neuropharmacology (week 10-12) Flashcards

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1
Q

two types of neurotransmitter receptors

A

ion channels (act like a gate for ions. When neurotransmitter binds to it, it opens up and allows certain ions to flow in, usually resulting in an action potential), and g-protein coupled (when a neurotransmitter binds, it turns GDP into GTP, which energises a second messenger inside the cell which binds to another receptor in the cell)

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2
Q

what is receptor specificity

A

neurotransmitters and their receptors bind like a lock and key. Their physical makeups fit together, and the receptors are highly specific, meaning only certain transmitters can activate certain receptors

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3
Q

neurotransmitters vs neuromodulators

A

A neurotransmitter strictly from synapses which diffuses across a cleft to effect one or two postsynaptic neurons, a muscle cell, or other effector cell, and is ither excitatory or inhibitory. Neuromodulators effect groups of neurons or effector cells with the correct receptors. Must not be from a synapse, and usually works with secondary modulators, and can provide longer effects, often changing the receptivity of neurons.

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4
Q

how can neuromodulators alter synapse functioning

A

can affect the presynaptic neuron by impacting neurotransmitter release, can affect the postsynaptic neuron by altering neurotransmitter function (firing pattern or excitability), or changes neural function or structure, impacting synaptic plasticity

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5
Q

where are neuromodulators made and how do they go around the brain

A

they are found deep in the brain, in some nucleus, and are transported through various long neurons

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6
Q

where are neurotransmitters made and how do they transport

A

neurotransmitters are synthesised in the cell body of the neuron, and then they are slowly transported through the axons to the synapse, however, release is fast, because they sit in the synapse ready.

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7
Q

how do drugs work on receptors

A

drugs can mimic neurotransmitters by being similarly shaped, meaning that their either antagonise (prohibit binding of neurotranmitters resulting in no stimulation) or agonise (overstimulate) the receptors, resulting in the effect felt by the user. Drugs can affect all stages of neurotransmitters.

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8
Q

what is the cycle of neurotransmitters

A

synthesis, release from synaptic vesicles, binds to receptors, +/- influence on postsynaptic neuron, broken down by enzymes, reuptake of transmitter, formation and storage in synaptic vesicles. Drugs can effect all stages.

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9
Q

glutamate and GABA overview

A

both true neurotransmitters, released by presynaptic neuron, directly effecting the likelihood of neurons firing.

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10
Q

glutamate synthesis

A

it is synthesised from glutamine, which is released from neighbouring cells. Note, glutamate can be turned into GABA and GABA can be turned into glutamate.

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11
Q

glutamate receptors

A

4 major types, 3 ion channels (NMDA receptor, AMPA receptor, Kainate receptor).

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12
Q

NMDA receptor information (drugs)

A

complex and only works if glycine is bound and magnesium is not. Alcohol is the most common antagonist, and also agonises GABA (inhibitory). PCP and ketamine also antagonise this receptor, causing dissociative hallucination.

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13
Q

what is GABA

A

it is an inhibitory neurotransmitter which reduces the likelihood that neurons fire for their non-preferred stimulus. They do this by increasing the selectivity, not determining what signals the glutamate chooses

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14
Q

GABA Synthesis

A

Glutamate can be turned into GABA and GABA can be turned into glutamate.

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15
Q

types of seizures

A

gereralised (most brain areas), partial (specific brain regions, can ble split into simple (change of consciousness, but no loss of consciousness), and complex (loss of consciousness)).

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16
Q

seizures and genetics

A

mostly genes involved in seizures are to do with incorrect ion channels. Most causes of seisures though, are due to abnormal brain tissue

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17
Q

what occurs when GABA function is impaired

A

Seizures

18
Q

How is dopamine synthesised

A

ingested as Thyrocine amino acid in food, converted by Thyrocine hydroxylase to L-Dopa, then turned into Dopamine by amino acid decarboxylase. (note its broken down by dopamine beta hydroxylase into noradrenaline)

19
Q

what is dopamine involved in

A

motor function, and reward systems in the brain (important in coding cost benefit for the neural systems)

20
Q

how is dopamine involved with rewards.

A

When an unexpected reward is given, there is a spike in dopamine. When the reward is habituated to a noise, the dopamine occurs after the noise, not after the reward. If the reward is not given after the signal, after the lack of reward, there is a suppression of dopamine

21
Q

what is EFT

A

Episodic Future thinking, and difficulties in it are associated with difficulties in appreciating and applying knowledge and benefits of delayed gratification.

22
Q

how do dopamine drugs like cocaine differ from normal dopamine functioning

A

when paired with a beep, unlike normal rewards, dopamine drugs like cocaine still release high levels of dopamine when the reward comes, meaning it perceives the drug as better than expected, cycling into addiction. Normal rewards release no extra dopamine when habituated to a bell.

23
Q

how do addiction and free will interact

A

drugs initiate “wanting” and cravings in addicted person,

24
Q

how is noradrenaline synthesised

A

dopamine is broken down by dopamine beta hydroxylase into noradrenaline

25
Q

what does noradrenaline break down into

A

noradrenaline breaks down in the adrenal gland into adrenaline, which explains its role in the fight or flight response. It can also be broken down into an inactive compound by monoamine oxidase.

26
Q

noradrenaline info (where from?)

A

part of the sympathetic nervous system (fight or flight), is involved in threat detection, and memory formation and retrieval. It is released from the Locus Coruleus (LC), of which, the highest activation is during highly positive and highly anxious experiences.

27
Q

explain noradrenaline (NA) and the four F’s

A

Fight, flight, freeze, fornicate. Noradrenaline invokes these evolutionarily significant states of arousal.

28
Q

prolonged LC/NA stimulation results in

A

Stress (when stimulation is from environmental factors), Anxiety (excessive and irrational “worry”), panic attacks (brief intense episodes as a result of random events, or internal thoughts)

29
Q

a low period of decision making results in

A

cells start to release more and more NA, resulting in variability in decision making, promoting a new decision

30
Q

how is performance associated with NA/LC activity

A

low levels of LC/NA activation = tired, vague and poor performance. high levels of LC/NA activation = restless, stressed, poor performance. optimal performance = moderate activity

31
Q

what is a visual marker for NA release

A

dilation of pupils (but it is also with cognitive and motor decisions)

32
Q

Seratonin (5-HT) overview (where synthesised and what it does)

A

5-HT acts as a neuromodulator, important in influencing sleep, mood, and hallucinations. Synthesised in the Raphe Nucleus (remember rassie erasmus)

33
Q

seratonin synthesis and degradation

A

synthesised in the raphe (remember rassie erasmus), ingested as amino acid tryptophan, turned into seratonin by tryptophan hydroxylase. Broken down by momamine oxidase (like dopamine and noradrenaline)

34
Q

depression and seratonin

A

brain imaging (and post mortem studies) showed a reduction in some types of serotonin receptors in the brain of unmedicated depressed people. a gene in the transport of serotonin has been linked to depression risk

35
Q

what are SSRI’s

A

they are drugs which treat depression through preventing the reuptake of seratonin into the presynaptic cell, leaving more available for the receptors

36
Q

theories of why SSRI’s are slow acting

A

a few theories, takes time for neurons to adapt to reducing stress response, and also possible it leads to neurogenesis, forming new pathways, alter gene expression

37
Q

what are some non-traditional neurotransmitters

A

peptides, lipids, nucleocides, gasses

38
Q

peptides info and example

A

amino acids broken down into singular peptides are able to be used as neurotransmitters (alongside being hormones). Common types are opioids (like heroin (full agonist), or the overdose preventing Naloxone (full antagonist), methadone is full agonist (slow), bulksoijwlek is partial agonist).

39
Q

lipids drugs

A

Endocanabinoids are a common lipid neurotransmitter. weed agonises partially

40
Q

nucleocides example and role

A

functional comoderators, roles in modulating other neurotransmitters. an example is adenosine, which is involved in promoting sleep and suppressing arousal. Caffeine blocks the receptors, building up the amount of adenosine

41
Q

gasses

A

use nitric oxide and carbon monoxide as transmitters. produced in the cell, and short lived.