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46 Cards in this Set

  • Front
  • Back
acethlcholine synthesis happens where?
in the cholinergic nerve terminal cytoplasm
Ach synthesized by the action of?
enzyme Choline Acetyltransferase (ChAT) on the precursors choline (Ch) and acetylcoenzyme A (acetyl-CoA)
choline is provided mainly through?
high-affinity sodium co-transport pumps (which require energy) located on the nerve terminal membrane
De Novo synthesis of Ch
occur to a limited extent
from choline-containing phospholipids
acts to provide enough Ch to make up for amt. lost in the synapse
Acetyl-CoA is synthesized from?
pyruvate & acetate, acetylating coenzyme A in mitochondoria
Hemicholinium-3 (HC-3) inhibits?
inhibit high affinity uptake carriers of Ch
leads to eventual depletion of Ach in the nerve terminal
Vesamicol inhibits?
inhibits Ach transport system on the vesicles
Botulinium Toxin (Bo Tox)
binds to sites on the nerve terminal
causes irreversible inhibition of the release of Ach from the nerve terminal
Bo Tox blocks?
blocks the ability of Ach vesicles to fuse with the internal nerve terminal cell wall and excytosis
black widow spider venom
triggers the exocytosis of Ach-containing vesicles
acetylcholinesterase catabolizes Ach to?
Ch and acetic acid
2 cholinergic receptors
muscarinic and nicotinic
muscarinic receptors
comprised of a family of receptors (M1-M5)
M1 location?
in autonomic ganglia and CNS
M2 location?
on supraventricular regions of heart
M3 location?
on smooth muscles
vascular endothelial cells
M1 & M3 are coupled to?
phospholipase C via G proteins
phosphatidylinositol polyphosphates(PIP)spilits into?
inositol 1,4,5 triphosphate (IP3) &
Diacylglycerol (DAG)
by activation of M1 & M3 receptors
water soluble (in cytoplasm)
act on IP3 receptors on the sarcoplasmic reticulum &
increase Ca release
lipid soluble (in cell memb)
along with increase Ca,
activates protein kinase C (PKC)
muscarinic Ach receptors
belong to a class of metabotropic receptors which use G proteins as their signalling mechanism
nicotinic receptors
use an ion-gated mechanism for signalling
Muscarinic receptors are found in?
parasympathetic nervous system
late EPSP in ganglia
blocked by Atoropine
selectively stimulated by Oxotremorine
excitatory post-synaptic potential
fairly selective M1 antagonist
mainly cardiac (decreases AV nodal conduction & SA automaticity, < HR)
blocked by Atropine
selective M2 antagonist
mainly at neuroeffector junctions (glands, smooth muscles)
blocked by Atropine
pupillary constriction
selective M3 antagonist
mainly in CNS
antagonized by Himbacine
exact importance and locations still unclear
nicotinic receptors
ganglionic receptors in both symp/para-symp and neuromuscular junctions
ganglionic nicotinic receptors stimulated by?
Ach & Dimethylphenyl-piperazinium (DMPP)
ganglionic nicotinic receptors antagonized by?
Trimethaphan (Arfonad)
neuromuscular nicotinic receptors stimulated by?
nicotine and Ach
Phenyltrimetyl ammonium (PTMA)
a selective agonist of neuromuscular nicotinic receptor
D-tubocurarine (Tubarine)
a non-depolarizing antagonist of neuromuscular nicotinic receptor
from snake venom
almost irreversible antagonist of neuromuscular nicotinic receptor
neuromuscular depolarizing blockers
Succ (Anectine)
initially stimulate receptor, then block
mainly muscarinic (M1, M2, ??)
inhibit further release of Ach
nicotinic autoreceptors found, but they tend to increase rather than inhibit Ach release
innervention on nerve terminal by another type of receptor
allows control of release by another system
receptors react to circulating neurotransmitter
paralysis of accomodation from para-symp drug
contraction of ciliary muscle
release the tension of suspensaory ligament
lens get thicker
relaxation of ciliary muscle
pulls ligament
makes lens thinner