tachyphlaxis?

A

tolerance after one drug administration

40
Q

How does tolerance work?

A
  1. Tolerance develops and dissipates to different effect of drugs, at different rates
  2. Tolerance will only develop in a circumstance where a drug places a demand on the homeostatic mechanisms
41
Q

What is metabolic tolerance?

A

rate of metabolism increases, usually due to an increase in enzymes used to break down the drug (enzyme induction)

42
Q

What is physiological tolerance?

A

homeostasis is mechanism by which the body maintains a constant internal environment; can result in tolerance

43
Q

What is behavioural tolerance?

A

through experience with a drug organisms can learn to decrease behavioral effect of the drug (both through classical and operant conditioning)

44
Q

What is conditioned tolerance?

A

environment drug is administered in can be a stimulus (CS) for the body’s effort to resist a drug -> eliciting physiol. Compensatory conditioned responses (CR) that decreases effect of drug/ increased tolerance

45
Q

What is sensitization (reverse tolerance)?

A

less common than tolerance, refers to increased effects of a drug usually following repeat administrations