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23 spring: pharm > Test 2: lecture 20-21 > Flashcards

Test 2: lecture 20-21 Flashcards

1
Q

what are the most common neurotransmitters

A

glutamate, gaba, glycine

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2
Q

gluatamte is the major — neurotransmitter

A

excitatory (allows + into the cell → depolarization)

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3
Q

what are the three major classes of ionotropic glutamate receptors

A

NMDA
Kainate
AMPA

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4
Q

all ionotropic glutamate receptors are — channels

A

cation (allow + through, let K out and Na into the cell)

are excitatory- will cause depolarization of the cell

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5
Q

ketamine will block

A

NMDA ionotropic glutamate receptor

will stop depolarization (calm it down)

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6
Q

too much glutamate will do what to neurons

A

cause cell death!

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7
Q

how can glutamate lead to neurotoxicity and cell death

A

glutamate allows Na into a cell and K out, if too active the increase in Na will cause H20 to come into cell and cause swelling → cell lysis

can also cause delayed apoptosis

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8
Q

how is glutamate removed from the synapse

A

reuptake by ecitatory amion acid transporters (EAATS)

glial cells will also reuptake glutamate, turns it into glytamine and brings it back to presynaptic neuron for recycling

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9
Q

Excitatory Amino Acid Transporters (EAATs) are powered by —

A

electrochemical gradient (Na/K)

glutamate will cause Na into the synapse, K into the cell

will pull glutamate back into presynaptic neuron for recycling

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10
Q

how does ischemia effect NMDA activation

A

decreased blood flow= loss of Na/K pump= loss of membrane potention in the synapse

no potential means glutamate released will not reuptake by EAATs- this leads to prolonged NMDA activation → too much Na into the cell → swelling → cell death

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11
Q

domoic acid

A

toxin in marine algae

agonist for kainate receptor (type of ionotropic glutamate receptor)

leads to headache, confusion, muscle weakness and coordination deficits

the BIRDS

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12
Q

— is the major inhibitor neurotransmitter in CNS. and is used for inhibitory control of —

A

GABA

Important in inhibitory control of interneurons

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13
Q

GABA is made from

A

glutamate

glutamic acid decarboxylase (GAD)

neuron can not release both GABA and glutamate= one or the other

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14
Q

reuptake of GABA

A

same as glutamate

by GABA specific EAAT and glial cells

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15
Q

two types of GABA receptors

A
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16
Q

GABA A receptors are —

A

Cl- channels

allow Cl into the cell= inhibitory = hyperpolarization

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17
Q

GABA B receptors are —

A

G protein coupled

are connected to K+ channels (move K+ out of cell) to cause membrane hyperpolarization

inhibitory

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18
Q

benzos bind to what receptors and will do what?

A

bind to GABA A receptors

make it easier to channel to open= increases Cl- into the cell = inhibitory/ hyperpolarization of the cell

benzodiazepam (valium), alprazolam (xanax)

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19
Q

barbiturates bind to what receptors and will do what?

A

bind to GABA A receptors

channels stay open longer= increases Cl- into the cell = inhibitory/ hyperpolarization of the cell

barbiturate= phenobarbital

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20
Q

what are some barbiturates?

A

sodium amytal, pentobarbital, phenobarbital

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21
Q

what are barbiturates used for in vet med

A

sodium amytal, pentobarbital, phenobarbital

used for sedation, anesthesia, and seizure control depending on the duration of action by the drugs.

causes respiratory depression in high dose = euthanasia

barbiturates bind to GABA A receptors and make them open longer allowing more Cl- into cell → inhibitory

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22
Q

what are some bad symptoms of barbiturate use

A

can cause confusion, imparied judgment and slow reflexes

lethal at high dose→respiratory depression

high tolerance

bad withdrawal

easily and commonly abused

sodium amytal, pentobarbital, phenobarbital - used for sedation, anesthesia, and seizure control in animals

binds to GABA A receptors and make them stay open longer= inhibitory

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23
Q

what are some Benzodiazepines

A

diazepam (Valium®), alprazolam (Xanax®).

24
Q

what are benzos used for

A

Short-acting BDZs used primarily as anxiolytics.

Long-lasting BDZs used as anxiolytics, muscle relaxants, anti-convulsants.

diazepam (Valium®), alprazolam (Xanax®).
bind to GABA A, and increased probablity of opening = inhibitory

25
Q

glycine is an — neurotransmitter

A

inhibitory

26
Q

where can you find glycine receptors

A

medulla and spinal cord inhibitory interneurons

27
Q

what will glycine do

A

will bind to ionotropic receptors and will open Cl channels

allows Cl- into the cell→ inhibitory

28
Q

strychnine

A

acts as competitive antagonist of glycine

plant from asia

if you have strychnine, you need more GABA to get to the same response

29
Q

how are peptide transmitter made

A
30
Q

two main classes of NT vesicles

A

large dense core vesicles → peptide transmitters

small synaptic vesicles → nonpeptide transmitters

31
Q

how are large dense core vesicles made vs small synaptic vesicles

A

large: made in soma of neuron and transported down axon to nerve terminal

small: made “on site” neurotransmittings already in the nerve terminal are packaged into vesicles

32
Q

if a nerve contains a classic neurotansmitter, can it also have peptide neurtransmitters?

A

yes

usually only 1 classical NT per nerve, but can have a bunch of peptide NT

33
Q

peptide transmitters typically acts via — receptors. Generally modulate ion channels activity — via G-proteins.

A

G-protein coupled

indirectly

often slow transmission, with longer range response (can travel to new synapse), and longer lasting

34
Q

what does it mean when peptide transmitters have longer range effect

A

they are released by neuron, but can float away to other synapase and cause signal there

usually slow transmission but responses generally last longer

35
Q

how does peptide NT become deactivated

A

peptidases will eat peptide NT into smaller inactive fragments

36
Q

what spinal tract carries pain to brain

A

spinothalamic tract

responds to heat, cold, mechanical and inflammation

37
Q

— respond to sharp, prickling, well localized and brief pain

A

Aδ
fast conduction
myelinated

38
Q

— nerves respond to dull ache, diffuse, long lasting pain

A

C
unmyelinated
slow conduction

39
Q

nociceptors use — as transmitters to secondary neuron

A

glutamate and substance P

40
Q

C fibers release —
Aδ fibers release —

A

C: glutamate and substance P

Aδ: glutamate only

41
Q

C fibers will release — for small/mild stimuli

A

glutamate

42
Q

C fibers release — for stronger stimuli and may signal persistent burning pain

A

substance P

C fibers: dull, diffuse, longer lasting pain, slower non myelinated

43
Q

substance P is degraded by

A

peptidases
* Neutral endopeptidase (NEP)
* Angiotensin converting enzyme (ACE)

44
Q

P substance binds to what type of receptors

A

neurokinin (tachykinin) receptors
NK1-3 maybe 4
mostly to NK1

all are GPCR that are linked to PLC activation (IP3 and DAG as second messengers).

45
Q

NK1 receptors prefer to bind to —

A

substance P

neurokinin (tachykinin) receptor

46
Q

where can you find substance P

A

skin- pain receptor

cardio: arterioles: cause low BP

respiratory: bronchoconstriction (asthma?)

GI tract: contracts GI

inflammatory: role in immune response, helps with migration of inflammatory cells

47
Q

what does substance P do in the brain

A

Possible roles involve mood (depression), anxiety, control of respiration, nausea, and emesis

48
Q

three opioid peptide families

A

endorphins
enkephalins
dynorphins

49
Q

what are the three main families of opiate receptors

A

μ (mu)
κ (kappa)
δ (delta)

µ and κ receptors associated with analgesia.

δ receptor not as important in analgesic effects of opiates May be important for the euphoric effects of these drugs.

50
Q

how do opioids effect pain

A

opioids (enkephalin, endorphins, dynorphins) are released from local inhibitory neurons

prevents release of NT(substance P and glutamate) from primary afferent nociceptors (C fibers)

51
Q

what will opioids do to brain

A

activated dopamine in brain cause sensation of pleasure, and mediate asaptations to stress and extreme pain

52
Q

how does nitric oxide get into cell

A

very small can just get into cells

very reactive radical, with short half life

53
Q

Nitric oxide likes to bind to

A

heme

will bind even better then oxygen

54
Q

what is a nitric oxide receptor and what happens when it bind

A

NO likes to bind to heme

will cause activation of soluble guanylyl cyclase which leads to ↑cGMP

cGMP will act as second messenger to:
* stimulate protein kinase G
* alter response of some ion receptors
* inhibit cAMP

55
Q

how does nitric oxide gas in the brain work

A

enters postsynaptic neuron and causes the formation of more NO

NO will move retroactivly into presynaptic neurons to cause release of cGMP

56
Q

NO acts on blood vessels as

A

endothelium derived relaxing factor (EDRF)

causes vasodilation and drop in blood pressure

23 spring: pharm (46 decks)

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