Neurobiology: Neurochemistry Answers – Flashcards

strings of AA, [smallest] in brain opioids: analgesic; internal heroin beta-endorphin, leu-enkephalin, met-enkephalin, dynorphin substance P, oxytocin, vasopressin, neuropeptide Y, somatostatin, vasointestinal polypeptide, cholecystokinin

adenosine, ATP methylxanthines (receptor blockers): caffeine, theophylline, theobromine

nontraditional gases: NO, CO cannabinoids: anandamide, 2-arachidonylglycerol

aka co-release, co-transmission ~2-4 NT released at one bouton (in different vessicles)

aka co-storage different NT in same vessicle

synthesis > storage > release/reception > inactivation

small NT: -substrates in all neurons, different enzymes produce the individual or combination NT -typically cytosolic > made at terminal near release site > transported into vesicle (ATP dependent) large NT: -pro-peptide made in cell body > vesicle > precursor convertases cleave NT from pro-peptide in vesicle > transport to terminal > release

vesicular storage- protect from degradative enzymes in cytosol

quantal, Ca dependent, exocytosis rest: reserve pool (storage) bound, releasable pool docked near Ca channel (active zone) depolarized (AP): Ca channel open > Ca influx > reserve pool detach, primed vessicles fuse with bouton > exocytosis fusion: v-SNARE + t-SNARE > SNARE complex > priming > Ca bind synaptotagmin (vesicle receptor) > fusion > exocytosis *C. botulinum toxin acts as a protease to degrade SNARE complex > prevent priming > block NMJ transmission (paralysis)

high AP activity, require more Ca larger vesicles, release at distant regions from active zone

small molecule: endocytosis > reformed > refilled > reused large molecule: retrieved but not reused

ionotropic: several protein subunits chemically gated ion channel (NT activation) spatially local, short action/duration metabotropic: second messenger (G-protein most common) > downstream physiological changes single protein crossing membrane 7x greater variety of changes (protein function/synthesis, tx, ion channels), spatial extent, longer latency/duration

NT binds GPCR > activate enzyme > conversion to second messenger cAMP system: NE binds beta-adrenergic receptor > G protein activated > adenylyl cyclase activated > ATP conversion to cAMP > protein kinase A activated > phosphorylation > change protein function

diffusion from synapse (not efficient) transporter reuptake of small NT (*NOT ACh) AChE degrades ACh > choline + acetate peptide diffuses to peptidase for break down