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GABA
type 1 nt, major inhibitory
what stains pv
basket cells and chandelier cells
what stains sst
martinotti cells and gabaergic projection neurons
what stains sht3ar
ngfc and bitufted cells
how is gaba made
glutmate + glutamate decarboxylaes (gabaergic neurons), plp is a cofactor how
how is gaba regulated
gad, 35% of gad bound to plp, competes with atp, but once camkii phosphorylates gad in intracellular calcium, increased affinity for plp
gaba storage
vgat loads in gaba with proton gradient atpase
gaba a receptor
ionotropic, conducts cl ions, pentameric, allosteric binding sites for drugsm
gaba b receptors
linked to increasing potassium channel condcutance, hyperpolarizes stronger than gaba a, inhibits adenylyl cyclase and calcium channels reducing synaptic transmission
what reuptakes gaba into cell
gat , gaba transporterh
how is gaba cleared from synaptic cleft
with gaba transaminase - gabat
glycine
type 2 aa nt, inhibitory in the brain stem and spinal cord, high concentrations,
glycine storage and synthesis
hypothesis: neurons take glycine from the extracellular space, hypothesis 2: neurons take glycine in nerve terminal from esrine using serine trans hydroxymethyltransferase which isnt unique to glycinergic neurons, and transported into vesicles with vgat
glycine receptors
ionotropic ligand gated, pentameric, permeable to cl, and gabaa and glycine are anchored to postsynapse with gephyrin protein, label receptors postsynaptically
how is glycine terminated
glyt-1 reuptakes it in glia, glyt-2 reuptakes it in neurons, labels glycinergic neurons, glyt -1 = 2 sodium and 1 cl, glyt -2 = 3 sodium and 1 cl tet
tetanus toxin
glycinergic inhibitory neurons = renshaw cells in spinal cord = negative feedback loop with motor neurons = no overexcitation, motor neuron ach at muscle cells and renshaw cells, and then glycine is released onto motor neurons to inhibit them, but blockade of this leads to tetanus, which stops vesicle release through cleaving vamp from core complex blocking renshaw signal inhibition