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
glycine is an --- neurotransmitter
inhibitory
26
where can you find glycine receptors
medulla and spinal cord inhibitory interneurons
27
what will glycine do
will bind to ionotropic receptors and will open **Cl channels** allows Cl- into the cell→ **inhibitory**
28
strychnine
acts as competitive antagonist of glycine plant from asia if you have strychnine, you need more GABA to get to the same response
29
how are peptide transmitter made
30
two main classes of NT vesicles
**large dense core vesicles** → peptide transmitters **small synaptic vesicles** → nonpeptide transmitters
31
how are large dense core vesicles made vs small synaptic vesicles
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
if a nerve contains a classic neurotansmitter, can it also have peptide neurtransmitters?
yes usually only 1 classical NT per nerve, but can have a bunch of peptide NT
33
peptide transmitters typically acts via --- receptors. Generally modulate ion channels activity --- via G-proteins.
G-protein coupled indirectly ## Footnote often slow transmission, with longer range response (can travel to new synapse), and longer lasting
34
what does it mean when peptide transmitters have longer range effect
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
how does peptide NT become deactivated
peptidases will eat peptide NT into smaller inactive fragments
36
what spinal tract carries pain to brain
spinothalamic tract ## Footnote responds to heat, cold, mechanical and inflammation
37
--- respond to sharp, prickling, well localized and brief pain
Aδ fast conduction myelinated
38
--- nerves respond to dull ache, diffuse, long lasting pain
C unmyelinated slow conduction
39
nociceptors use --- as transmitters to secondary neuron
glutamate and substance P
40
C fibers release --- Aδ fibers release ---
C: glutamate and substance P Aδ: glutamate only
41
C fibers will release --- for small/mild stimuli
glutamate
42
C fibers release --- for stronger stimuli and may signal persistent burning pain
substance P C fibers: dull, diffuse, longer lasting pain, slower non myelinated
43
substance P is degraded by
peptidases * Neutral endopeptidase (NEP) * Angiotensin converting enzyme (ACE)
44
P substance binds to what type of receptors
**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
NK1 receptors prefer to bind to ---
substance P ## Footnote neurokinin (tachykinin) receptor
46
where can you find substance P
**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
what does substance P do in the brain
Possible roles involve mood (depression), anxiety, control of respiration, nausea, and emesis
48
three opioid peptide families
endorphins enkephalins dynorphins
49
what are the three main families of opiate receptors
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
how do opioids effect pain
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
what will opioids do to brain
activated dopamine in brain cause sensation of pleasure, and mediate asaptations to stress and extreme pain
52
how does nitric oxide get into cell
very small can just get into cells very reactive radical, with short half life
53
Nitric oxide likes to bind to
heme will bind even better then oxygen
54
what is a nitric oxide receptor and what happens when it bind
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
how does nitric oxide gas in the brain work
enters **postsynaptic neuron** and causes the formation of **more NO** NO will move **retroactivly** into presynaptic neurons to cause release of **cGMP**
56
NO acts on blood vessels as
endothelium derived relaxing factor (EDRF) causes vasodilation and drop in blood pressure