NeuroPharm Flashcards

1
Q

What are excitatory amino acids? (2)

A

glutamate

aspartate

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2
Q

What are inhibitory amino acids? (2)

A

GABA

glycine

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3
Q

What are monoamines? (3)

A

serotonin, dopamine, NE

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4
Q

What are the glutamate ionotropic glutamate receptors? metabotropic?
What are the general functions of them?

A

ionotropic: synaptic plasticity, learning/memory
Kainate
AMPA
NMDA

metabotropic: memory
mGluRs

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5
Q

What produces glutamate? What is the functional role of glutamate?

What happens if you have excess glutamate? deficiency?

A

pyramidal cells - synaptic plasticity, learning, memory

excess: excitotoxicity -> AD, ALS, neuropathic pain
deficiency: schizophrenia

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6
Q

There are 3 GABA receptor subtypes: A, B, and C, all of which produce hyperpolarization. Give an example of an agonist of each receptor?

A

GABA-A: barbituates and benziodiazepines

GABA-B: baclofen

GABA-C: not modulated by any of these agonists!

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7
Q

What type of receptor are nicotininc receptors? muscarinic receptors? Do they cause EPSP or IPSP?

A

nicotinic: ionotropic –> EPSP
muscarinic: metaotropic
M1, 3, 5 (Gq) –> EPSP
M2, 4 (Gi) –> IPSP

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8
Q

How would you treat organophosphate poisoning? (2 agents)

A

atropine + 2PAM (pralidoxime)

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9
Q

What are agonist of ACh receptor? antagonists?

A

Muscarine (M1, 2)
Carbachol (M1-5)
Pilocarpine (M3)

AChE inihibitors
Donepezil
Tacrine
Galantamine
Rivastigmine

Antagonists:
Atropine
Scopolamine

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10
Q

ACh is made and released at the NMJ. What enzyme is responsible for this? What happens if there is a deficiency in this enzyme?

A

ChAT

deficiency of this enzyme –> Alzheimer’s Disease

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11
Q

What are some monoamine drug targets?

A

MAO - normally breaks down catecholamines + serotonin in the synaptic cleft. Inhibitors of this results in an increase of NTs in the synaptic cleft

5HT reuptake transporter - inhibitors prevent uptake of the NT, resulting in an increase of NT in the synaptic cleft

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12
Q

Where is dopamine made? What are its functional roles?

What breaks down dopamine?

A

VTA and substantia nigra

behavior, cognition, motor, motivation, reward, addiction

MAO, COMT

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13
Q

What are the 4 different dopaminergic pathways?

A

nigrostriatal: substantia nigra –> striatum
mesolimbic: VTA –> nucleus accumbens + amygdala
mesocortical: VTA –> cortical
tuberoinfundibular: hypothalamus –> pituitary

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14
Q

What are some pharmacological agents that restores dopaminergic tone?

A

LevaDOPA - precursor of dopamine
COMT-inhibitors
Dopamine agonists
DOPA-decarboxylase inhibitors

Cocaine, methylphenidate - prevents DA reuptake
Amphetamines - induces DA release

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15
Q

Where is NE made? What are its functional roles?

What breaks down NE?

A

locus coeruleus + caudal raphe nucleus

arousal, attention, focus

MAO, COMT

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16
Q

What is a pharmacological agent that would be used to reduce NE tone?

A

clonidine (a2 agonist) - reduces NE release, which helps with neuropathic pain, opioid detox, ADHD, Tourettes

17
Q

Where is Serotonin made? What are its functional roles?

What breaks down Serotonin?

A

raphe nucleus

anger, aggression, mood, sleep, sexuality, appetite, pain

MAO

18
Q

What is a pharmacological agent that would be used to increase serotonin?

A

SSRIs, or agonists of the 5HT receptors

19
Q

Why does benadryl cause drowsiness?

A

Histamine binds H1-3 and its activation causes arousal. Anti-histamines (agents that block receptor activation), like benadryl, cause drowsiness

20
Q

What are symptom that manifest as a result of dysfunctional production of NE?

A

depression
ADHD
phobias
pain

21
Q

What is the functional role of cannabinoids?

What are some agonists of cannabinoid receptors?

A

Cannabinoids bind to CB1 and inhibits GABA/Glutamate release, thus reducing the GABA-inhibition of dopaminergic neurons in the VTA -> nucleus accumbens.
This results in an outpouring of dopamine, resulting in a REWARD state

agonists: anandamine, THC, cannabidiol (CBD)

22
Q

What is the functional roles of opioids?

What are some exogenous and endogenous agonists of cannabinoid receptors?

A

opioids inhibit GABA release (similar to cannabinoids)

exogenous agonists: morphine, codeine, heroin
endogenous agonists: endorphins, enkephalins, dynorphins