L12 - Neuropharmacology Flashcards

1
Q

What does neuropharmacology study?

A

How chemicals like drugs and neurotransmitters affect neuronal function in the nervous system

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2
Q

What are endogenous chemicals in neuropharmacology?

A

Neurotransmitters

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3
Q

What are exogenous chemicals in neuropharmacology?

A

Drugs

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4
Q

What role do calcium channels play in neurotransmitter release?

A

Calcium influx triggers vesicle fusion with the presynaptic membrane, which releases neurotransmitters into the synaptic cleft.

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5
Q

How are neurotransmitters cleared from the synaptic cleft?

A

Through reuptake by transporters, enzymatic breakdown or diffusion away from the cleft

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6
Q

What is the synaptic cleft?

A

Small gap between presynaptic and postsynaptic neurons where neurotransmitter transmission occurs

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7
Q

How do neurotransmitters binding to receptors affect the postsynaptic neuron?

A

It can cause either excitation (EPSP) or inhibition (IPSP) depending on the receptor type

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8
Q

What is the role of ionotropic receptors?

A

They directly regulate ion fluxes through ion channels

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9
Q

What happens when acetylcholine binds to a nicotinic receptor?

A

Sodium channels open, causing depolarisation (Excitatory Postsynaptic Potential - EPSP).

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10
Q

How does GABA binding to GABA-A receptors affect the cell?

A

Chloride channels open, causing hyperpolarisation (Inhibitory Postsynaptic Potential IPSP)

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11
Q

What is the difference between metabotropic and ionotropic receptors?

A

Metabotropic receptors regulate intracellular metabolic reactions often through G-protein mediated systems and have slower, longer-lasting effects.

Ionotropic receptors directly regulate ion fluxes through ion channels causing rapid ad short-lasting effects

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12
Q

Give an example of a metabotropic receptor?

A

Muscarinic acetylcholine receptors

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13
Q

what are 3 examples of ionotropic receptors?

A

Glutamate receptors, GABA-A receptors, nicotine acetycholine receptors

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14
Q

Name a serotonin receptor that’s ionotropic?

A

the 5HT-3 receptor

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15
Q

What is a receptor agonists?

A

A substance that mimics the action of the native neurotransmitter at a receptor

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16
Q

What is a receptor antagonist?

A

Substances that bind to a receptor but don’t activate it, blocking neurotransmitter binding

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17
Q

What are Barbiturates and how do they differ from BZs in terms of safety?

A

Barbiturates are drugs that act as CNS depressants

They have a higher risk of dependence and fatal respiratory depression compared to BZs

18
Q

How do BZs modulate GABA-A receptors?

A

They enhance the effect of GABA by binding to an allosetric site (location on the receptor that’s separate from the active site), increasing chloride influx and inhibition

19
Q

What does the Diazepam Binding Inhibitor (DBI) do?

A

DBI is an endogenous modulator of GABA-A receptor fucntion, affecting inhibition in the brain

19
Q

What are presynaptic receptors?

A

receptors located on the neurone terminals that modulate neurotransmitter release

20
Q

What’s the role of autoreceptors?

A

The provide negative feedback to reduce neurotransmitter release, synthesis or storage

21
Q

How do heteroreceptors differ from autotrceptros

A

Heterorecptors modulate neurotransmitter release of another neuron and autoreceptos modulate thier own neuron’s transmitter release

22
Q

Can heteroreceptors be excitatory?

A

Yes - heteroreceptors can enhance neurotransmitter release in the second terminal

23
Q

What do Monoamine Oxidase Inhibitors (MAOIs) do?

A

They inhibit monoamine oxadise enzymes, preventing neurotransmitter breakdown and increasing levels in the synaptic cleft

24
Q

How do SSRIs alleviate the symptoms of depression?

A

They block serotonin reuptake, increasing the avaliability in the synpatic cleft

25
Q

What drug(s) prevent action potentials by blocking sodium channels?

A

Tetrodotoxin or some local anesthetics

26
Q

Name a drug that inhibits neurotransmitter reuptake

A

Cocaine - blocks dopamine reuptake, increasing its concentration in the synaptic cleft

27
Q

Which drug increases dopamine sythesis?

A

L-DOPA is used to increase dopamine synthesis in Parkinson’s disease

28
Q

What drug is used to prevent neurotransmitter storage?

A

Reserpine blocks the storage of neurotransmitters like dopamine, norepinephrine and serotonin in vesicles

29
Q

How does reserpine affect neurotransmitter availability?

A

It prevents neurotransmitter storage in vesicles, reducing availability for release

30
Q

What is the biological basis of reward and addiction?

A

Reward + addiction are linked to the dopaminergic pathways in the brain, particularly the mesolimbic dopamine system

31
Q

How is dopamine involved in addiction?

A

Drugs of abuse increase dopamine release in the nucleus accumbens, reinforcing drug-seeking behaviour

32
Q

What is the primary neurotansmitter associated with Sz?

A

Dopamine –> overactivity in dopaminergic pathways contributes to Sz symptoms

33
Q

What neurotransmitter imbalance is implicated in depression?

A

Reduced levels of serotonin, norepinephrine and dopamine

34
Q

How are dopamine antagonists used in Sz treatment?

A

They block dopamine receptors, reducing overactivity linked to psychotic symptoms

35
Q

What are benzodiazepines used for clinically?

A

Treating anxiety, insomnia and muscle relaxation

36
Q

Why are barbiturates less commonly used now?

A

Due to high potential for dependence ad fatal respiratory depression

37
Q

What is the difference between ionotropic and metabotropic receptors?

A

Ionotropic receptors directly gate ion channels, while metabotropic receptors modulate intracellular reactions.

38
Q

Why is it important to understand drug mechanisms in neuropharmacology?

A

To relate drug actions to their therapeutic uses and side effects.

39
Q

What natural source produces atropine?

A

Atropine is derived from the deadly nightshade plant (belladonna).

40
Q

What is nicotine’s mechanism of action?

A

It acts as an agonist at nicotinic acetylcholine receptors.