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PYB260 > Week 2 - Neurobiology > Flashcards

Week 2 - Neurobiology Flashcards

1
Q

Models of addictive behaviour - drug use models

A
  • disease model
  • physical dependence model
  • positive reinforcement model
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2
Q

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 year was addiction added to the DSM?

A

1987

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4
Q

Strengths of the disease model

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

Limitations of the disease model

A
  • what is the disease?
  • may reduce individual responsibility for behaviour
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6
Q

Physical dependence model

A

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

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7
Q

Drug administration and withdrawal effects

A
  • repeated drug administration - body learns to adjust to drug-induced changes
  • drug removes - body readjusts again (withdrawal)
  • withdrawal symptoms are usually opposite symptoms incurred by drug
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8
Q

How can withdrawal symptoms be stopped?

A

by re-administering the drug, or a similar drug (cross-dependence)

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9
Q

Strengths of physical dependence model

A

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

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10
Q

Limitations of physical dependence model

A

cannot account for:
- individual differences as well as the disease model can
- substances of addiction that show little to no withdrawal sickness
- voluntary withdrawal (despite symptoms)

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11
Q

How does the psychological dependence model attempt to refine the physical dependence model?

A
  • circular reasoning
  • difficult to assess outward manifestations
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12
Q

Positive reinforcement model

A
  • drugs are self-administered because they act as a positive reinforcer (operant conditioning)
  • drugs that are self-administered by animals even in the absence of physical dependence/withdrawal
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13
Q

What is a positive reinforcer?

A

any stimulus that increases the frequency of a behaviour it is contingent on

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14
Q

Limitations of positive reinforcement model

A
  • can the positive consequences of behaviour outweigh the costs?
  • circularity: drug is a positive reinforcer because of increased drug taking behaviour; then positive reinforcement cannot explain drug taking
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15
Q

Strengths of the positive reinforcement model

A
  • accounts for drug-taking behaviour in absence of dependence/withdrawal
  • compatible with disease/physical dependence model
  • compatible with general model of reinforcement
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16
Q

How does classical & 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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17
Q

why do positive reinforcers activate motivational circuits?

A

because it may increase likelihood of behaviour repeating

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18
Q

What does the motivational circuit rely on?

A

activity of neurotransmitters

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19
Q

Incentive salience

A

A strong motivation for rewarding stimuli (natural and acquired)

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20
Q

neuroanatomy of motivation & reinforcement

A
  • ‘wanting’ vs ‘liking’ in reinforcement
    • ‘pleasure centres’
  • drugs as reinforcers
  • stress & reinforcement
  • addiction
    • drugs alter the functioning of the motivation system & behaviour
    • increase dopamine in mesolimbic dopamine system
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21
Q

Incentive Sensitisation Theory

A

with repeated administration of a drug, the reinforcing effects (incentive value) and related stimuli become sensitised.
- increased sensitisation of the dopamine response in mesolimbic dopamine system & motivation circuitry, leads to;
- increased intensive salience being acquired of the drug and associated stimuli

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22
Q

Drug craving

A

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

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23
Q

Strengths of the Incentive Sensitisation Theory?

A
  • accounts for the development of addiction over time/use
  • explain craving triggers (associated stimuli that have acquired incentive salience) & priming effects
24
Q

Hendonic dysregulation & adaptation (HD&A) is the modern version of which model?

A

the physical dependence model

25
Q

Allostatic process of HD&A

A
  • repeated use &/or cessation of use, there’s an opposite compensatory response (depression) - disrupted neurotransmitter functioning & neuroadaptation
  • contrast to homeostasis (changing/lowered set point in brain)
  • increases tolerance to pleasurable (liking) effect of drug & increases insensitivity to pleasure
26
Q

Dysphoria

A

withdrawal mechanism of psychological dependence - can explain relapse long after physical withdrawal symptoms are gone

27
Q

Disruption of brain control circuits

A

A dysfunction in information processing and integration amongst multiple brain regions

28
Q

circuits that regulate

A
  1. reward/saliency - (nucleus accumbens & ventral tegmental area)
  2. motivation/drive (orbitofrontal cortex & motor cortex)
  3. memory/conditioning - (amygdala & hippocampus)
  4. inhibitory control/executive function - (dorsolateral prefrontal cortex & anterior cingulate gyrus)
    - all interconnected circuits; receive input from dopamine neurons
29
Q

neurons

A

responsible for receiving sensory information, integrating & storing information & controlling muscles & glands.
- connected to each other via synapses

30
Q

cell body (soma)

A

contains the nucleus

31
Q

nucleus

A

contains genetic information & controls metabolism of the cell

32
Q

membrane

A

surrounds the cell; semipermeable; filled with cytoplasm

33
Q

dendrites

A

fibres extending from axon; connect to other cells

34
Q

axon

A

length of the neuron

35
Q

axon hillock

A

place where axon is attached to cell body

36
Q

myelin sheath

A

fatty substance surrounding the axon

37
Q

terminal buttons

A

swelling at the end of the axon

38
Q

what are neurotransmitters

A

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

39
Q

Stimulation of the axon

A
  • action potential (AP)
  • the breakdown & restoration of the restin potential (firing; all or non 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
40
Q

Stimulation of dendrites & cell body

A

postsynaptic potentials (PSPs): graded; excitatory (EPSP) vs inhibitory (IPSP) summation across time & space

41
Q

Action at a synapse

A
  • neurotransmitters - effects depend on receptor site and binds to;
  • receptors - ionotropic vs metabotropic
  • second messengers
42
Q

Types of neurotransmitters

A
  • Acetylcholine (ACh)
  • Monoamines:
  • Catecholamines (CA)
    • Epinephrine (E)
    • Norepinephrine (NE)
    • Dopamine (DA)
  • Serotoninc or 5-Hydroxytryptamine (5-HT)
  • Adenosine
  • Endocannabinoids
  • Amino Acides
  • Opiod Peptides
    • Enkephalines or Endorphins
43
Q

Neurotransmitter action

A

most drugs work by interfering with the chemical process that occurs at a synapse

44
Q

How do drugs alter the synaptic process

A
  1. mimicking neurotransmitters & occupying their receptor sites
  2. decreasing activity of enzymes that create or destroy neurotransmitters
  3. althering neutrotransmitter reuptake
  4. altering the activity of a second messenger
  5. interfering with ion channels
  6. changing the amount of neurotransmitter released
45
Q

How do drugs have an effect on Acetylcholine (ACh)

A
  • Acetylcholinesterase (AChE) - enzyme in synapse which normally breaks down Ach
  • Drugs may interfere with AChE or with receptor sites
  • Insecticides, Nerve Gases
  • Cholinergic synapses
  • Nicotinic
  • Stimulated by nicotine
  • Blocked by curare & Botox
  • Muscarinic
  • Stimulated by muscarine
  • Blocked by atrophine & scopolamine
46
Q

Plasticity of physiology and neurophysiology

A

CNS is not static - changes may take place in the CNS in response to drug taking
such plasticity may account for another aspect of drug taking - tolerance

47
Q

Tolerance

A

decreased effectivence (or potency) of a dryg usually resulting from repeated administrations; necessity of increased dose to maintain its effect

48
Q

cross-tolerance

A

tolerance to one drug diminishes the effect of another drug

49
Q

what is acute tolerance and tachyphlaxsis

A

tolerance after one drug administration

50
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
51
Q

Metabolic tolerance

pharmacokinetic tolerance

A

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

52
Q

physiological tolerance

pharmacodynamic tolerance

A

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

53
Q

behavioural tolerance

A

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

54
Q

conditioned drug tolerance

A

environment drug is adminstered in can be a stimulus for the body’s effort to resist a drug leads to eliciting phys. compansatory conditioned responses that decrease effect of drug/increase tolerance

55
Q

sensitisation (reverse tolerance)

A

less common than tolerance, refers to increase effects of a drug usually following repear administrations
- cross-sensitisation to other drugs

56
Q

Diagnostic criteria of identifying people with addictions

A
  • DSM-IV-TR
  • DSM-5
  • ICD-11

PYB260 (10 decks)

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