02. Recreational Drugs Flashcards

1
Q

Describe heroin.

A

-Heroin is a highly addictive opiate drug. It is taken recreationally for a euphoric ‘high’.
-Heroin has depressant effects on the CNS, it slows down activity, including neurons involved in pain.
-This is why opiates are valued as analgesics (painkillers).

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2
Q

How does heroin effect the transmission process in the CNS?

A

-Heroin is usually injected intravenously and flows through the bloodstream to the brain. Once in the brain it is broken down into morphine (a closely related opioid).
-Morphine binds to specific opioid receptors at the synapse- mu receipts in the cerebral cortex, lambic system and hypothalamus. This releases dopamine (feelings of pleasure).
-Receptors for heroin/morphine exist in the body because the CNS has its own opioid system.
-Endorphins and enkephalins are the bodies natural painkillers. Heroin takes advantage of this system by binding with the natural opioid receptors to enhance its effects.
-Heroin is an agonist drug because it mimics the action of another chemical, ie it binds to the natural opioid receptors because it has a complimentary shape, thus increasing the levels of dopamine.

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3
Q

What are the long terms effects of heroin on neural transmission?

A

-Repeated heroin use leads to downregulation.
-Regular use means the opioid receptors on the postsynaptic neuron are constantly binding with morphine molecules.
-This desensitises the receptors to the effect of the drug.
-Therefore more of the drug is needed to have the same effect (tolerance).

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4
Q

Describe cocaine.

A

-Cocaine is an illegal and addictive drug. It is taken recreationally for stimulating effects (it speeds up the body, eg heart rate).
-Cocaine is very fast acting and has immediate effects on neural transmission within the brain.
-Users experience a ‘come down’ after taking it due to depleted levels of dopamine and the bodies need to recover.

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5
Q

How does cocaine effect the transmission process in the CNS?

A

-Cocaine works on the reward pathway and dopamine receptors in the brain.
-Cocaine draws on the idea that there is reuptake by the presynaptic neuron or neurotransmitter left in the synaptic gap.
-Cocaine blocks the binding site on the reuptake receptor, or transporter molecule, and stops the reuptake of dopamine back into the presynaptic neuron.
-This blocking of reuptake means there is excess dopamine in the synapse because it is not being reabsorbed.
-This excess of dopamine leads to over stimulation at the postsynaptic receptors.
-Therefore there is more dopamine than usual creating intense feelings of pleasure, or euphoria.

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6
Q

What are the long term effects of cocaine on neural transmission?

A

-The continuous binding of dopamine to the dopamine receptors is overstimulating and negatively affects the neural transmission.
-Overtime the dopamine receptors become damaged, changing shape which prevents neurotransmitters binding successfully.
-The number of dopamine receptor sites will also decrease.
-This leads to desensitisation and more dopamine is required to stimulate the post synaptic neuron to a ‘normal level’.
-As there is a loss of response to the drug, more is needed to experience the same effect (tolerance).
-A person becomes addicted because they crave the intense pleasure experienced, due to activation of the dopamine reward pathway, and therefore want to take the drug again because it is rewarding.

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7
Q

Describe Straiker and Mackie’s finding on neurotransmitters.

A

-Straiker and Mackie used hippocampal neurons from mice with the human CB1 receptor in order to study the effects of cannabis.
-Study found that the mice exhibit similar addictive behaviours to humans when dosed with cannabis as excess dopamine was found in the neural pathway.
-This suggests that neurotransmitters and the reward system work in similar ways, therefore giving us evidence to support neurotransmission in humans.

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8
Q

Describe the problems with animal research.

A

-A weakness is problems with using mainly non-human animal studies to understand drug effects on human CNS transmission.
-The basic transmission processes in mammals are similar. But some differences arise because the human brain is more complex than the rat brain.
-For example, isolating the effects of just one neurotransmitter greatly oversimplifies the process.
-It is very unlikely that the complexity of recreational drug effects on transmission can be explained by just one mode of action of a drug. The interactions of dopamine with other neurotransmitters systems (eg noradrenaline, serotonin, GABA) are not well understood.
-This means that extrapolation from non human animals to humans is risky and should be undertaken only very cautiously.

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9
Q

Describe Nora Volkow et al’s findings.

A

-Evidence of drug effects on CNS transmission comes from studies of humans aswell.
-For example, Nora Volkow et al used PET scans to track the activity of dopamine transporters during a cocaine induced ‘high’.
-They found that the extent to which cocaine occupied dopamine transporters correlated positively with the course of the subjective experience. In other words, subjective experience intensified as more dopamine transporters were occupied by cocaine and declined as they became less active.
-This supports the view that evidence from animal models is valid, as human studies produce similar results.

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10
Q

Describe the real life application.

A

-As our knowledge of drug effects on the CNS transmission grows, more treatments for addiction become available.
-For example, once heroin was identified as an agonist that binds to opiate receptors, other drugs were developed with a reverse mode of action.
-Naloxone

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