Lecture 3 Flashcards
endogenous vs exogenous
endogenous = made in the body (Ach) exogenous = made outside the body (nicotine and muscarine)
acetylcholine neuron/receptor name
cholinergic neuron and receptor
epinephrine neuron/receptor name
adrenergic neuron and receptor
dopamine neuron/receptor name
dopaminergic neuron, D1, D2 … receptor
serotonin neuron/receptor name
serotonergic neuron, 5HT receptor
glycine neuron/receptor name
glycinergic neuron and receptor
GABA neuron/receptor name
GABAinergic neuron and GABA receptors
glutamate neuron/receptor name
glutamergic neuron, NMDA and AMPA receptors
acetylcholinesterase
on postsynaptic neuron, breaks down Ach to be reused in presynaptic neuron
where Ach used and where excitatory/inhibitory
excitatory = somatic motor neuron, autonomic motor neuron, CNS inhibitory = autonomic motor neuron
nicotinic receptors - mechanism, naming, where found
nonspecific LGIC but inward flow of Na+ dominates because down electrical and concentration gradient vs K+ going down concentration but against electrical , always excitatory, found in autonomic ganglia and skeletal muscle
muscarinic receptors - mechanism
GPCR, based on G protein type and channel that is open or closed effect may be different
M3/M5 - location, mechanism, effect
GI, smooth muscle, gland Ca2+ channel opens and muscle contraction
M2 - location, mechanism, effect
heart, K+ channel opens causing hyperpolarization, inhibition of intrinsic heart rate
botulinum toxin - effect and mechanism
flaccid paralysis, SNARE complex frozen and cant change conformation, no Ach released
curare - effect and mechanism
nicotinic antagonist, flaccid paralysis
A-bungarotoxin
nicotinic and muscarinic antagonist
saxitoxin
blocks Na+ VGIC so no action potential generated
tetrodotoxin
blocks Na+ VGIC so no action potential generated
strychnine
blocks glycine receptor (so no inhibition)
spastic vs flaccid paralysis
spastic = eternally contracted because too much Ach vs flaccid = no contraction at all because no Ach
GABA and glycine location
GABA = brain
glycine = spine
both inhibition by Cl-
ex of glycine in UMN and LMN
UMN –> releases glycine –> inhibition of Ach release by LMN –> no skeletal muscle stimulation
monoamines - list them
- catelochamines = tyrosine –> dopamine, epinephrine, norepinephrine
- tryptophan –> serotonin
- histidine –> histamine
presynaptic reuptake receptors
on presynaptic neuron, takes up NT so it doesnt remain in synaptic cleft and cause over stimulation
monoamine oxidase MAO
found in presynaptic neuron, breaks down NT
MAO inhibitors
prevents MAO from breaking down NT so more NT in synaptic cleft
MAO receptor mechanisms
mostly LGIC but sometimes GCPR with cAMP secondary messenger
GPCR with cAMP
NT –> receptor –> G protein dissociation –> adenylate cyclase –> ATP to cAMP –> protein kinase activated –> other proteins phosphorylated
serotonin - function and where found
found raphe nuclei, role in mood, cerebral circulation, behavior, appetite, libido
SSRI - mechanism and uses
serotonin reuptake inhibitor, increases amount of serotonin by preventing reuptake, treats depression, anxiety, migraine
nigrostriatal system - function, start and end, relation to parkinsons
- initiate movemetn adn complex coordinated movement
- death of neurons in this system causes Parkinsons
- substantial nigra to corpus striatum
mesolimbic dopamine system - start and end (many), relation to schizophrenia and Parkinsonian side effects
- VTA –> nucleus accumbens, amygdala, hippocampus, prefrontal cortex, frontal cortex
- schizophrenia = overactive mesolimbic system, hallunciatiosn
- treated by decreasing dopamine which affects nigrostrial and causes Parkinsonian side effect
VTA receptors and relation to drugs
VTA receptors for Ach and GABA, means can be stimulated by nictoine, opiods, cannabinoids etc and explains addiction from drugs
cocaine and amphetamines
neurotransmitter reuptake inhibitors - cocaine triple reuptake inhibitor of serotonin, dopamine and norepinephrine, amphetamine on reputake inhibitor of norepinephrine
glutamate - receptors and effect
NMDA, AMPA, excitatory
NO effects
smooth muscle relaxation and blood vessel dilation (due to relaxation)
