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HC > Drugs > Flashcards

Drugs Flashcards

1
Q

Communication in the brain

A 
Electricity 
- action potentials 
- high enough - release 
Chemistry 
- neurotransmitters 
- carry info 
- define quality of content
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2
Q

Neurotransmitters

A
  • l-glutamine and GABA
  • perform vital functions in the CNS, excitatory and inhibitory
  • dopamine - increase HR and BP, memory and attention
  • serotonin - depression, suicide and impulsiveness
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3
Q

Modes of Action

A
  • usually react with receptors (“lock and key”)
  • agonist or antagonist of NT and NM
    • naturally secreted substance that acts like NT
    • not restricted to synaptic cleft, diffuses through extracellular fluid
  • agonist - drug that facilitated effect of NT on postsynaptic cell
  • antagonist - inhibits or opposed effects of NT on postsynaptic cell
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4
Q

How do drugs work?

A

Alter presynaptic events

Affect processes in the axon (conduction of action potentials)

Affect synthesis and storage of NT and NM

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5
Q

Neural mechanisms

A

All natural reinforcers cause release of dopamine in nucleus accumbens

Addictive drugs also trigger the release of dopamine

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6
Q

Drug effects

A

Drugs can:

  • stop chemical reactions creating NT
  • empty NT from vesicles where stored to protect from breakdown
  • block NT entering/leaving vesicles
  • bind to receptor in place of NT
  • prevent NT returning to sending neuron (reputable)
  • interfere with second messenger
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7
Q

Messengers

A
  1. Neurotransmitters
  2. Chemical produced when G protein activate another enzyme
    - carries signal to open ion channel or cause other events in the cell

G protein - conveys messages to other molecules

Reuptake - reentry of NT liberated by terminal button back though membrane and terminating post

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8
Q

Synaptic Events

A

Interfere reuptake mechanisms

Affect activation of receptor molecules (e.g. antipsychotics may block dopamine receptors, dopamine antagonist)

Alter number of receptor molecules (alcohol increases GABA receptors)

Alter second messenger activity

May affect the release of synaptic transmitters

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9
Q

Neural mechanisms

Cocaine

A

Inhibits the active uptake of dopamine and norepinephrine into neuron terminal allowing accumulation of transmitters in synapses

Accumulation of dopamine and it’s action an receptors is responsible for the stimulant, euphoric activity of the drug, and consequent abuse

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10
Q

Tolerance

A
  • must take larger and larger amounts to be effective

- will suffer withdrawal symptoms if they stop taking the drug

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11
Q

Caffeine

A
  • stimulates CNS: increase alertness, wakefulness, ability to work and concentrate
  • enhance cognition and stimulate encoding
  • competes with NT adenosine (inhibits release of cataholamines)
    • class of amines, include dopamine and epinephrines
  • acts as cateholaminergic agonist
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12
Q

Warburton (1995)

A
  • regular coffee drinkers prescribed caffeine
  • computer cognitive tasks
  • improve cognitions (attention, problem solving, delayed recall)
  • not immediate recall or working memory
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13
Q

Caffeine research

A
  • focus on effects of cognitive performance
  • evidence mixed (Van der Stelt and Snel, 1998)
  • mood results also mixed
  • positive often attributed to arousal from caffeine
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14
Q

Caffeine Research Critique

A

Methodology issues
- inconsistent (Lieberman, 1987)

Design issues

  • dietary doses, weight related doses, dose dependency
  • within vs between subjects
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15
Q

Participant variables

A
  • use of other drugs
  • interactions (caffeine and nicotine, alcohol, other drugs)
  • sex (menstrual cycle), age, personality

Controls - washout period, dosage, time of day

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16
Q

Alcohol

A
  • wide range of CNS effects
  • increase GABA receptors
  • dopamine release
  • opiate antagonists suppress consumption in rats (Froelich et al, 1990)
  • genetic vulnerability and stressful environment cause alcoholism (McGue, 1999)
17
Q

Effects of Alcohol

A
  • neg affect of basic perceptual, simple performance measures and complex tasks
  • biphasic: stimulation through depression
  • driving: even at low dose impair psychomotor coordination and sustained attention
  • acute alcohol cons impairs WM
  • chronic alcohol cons impairs LTM
  • protective effect of low/moderate cons and dementia (Panza et al, 2012)
18
Q

Nicotine

A
  • acts mostly on ANS
  • stimulation of reward centre
  • cholinergic agonist: interacts with cholinergic receptors (crucial in cog)
  • biphasic: stimulant and depression
19
Q

Nicotine Research

A
  • twin studies show genetic component (65%) (Lerman et al,1999)
  • only 20% attempts to quit successful (Schelling, 1992)
  • enhance performance of cog tasks in humans and animals (Pritchard and Robinson, 1998)
  • reaction time and errors in smokers (Pritchard and Robinson, 1998)
  • short term but not long term memory (Heishman et al, 2010)
20
Q

Lack of Nicotine

A 
Withdrawal 
Heart and BP changes 
Sleeping problems 
Anxiety, irritability, impatience, hostility, depression 
Difficulty concentrating 
Restlessness 
Increased appetite and weight gain
21
Q

Alcohol and Nicotine

A

Often taken in combination but few studies

Alcohol associated with increase cigarette consumption (Istavan and Matarazzo, 1984)

22
Q

Alcohol and Caffeine

A

Caffeine used as cure but no clear evidence

May reduce alcohol absorption

23
Q

Nicotine and Caffeine

A

Nicotine reduces half life of caffeine

Both show to improve performance

Caffeine intake doesn’t increase smoking -link may have non pharmacological basis

24
Q

Summary

A
  • major drugs mimic structure of NT
  • NT underlie every though, emotion, memory, learning
  • carry signals between all nerve cells or neurons in the brain
  • neurochemistry supporting addiction: places, people and objects associated with drugs imprinted on the brain

HC (2 decks)

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