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Unit 19 > NT > Flashcards

NT Flashcards

1
Q

What condition is lystergic acid diethylamide used in?

A

depression

its a serotonin agonist

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2
Q

What kind of medicine (agonist, antagonist etc) for what NT is lystergic acid diethylamide?

A

serotonin agonist

used in treating depression

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3
Q

What disorder are SSRI’s commonly used in?

What are their mechanism of actions?

A

depression

Inhibits the reuptake of serotonin into the presynaptic cleft

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4
Q

What is another class of medications that works in a similar way to SSRI’s?

What makes them different

A

tricyclics: both inhibit the reuptake of serotonin.

They block the reuptake of BOTH serotonin and NE

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5
Q

What kind of disorder is MAO inhibitor used for

what is its mechanism of action

A

depression/mood disorder

Serotonin is normally oxidized after reuptake, MAO stop this process therefore leaving more active serotonin in the cleft after re-uptake

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6
Q

What is electroconvulsive therapy used for?

through what mechanism of action?

A

depression/mood disorder

increases 5HT transmission, increases sensitivity of 5HT receptors in hippocampus, and increases number or 5HT receptors

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7
Q

Cholinergic drugs are prescribed to do what?

what is an example of a disorder this may be used in

A

increase ACH

Alzeihmers

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8
Q

Extrapyramidal motor respnse what kind of mediation is given? and why?

A

Extrapyramidal motor response = parkinsonion tremor

benztropine

ACH inhibitor

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9
Q

if someone is getting motion sickness, what NT is involved

is it high or low?

A

ACH is high

so you give them a receptor antagonist (scopolamine patch)

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10
Q

what kind of medication is a scopolamine patch?

A

ACH antagonist: decreases the ACH in the system

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11
Q

what NT are amino acids?

A

glutamate

GABA

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12
Q

what NT hyperpolarizes the cerebral cortex

A

GABA

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13
Q

what NT hypopolarizes the cerebral cortex?

A

Glutamate

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14
Q

Glycine is associated with what NT?

A

GABA

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15
Q

Asparate is associated with what NT?

A

Glutamate

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16
Q

What are the two major locations of GABA in the CNS?

A

striatopallidal pathway: extrapyramidal motor response

interneurons t/o the brain

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17
Q

Why is GABA so widely distributed in the brain

A

the interneurons in the brain having GABA allow the brain membranes to stabilize and prevent repetitive firing of neurons. Without this you could have seizures.

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18
Q

Decreased GABA may lead to what?

A

seizures

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19
Q

what is the mechanism of action of BDZ and barbituates

A

increase GABA therefore are anticonvulsants

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20
Q

drugs that block GABA reputake are convulsants or anticonvulsants?

A

anticonvulsants: there is more availability of GABA

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21
Q

after stroke what happens to GABA in perilesional area?

A

increase in GABA as protection mechanism

THIS CAN BE A BARRIER TO PLASTICITY IF THIS PERSISTS

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22
Q

suppression of GABA in perilesional cortex after stroke leads to decreased or increased motor recovery/

A

increased!

This was found through a study where they used an inverse agonist or deleted parts of receptors suing Gabra, so GABA receptors weren’t available

23
Q

We know that glutamate is at 80% of the CNS synapses, how is its action terminated

A

uptake of excessive glutamate through EAATS (excitatory amino acid transporters)

24
Q

arousal is mainly associated with what three NT?

A

NE, EPI, AH

25
Q

Mood is mainly associated with what NT?

A

serotonin

26
Q

Motivation is mainly associated with what NT?

A

dopamine

27
Q

Executive function is mostly associated with what NT?

A

ACH (think Alzeihmers)

28
Q

Action planning and selecting is mostly associated with what NT?

A

Dopamine (think reward system and the BG tagging things)

29
Q

Action is most associated with what NT?

A

glutamate

30
Q

Expectation of reward and reward is most associated with what NT?

A

Dopamine

31
Q

what two neuronal bodies are associated with the thalamic pathway of the ascending arousal system?

A

pedunculopontine (PPT)

laterodorsal tegmental (LDT)

32
Q

what are the two pathways of the ascending arousal system?

A

thalamic and extra thalamic

33
Q

What NT does the thalamic pathway of the ascending arousal system work through?

A

ACH

34
Q

Pedunculopontine and laterodorsal tegmental nucleu are assoicated with which arousal pathway/

A

thalamic: they innervate the thalamus leading to activity

35
Q

what are the PPT and LDT most active?

A

during wakefulness and REM sleep (dreaming)

36
Q

the extrathalamic pathway is comprised of single or multiple systems?

A

multiple systems with different NT. Everything other than the ACH is here witht heir corresponding cell bodies

They each work in a coordinated manner, to create overlapping redundancy and contribute to sustain wakefulness

37
Q

AD can be caused by one of two mechanisms

A

decreased ACH

OR

Reduction in ACH receptors

38
Q

executive funciton and memory problems is what disease state?

What NT is associated?

A

AD

ACH

39
Q

Two main tx for AD relating to ACH and its receptors

A

Acetylcholinesterase inhibitors: reduces reuptake/destruction of ACH

Stimulation of ACH receptors

40
Q

Acetylcholinesterase inhibitors increase or decrease ACH?

A

increase: reduces the re-uptake/destruction of ACH

41
Q

what are the three main things we know exercise does in terms of NT

A

increases dopamine

increases 5HT

increases noradrenaline

42
Q

Sometimes one NT is associated with one medical diagnosis but we know that they work symbiotiacally to produce interaction efffects why is this important

A

all sx are not addressed by a single agonist

43
Q

NT mechanisms often differ or stay the same with disease?

A

differ. duh.

44
Q

true or false: one NT generally shows the same sx for many disesase?

A

true

45
Q

True or false: more than one NT is implicated in a single disease

A

true

46
Q

true or false: pharmacological intervention alone is insufficient?

A

true and they may have side effects

47
Q

Achetylcholinesterase mechanism of action

A

normally cholinesterase breaks down ACH so this drugs stops that from happening increasing available ACh; used in AD

48
Q

what is a side effect of antipsychotics? what is the mechanism of action that causes this?

A

inhibition

dopamine antagonist: blocks D2,3 and 4

49
Q

L-Dopa premotes what?

A

plasticity

50
Q

would acetylcholinesterase increase or decrease plasticity?

A

increase!

51
Q

would acetylcholinesterase increase or decrease plasticity?

A

increase!

52
Q

antipsychotics reduce or increase plasticity?

A

reduce!

53
Q

D-cycloserine is excitatory or inhibotory in nature?

A

excitatory: works on NMDA receptors like glutamatee

Unit 19 (4 decks)

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