exam 1 study night Flashcards
acetylcholine
excitatory
in PNS at neuromuscular junctions
released by cholinergic neurons
implicated in Alzheimers
neurons release ACh
cholinergic
at neuromuscular junctions
synthesis of Ach
choline and acetyl coA in cytoplasm of synaptic terminals
- cholinergic
AChe
destroys/inhibits ACh
releases choline to resume for synthesis
nerve gas sarin
inhibits AChe
Ache inhibits ACh
inhibit Ache = buildup of ACh in synaptic cleft and overtime. receptors causes desensitization
ACh receptors
- nicotinic - ligand gated ion channel bind nicotine and ACh.
ion channel permeable to K+ and Na
- Na larger driving force = depolarization due to Na+ influx - muscarinic - cholinergic receptor stimulated by Ach and muscarine . g protein or 2nd messenger coupled
nicotinic receptors
for ACh
ligand gated ion channel binds nicotine and Ach
permeable for k and Na
Na has greater driving force and Na influx causes depolarization
cholinergic
neurons release Ach
atropine
antagonist of muscarine receptors of Ach
antagonist of muscarine Ach receptors
atropine
Alzeihmers
depleted cholinergic neuron
increase beta amyloid proteins cause cell deth
biogenic amines
catecholamines and serotonin
small charged synthesized from Rs
DA, NE, Epi, Sero, Hist.
catecholamines
DA, NE, Epi (Y) –> L-dopa by rate limiting enz
epinephrine is NOT common NT in CNS but is major hormone of adrenals
Epi
major hormone from adrenals. not common NT
catecholamine
MAO
breaks down catecholamines
MAO inhibitors
drugs increase NE and DA in synapse by slowing down degradation
receptors for Epi and NE
METABOTROPIC 1. alpha androgenic:
a1 - act on postsynaptic nerve to change activity go K+ channels
a2 = act presynaptic to inhibit NE release
2. beta-androgenic
1,2,3 - stimulatory G proteins messenger increase cAMP in postsynaptic cell
CATECHOLAMINE RECEPTOR
metabotropic
serotonin
prod from W essential
slow onset
excitatory effect on muscles
inhibitory on sensations
NO activity during sleep
5-HT monoamine hormone
SRRI
inactivate presynaptic transport which mediates serotonin reuptake in presynaptic cell which increases the conc. of NT
By blocking its reuptake, SSRIs increase the concentration of serotonin in the synaptic cleft, enhancing neurotransmission
AA NT
glutamate and GABA, glycine
glutamate
AA NT
EXCITATORY
50% excitatory synapses in CNS
majority inotropic receptors
glutamate receptors
mostly inotropic in postsynaptic membranes
- AMPA, excitatory
- NMDA
channels
AMPA and NMDA receptors
channels
show cooperatively
receptors for glutamate excitatory in postsynaptic membranes
implicated in LTP
LTP
excitatory NMDA and AMPA implicated
lasting changes in strength of signal for learning and memory
glutamate LTP Mechanism
- presynaptic neuron fires AP, glutamate released and binds both AMPA and NMDA on postsynaptic membrane.
- AMPA rec. fun like excitatory postsynaptic rec. channel becomes permeable to both K and Na and NA influx depolarizes EPSP of postsynaptic cell
NMDA channels mediate Ca flux
when depolarized, Ca enters postsynaptic cell - Ca ions activate 2ndmessanger cascade with kinases and LTP
after LTP
subsequent APs will cause greater depolarization of postsynaptic membrane
NMDA receptors
excitatory postsynaptic channel receptor for glutamate
1. mediate Ca influx
2. excitotoxicity - injury spreads to adj. areas
when glutamate containing cells die, glutamate excessively stims AMPA and NMDA nearby causing accumulation of toxic conc. Ca and cell death
GABA
AA NT
INHIBITORY NT
Modified glutamate
can bind inotropic or metabotropic
sev binding sites
GABA receptors
iono or metabotropic
- inotropic increases Cl flux into cell = hyper polarization IPSP postsynaptic
GABA drugs
increase Cl flux thru GABA receptor
ethanol from alc target gaba
ethanol on GABA
stimulates GABA synapses and inhibits excitatory glutamate synapses
overall depression of activity