Synapses

Question 1

Difference b/w Ionotropic and Metabotropic Rs

Answer 1

Ion channels vs. IC messenger activators

Question 2

2 PNS Uses/Locations of ACh

Answer 2

Neuromuscular junction

Parasympathetic

Question 3

Synthesis of ACh

Answer 3

Choline acetyltransferase (CAT) joins Acetyl-CoA and Choline in cytoplasm of nerve terminals

Question 4

Degradation of ACh

Answer 4

Acetycholinesterase in synapses (postsynaptic membrane and glial cells) breaks it down

Question 5

Botulism Toxin

Answer 5

Blocks release of ACh into synapse

Question 6

Black Widow Spider Venome

Answer 6

Opens cation channels, causing massive ACh release and then none is left (respiratory difficulties)

Question 7

Tubocurarine Chloride

Answer 7

Arrow poison that blocks nAChRs, so a paralyzer in some surgeries

Question 8

Neostigmine and Eserine

Answer 8

Reversible ACh-esterase inhibitors (used in myasthenia gravis)

Question 9

Nerve Gas

Answer 9

Irreversible ACh-esterase inhibitor, treated w/ atropine or 2-PAM

Question 10

Atropine

Answer 10

Antagonist for mAChRs

Question 11

Different Locations of nAChR and mAChR

Answer 11

neuromuscular junctions vs. heart

Question 12

2 ACh Related Diseases

Answer 12

Myasthenia gravis - reduced # of nicotinic Rs causes muscle weakness
Congenital Myasthenic Syndrome - muts in CAT cause similar symptoms

Question 13

3 Biogenic Amines & Catecholemines

Answer 13

DA
EPI
NOR

Question 14

NOR Function

Answer 14

Primary Postganglionic NT for sympathetic nervous system

Question 15

Tyrosine Hydroxylase (location, rxn, and notable point)

Answer 15

Only found in neurons and adrenal medulla

Rate limiting step in catecholamine biosynth, converts Tyr to DOPA

Question 16

Reserpine

Answer 16

Tranquilizer that inhibits DA (and also 5HT) transport into vesicles, depleting CATs available for release bc Dopamine Beta-Hydroxylase is localized w/in vesicles and NOR production happens there

Question 17

CAT Degradation

Answer 17

MAO in mt and COMT in cytoplasm, so they must be taken up into cells for degradation unlike ACh

Question 18

Alpha-methyl-DOPA

Answer 18

False transmitter, acts as sedative bc acts like DOPA to be packaged and shit but can’t react w/ Rs

Question 19

Cocaine Mech

Answer 19

Blocks reuptake of CATs

Question 20

2.4 CAT Rs

Answer 20

Dopaminergic: D1 Gs stimulates adenylyl cyclase, D2 Gi inhibits adenylyl cyclase which stimulates Ca influx
Adrenergic: alpha in smooth muscle prefers NE and works through IP3/DAG. Beta in striated muscle prefers EPI and activates adenylyl cyclase and cAMP

Question 21

Primary Role of 5HT

Answer 21

Regulate motility

Question 22

AA Precursor of 5HT

Answer 22

Trp

Question 23

Prozac Mech

Answer 23

SSRI, inhibits 5HT transport out of synaptic cleft

Question 24

2 Fates of 5HT

Answer 24

Breakdown by MAO or in pineal gland conversion to melatonin

Question 25

LSD Mech

Answer 25

Mimics 5HT at 5-HT2A R

Question 26

Glutamine-Glutamate Cycle

Answer 26

Glu synth’d by glutaminase (or Krebs) and reuptaken into glials, post, and presyn cells and degraded to gln by glutamine synthetase for transport

Question 27

Glutamate Role

Answer 27

Primary excitatory NT, opens ionotropic Na/K Rs and also metabotropic Rs

Question 28

Ischemia NT Effect

Answer 28

Release glutamate, which then opens up NMDA R, a Ca channel causing cell death

Question 29

GABA Synth

Answer 29

From glu in nerve terminals via glutamic acid decarboxylase (GAD)

Question 30

GABA Degradation

Answer 30

Taken up by all 3 cells also but GABA-transaminase shunts into Krebs as succinate

Question 31

3 Medications for Epilepsy

Answer 31

Benzodiazpines: agonist for ionotropic GABA Rs
GABITRIL: GABA reuptake inhibitor
SABRIL: inhibits GABA transaminase and thus breakdown

Question 32

5 Differences b/w Small NTs and Neuropeptides

Answer 32

1. Synthesized in soma not at terminal
2. No reuptake mechs
3. No specific degradative enzymes
4. Colocalized w/ other NTs
5. Released at very low concs