Synapses Flashcards
Difference b/w Ionotropic and Metabotropic Rs
Ion channels vs. IC messenger activators
2 PNS Uses/Locations of ACh
Neuromuscular junction
Parasympathetic
Synthesis of ACh
Choline acetyltransferase (CAT) joins Acetyl-CoA and Choline in cytoplasm of nerve terminals
Degradation of ACh
Acetycholinesterase in synapses (postsynaptic membrane and glial cells) breaks it down
Botulism Toxin
Blocks release of ACh into synapse
Black Widow Spider Venome
Opens cation channels, causing massive ACh release and then none is left (respiratory difficulties)
Tubocurarine Chloride
Arrow poison that blocks nAChRs, so a paralyzer in some surgeries
Neostigmine and Eserine
Reversible ACh-esterase inhibitors (used in myasthenia gravis)
Nerve Gas
Irreversible ACh-esterase inhibitor, treated w/ atropine or 2-PAM
Atropine
Antagonist for mAChRs
Different Locations of nAChR and mAChR
neuromuscular junctions vs. heart
2 ACh Related Diseases
Myasthenia gravis - reduced # of nicotinic Rs causes muscle weakness
Congenital Myasthenic Syndrome - muts in CAT cause similar symptoms
3 Biogenic Amines & Catecholemines
DA
EPI
NOR
NOR Function
Primary Postganglionic NT for sympathetic nervous system
Tyrosine Hydroxylase (location, rxn, and notable point)
Only found in neurons and adrenal medulla
Rate limiting step in catecholamine biosynth, converts Tyr to DOPA
Reserpine
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
CAT Degradation
MAO in mt and COMT in cytoplasm, so they must be taken up into cells for degradation unlike ACh
Alpha-methyl-DOPA
False transmitter, acts as sedative bc acts like DOPA to be packaged and shit but can’t react w/ Rs
Cocaine Mech
Blocks reuptake of CATs
2.4 CAT Rs
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
Primary Role of 5HT
Regulate motility
AA Precursor of 5HT
Trp
Prozac Mech
SSRI, inhibits 5HT transport out of synaptic cleft
2 Fates of 5HT
Breakdown by MAO or in pineal gland conversion to melatonin
LSD Mech
Mimics 5HT at 5-HT2A R
Glutamine-Glutamate Cycle
Glu synth’d by glutaminase (or Krebs) and reuptaken into glials, post, and presyn cells and degraded to gln by glutamine synthetase for transport
Glutamate Role
Primary excitatory NT, opens ionotropic Na/K Rs and also metabotropic Rs
Ischemia NT Effect
Release glutamate, which then opens up NMDA R, a Ca channel causing cell death
GABA Synth
From glu in nerve terminals via glutamic acid decarboxylase (GAD)
GABA Degradation
Taken up by all 3 cells also but GABA-transaminase shunts into Krebs as succinate
3 Medications for Epilepsy
Benzodiazpines: agonist for ionotropic GABA Rs
GABITRIL: GABA reuptake inhibitor
SABRIL: inhibits GABA transaminase and thus breakdown
5 Differences b/w Small NTs and Neuropeptides
- Synthesized in soma not at terminal
- No reuptake mechs
- No specific degradative enzymes
- Colocalized w/ other NTs
- Released at very low concs
