Lecture 12 Flashcards

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1
Q

What are drugs?

A

Two types - illegal = cocaine, opiates, LSD and legal = nicotine, alcohol and caffeine. Tend to imitate substances already present in our nervous system, particularly those that affect transmission at the synapse.

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2
Q

How do drugs work

A

Drugs can affect transmission at the synapse in two ways: Antagonist = inhibit transmission at the synapse and block neurotransmitters. And Agonist = facilitate transmission at the synapse and increase effects of neurotransmitter, or mimic the neurotransmitter. Some drugs do both of these. Drug has a high affinity for a receptor if it binds to that receptor and has a high efficacy if it has tendency to activate that receptor. Most drugs stimulate the release of dopamine particularly in the nucleus accumbens = a small subcortical area rich in dopamine receptors. Drugs = sustained bursts of dopamine = inhibition of GABA = increases activity in nucleus accumbens. They work through stimulants - amphetamine = stimulates dopamine synpases by increasing the release of dopamine from presynaptic terminal. Cocaine = blocks the reuptake of dopamine, thus prolonging effects. More dopamine = widespread reduction in activity in most of the brain apart from nucleus

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3
Q

Why do drugs increase arousal

A

Excitement, confidence and alertness - decreases background noise - increases the clarity of signals

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4
Q

How do opiates work

A

Morphine & heroin = increases relaxation, decrease sensitivity to pain. Mini endorphins, so opiates attach to specific endorphin receptors: 1 = inhibits GABA so increases dopamine, but also blocks a hindbrain area that usually releases norepinepherine - reduction in norepinepherine reduces memory storage and reduces stress

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5
Q

How does marijuana work

A

Contains cannabinoids and bind to specific cannabinoid receptors widespread in the brain. 1 = inhibit GABA release = perception of heightened awareness. 2 = Cannabinoid receptors abudant in hypothalamus = increases appetite

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6
Q

How does Botox (Botulinium toxin) work

A

Deadly neurotoxin released by bacteria found in decaying food. Antagonist and blocks the release of acetylcholine at neuromuscular junctions - paralysis, but in small doses can be used to reduce muscle tremors and cosmetically

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7
Q

How do drugs relate to addictions

A

Many addictive substances increase activity at dopamine synpases, particularly in the nucleus accumbens. Sensitization of the nucleus accumbens = becomes more sensitive to substances after repeated use, increased ability to release dopamine in response to the substance, reduced sensitivity to other things. Withdrawal = cravings for the drug, relapose causes increased sensitivity, user learns that the drug relieves distress associated with withdrawal, and so craves it more during future withdrawal

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8
Q

What’s the difference between wanting and liking?

A

Drugs increase the need for the substance even if the experience is not pleasant - mice with increased dopamine production showed no more pleasure in food, but made more effort to get it. Mice with decreased dopamine production made less effort to get food, but ate just as much

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9
Q

Can we counter addiction

A

Varenicline is a treatment for smoking = partial nicotine receptor agonist. Addiction to legal drugs can be hard to define - addiction = continues use of a substance when it interfers with your life

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10
Q

Discuss the two types of alcoholism

A

Type 1 = late onset (after 25), gradual onset and equal in men and women - it is less severe and fewer relatives with alcoholism. Type 2 = Early onset (before 25) and rapid onset, more men than women, Severe and more relatives with alcoholism. Genes might influence alcoholism in many ways e.g. coding for an increase in risk taking behaviour, coding for an increased stress response = more likely to relapse after quitting.

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11
Q

Do sons of alcoholic fathers show predispositions to alcoholism?

A

Show less than average intoxication - better tolerance to alcohol! Show greater decrease of stress when drinking and have slightly smaller amygdala

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12
Q

Discuss depression with definitions and traits

A

Clinical/major depression = feelings of extreme sadness and helplessness, server enough to interfere with daily life and can last for weeks or months. This is twice as common in women than men and 5% of adults have clinically significant depression. Postnatal depression is depression after giving birth - 20% women, but only 0.1% is long-lasting.

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13
Q

What causes depression

A

Moderate degree of heritability to depression, but not specific to depression! Relatives are also more likely to suffer from anxiety disorders, substance abuse and bulimia. More common among relatives of women with early onset depression. Low serotonin turnover associated with aggression and depression so genes controlling serotonin have been implicated. Caspi et al (2003) found that gene controlling the serotonin transporter protein controls the ability of an axon to reabsorb serotonin. This gene affects how people cope with life experiences - two short forms of the gene results in a higher chance of depression in response to stressful life events

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14
Q

Discuss what bipolar disorder is and the different types

A

Unipolar disorder = varying between normality and depression. Bipolar disorder = varying between mania and depression (manic depression). Mania = restless activity etc. Increased metabolism during manic phases and possible genetic component - more common in monozygotic twins but this seems to increase risk rather than cause. It is treated with lithium salts which block synthesis of arachidonic acid

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15
Q

What is SAD

A

Seasonal Affective Disorder. Depression associated with one season (usually winter) and is commor near the poles where the nights are long. It is less severe than major depression and light therapy can treat it

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16
Q

Discuss schizophrenia and what it is

A

Schizophrenia = split mind, but is not related to multiple personality. Split refers to a division between emotions and intellectual experiences and behaviour. Some patients show inappropriate emotions expression that seems detached from current circumstances. Behavioural symptoms include positive and negative. Positive = psychotic and disorganised. Negative = poor social skills and speech. Not all patients exhibit all symptoms - difficult to diagnose, often confused with other conditions and difficult to pinpoint a specific brain area. Demographics = more in men, earlier onset in men, 1% of population and equal in all cultures and populations (this implies a genetic basis). It is likely in closely related individuals but it may not be one gene but instead a combination of genes interacting with the environment

17
Q

How does schizophrenia develop

A

Neurodevelopmental hypothesis = abnormalities in the development of the nervous system before birth and in the newborn. Infections, poor nutrition and complicated delivery increase chance of schizophrenia slightly as well as some slight brain abnormalities in patients, suggesting changes during development. Brain abnormalities = ventricles are larger so less space for brain cells, prefrontal cortex is damaged, cell bodies are smaller in the hippocampus and prefrontal cortex, less lateralisation than most people and thus more likely to be left handed

18
Q

What happens at the synapse in schizophrenia patients

A

Abused drugs are associated with an excess of dopamine, and can cause psychosis - dopamine hypothesis of schizophrenia = excess activity of dopamine synapses. Patients have twice as many dopamine receptors than other people, but normal levels of dopamine are found when measured directly. It is also associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex = deficient activity at glutamate synpases. Related to dopamine - dopamine inhibits glutamate release and glutamate activates neurons that inhibit dopamine. PCP inhibits glutamate receptors and produces similar symptoms to schizophrenia.