Drugs And Addiction Flashcards

(33 cards)

1
Q

What are drugs?

A

Imitate substances already present in our nervous system, particularly those that affect transmission at the synapse

  • drugs= mainly from plants
  • plant produces chemical to attract insects, to stop being eaten etc
  • nervous system of many animals = similar
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2
Q

How do drugs work?

A

Can affect transmission at synapse in 2 way:

  1. Antagonist — blocks NT
  2. Agonist— increase effect of NT/ mimics NT
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3
Q

How to drugs work? (Receptors)

A

Drunk has high AFFINITY for receptor, if it BINDS to that receptor

Drug has high EFFICACY if it has tendency to ACTIVATE that receptor

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4
Q

How to drugs work? Brain

A

Drugs stimulate release of dopamine — in nucleus accumbens

Drug» bursts of dopamine» inhibits GABA» increases activity in nucleus accumbens

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5
Q

What is the nucleus accumbens?

A

Small subcritical area rich in dopamine receptors

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6
Q

Drug stimulants: agonists

A

Amphetamine (speed)
- stimulates dopamine synpases by increasing release of dopamine from presynaptic terminal

Cocaine
- blocks reputable of dopamine, prolonging effects

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7
Q

What does more dopamine result in?

A

Widespread reduction in activity in most f brain (apart from nucleus accumbens)

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8
Q

How do drugs work? Opiates:

A

Morphine + Heroin
- both increase relaxation, decrease sensitivity to pain
- mimics endorphins (naturally occurring chemical in brain)
- opiates attach to specific endorphin receptors

  1. Inhibit GABA - increase dopamine
  2. Also blocks hindbrain area that usually releases norepinephrine
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9
Q

What does reduction in norepinephrine result in?

A

Reduces memeory storage +reduces stress

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10
Q

How does marijuana work?

A
  • Contains cannabinoids
  • bind to specific cannabinoid receptors (widespread in brain)
  1. Inhibit GABA release (increase dopamine release in nucleus accumbens) = perception of high extended awareness
  2. Cannabinoid receptors abundant in hypothalamus (feeding)= increased appetite
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11
Q

How do drugs work? Botox

A
  • deadly nerutoxin released by bacteria found in decaying food
  • ANTAGONIST
  • Blocks release of acetylcholine at neuromuscular junctions - paralysis
  • in small doses can be used to reduce muscle tremors and cosmetically
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12
Q

How do drugs relate to addiction?

A

Many addictive substances increase activity at dopamine synapses
Particularly in nucleus accumbens

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13
Q

Different between wanting and liking

A

-Drugs increase NEED for substance even if experience = not pleasant

  • Mice with increased dopamine production showed no more pleasure in food, but made more efforts to get it
  • Mice with decreased dopamine production made less effort to get food, but ate just as much
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14
Q

Drug addiction: Sensitisation of Nucleus Accumbens

A
  • becomes more sensory to substance after repeated use
  • increased ability to release dopamine in response to substance
  • reduced sensitive to other things
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15
Q

Drug addiction: Withdrawal

A
  • craving for drug
  • relapse causes increased sensitivity
  • user learns that drug relieves distress associates with withdrawal, and so craves it more during future withdrawal
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16
Q

Can we counter addiction?

A

Treatment from smocking:

Varenicline = partial nicotine receptor agonist

Varenicline stimulate + binds&raquo_space; nicotine, timulattes nictoine rectors= increased dopamine

17
Q

What considers something to be addition?

A

Continues use of substance that interfered with you life

18
Q

Alcohol and areas of brain:

A

Alcohol acts on many brain areas— mainly inhibitory effects

19
Q

2 types of alcoholism:

A
  1. Late onset, gradual onset, equal men and women, less severe, few relatives with alcoholism
  2. Early onset, rapid onset, more men than women, severe, more relatives with alcoholism
20
Q

Genes and alcoholism

A

Genes may influence alcoholism in many ways

  1. Coding for increase in risk taking behaviour
  2. Coding for increased stress responce= more likely to relapse after quitting
21
Q

Do sons of alcoholic fathers show predispositions to alcoholism?

A
  1. Show tolerance to alcohol
  2. Greater decrease of stress when drinking
  3. Smaller amygdala (increases risk taking).
22
Q

Depression, what causes it?

A

Clinical depression:
- feelings of extreme sadness
- severe enough to interfere with daily life
- twice as commen in women

Causes:
- degree os heritability to depression, but not specific to depression (relatives likely to suffer from bulimia, anxiety, substance abuse)
- more common among relatives of women with early onset depression

  • suggested that postnatal depression runs in families
23
Q

Depression and Seratonin

A

Low seratonin associated with aggression and depression

So genes controlling seratonin have been implicated
- gene controlling serotonin transporter protein
-this protein control ability of axon to re absorb serotonin

24
Q

Genes controlling serotonin: short and long types

A

This gene affects how people cope with life experiences

Short and long types:

  • 2 short forms of gene = more likely to have depression in responce to stressful stimuli
25
Bipolar Disorder
Unipolar disorder: varying between normality + depression Bipolar disorder: varying between mania + depression
26
What is mania ?
Restless activity, excitement, confidence, rambling speech
27
What happen with bipolar?
Increased metabolism during manic phases Possible genetic component— more common in monozygotic twins Treated with lithium salts— bocks synthesis of acid associated with brain inflammation
28
What is Seasonal Affective Disorder (SAD) ?
- depression associated with one season (winter) - common near poles were nights are long - less severe than major depression - light therapy as treatment (affects biological clock)
29
Schizophrenia
Split mind. Not related to dissociative identity disorder. Split refers to diviso between emotional and intellectual experiences and behaviour Some patients show innaprotirte emoonal expression that seeks detached from current circumstances Symptoms: hallucinations, thought disorder, movement disorder, psychotic, disorganised, poor social interactions, poor speech Difficult to diagnose- often confused with other conditions Difficult to pinpoint specific brain area More common in men Earlier onset on men
30
Schizophrenia- is there one gene for it?
May not be one gene,instead combination of genes interacting with environment
31
How does schizophrenia develop?
Neurodevelopmental hypothesis = abnormalities in development of nervous system before birth and in newborn 1. Infections, poor nutrition, complicated delivery —- only increases Schizophrenia chance slightly 2. Some slight brain abnormalities in patients, suggesting subtle changes during development
32
Brain abnormalities in schizophrenia
1. Ventricles larger— less space for brain cells 2. Prefrontal cortex damaged (work in memeory impaired) 3. Cell bodies smaller in hippocampus and prefrontal cortex 4. Less ,arterialisation than most ppl- more likely to be left handed
33
Schizophrenia: what is happening at the synapse?
Abused drugs associated with excess of dopamine— can cause psychosis Dopamine hypothesis of schizophrenia = excess activity of dopamine synapses Schizophrenia patients have 2x as may dopamine receptors that others Associated with lower than normal release of glutamate + fewer re perons in prefrontal cortex Glutumate hypothesis of schizophrenia = deficient activity at glutamate synapses Dopamine inhibits glutamate release and glutamate activates neurons that inhibit dopamine