Lecture 11 Flashcards

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1
Q

What are drugs?

A

Substances that tend to imitate other substances that are already present in the nervous system, usually those that are involved with the transmission at the synapse. Most drugs come from plants that use the chemicals to attract insects or to prevent being eaten.

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2
Q

What are the two types of ways drugs affect the synapse?

How do drugs work?

A

They can affect the synapse antagonistically; inhibits transmission by blocking the neurotransmitter, or agonistically; facilitates transmission at the synapse by increasing the effects of the neurotransmitter or mimicking it. Some drugs can cause both effects. Drugs can have a high affinity for a receptor and they can have a high efficacy for one, meaning they activate it. Most drugs stimulate the release of dopamine, mainly in the nucleus accumbens (small subcortical area rich in dopamine). The increased release of dopamine inhibits GABA which increases the activity in the accumbens.

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3
Q

How do stimulants work?

A

Stimulants such as amphetamine, aka speed, and cocaine are dopamine agonists causing the accumulation of dopamine in synaptic cleft. Speed stimulates the release of dopamine in the presynaptic terminal. Cocaine blocks the reuptake of dopamine, so this drug has prolonging effects. Increased dopamine reduces activity in most ofthe brain which causes arousal as there is less background noise. After the effects wear away, you crash because the dopamine isn’t replaced quickly enough.

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4
Q

How do opiates work?

A

Opiates such as morphine and heroin increase relaxation and decrease sensitivity to pain. They mimic endorphins by attaching to endorphin receptors. This inhibits GABA which increases dopamine but it also blocks norepinephrine in the hindbrain reducing memory and stress.

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5
Q

How does marijuana work?

A

It contains cannabinoids which bind to cannabinoid receptors in the brain, this also inhibits GABA etc. They also increase apetite as the receptors are abundant in the hypothalamus.

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6
Q

How does botulinium toxin work?

A

This is commonly known as botox. It’s released by bacteria in decaying food, it’s a deadly neurotoxin. Botox is an antagonist because it blocks the release of acetylcholine which causes paralysis. In small doses, it can be used cosmetically.

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7
Q

How does addiction work?

A

Kalat found that when mice had increased dopamine production, they had no increased pleasure for food, they just tried harder to get it. The opposite was found with decreased dopamine production. This shows that drugs increase the need for the substance but this isn’t related to pleasure. Over time, the nucleus accumbens becomes more sensitive to substances after repeated use, this increases dopamine release in response to the substance, however, it becomes less sensitised to other things. If one then withdraws from the substance, they crave it. Then, if they relapse, they become even more sensitive and realise they need the drug to relieve the distress, making withdrawal even harder.

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8
Q

What drug can be used to reduce nicotine addiction?

A

Vareniciline, it works by causing the same effect as nicotine.

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9
Q

What are the two types of alcoholism?

side note: alcohol has mainly inhibitory effects

A

Type 1: Late and gradual onset, less severe and no gender differences found. No genetic basis.
Type 2: Early and rapid onset, more severe and more prevelant in men. Possible genetic basis.

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10
Q

Discuss alcohol and genetics

A

There isn’t a specific gene for alcoholism. However, there could be genes that code for an increase in risk taking behaviour or increased stress responses which would make one more likely to relapse.
Research has shown that sons have more tolerance for alcohol, they have a larger reduction in stress when they drink and they have a smaller amygdala (associated with risk taking).

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11
Q

Discuss depression

A

It’s a disorder that causes extreme sadness and feelings of helplessness. It interferes with one’s life, it’s more prevelant in females and about 5% of adults have clinical depression. There’s a moderate degree of heritability but it isn’t specific to depression, it’s an increased chance of developing disorders like anxiety, substance abuse, depression and so on. Low levels of serotonin are associated with depression (as well as aggression) so genes are involved. Caspi found that it was the gene controlling the serotonin transporter protein. If you have 2 short versions of the gene, you are more likely to develop depression after a stressful event. 20% of women get post partum depression and Murphy-eberenz found heritability of post partum depression.

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12
Q

Discuss bipolar disorder

A

There are two types: unipolar (varying between normaility and depression) and bipolar (varying between mania and depression). People have increased metabolism during manic phases. There is concordance found but related to increased risk, not a direct cause. You can treat it via lithium salts which prevent arachidonic acid being synthesised.

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13
Q

Discuss seasonal affective disorder

A

When one gets depressed during winter, it’s less severe than depression. Light therapy can treat it.

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14
Q

Discuss schizophrenia

A

Commonly known as split mind because there is a division between emotion/intellect and behaviour. Their emotions often seem detached from their circumstances. Scizophrenia can cause hallucinations and delusions. The disorder can be acute or chronic. Positive symptoms (additions): psychotic symptoms like hallucinations and disorganised symptoms like odd emotional displays. Negative symptoms: poor speech, poor social interactions etc. Not all patients show all symptoms, making it hard to diagnose and hard to find a specific brain area. Although, PET scans have found activations in the hippocampus, thalamus and auditory cortex. The disorder is more common in men and about 1% of the population have it. There are equal proportions across all cultures, suggesting that genes are involved. There is a strong concordance but it could be a combination of genes interacting with the environment. The neurodevelopmental hypothesis believes that it is caused by abnormailities in the development of the nervous system due to infections, deficiencies etc. Schizophrenics also seem to have brain abnormalities, for example larger ventricles in the brain leaving less space for cells. This varies greatly among patients though. Also, some have damaged prefrontal cortexes, smaller cell bodies in areas associated with working memory and less lateralisation. There is also large variation of these findings. Excess activity of dopamine synapses (drugs) can cause psychosis. Schizophrenics have twice as many dopamine receptors but normal levels of dopamine. Also deficient activity of glutamate synapses can cause psychosis, dopamine inhibits glutamate which is involved with the inhibtion of dopamine release. PCP inhibits glutamate release also. The cause of schizophrenia is still unknown as there are many different hypotheses.

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