MCP 28: Synaptic Transmission Flashcards
neuromuscular junction (NMJ)
allows for nerve control of skeletal muscle, point of contact between nerve and muscle
end plate
AKA the neuromuscular junction
end plate potential (EPP)
not an action potential, depolarizes the cell so enough voltage gated Na+ channels open to produce an action potential in the muscle
excitatory postsynaptic potential (EPSP)
AKA end plate potential
excitation-secretion coupling
process by which depolarization increases free cytosolic calcium that in turn induces vesicle fusion and exocytosis of neurotransmitter from the presynaptic membrane
active zone
in the presynaptic membrane, NT-containing vesicles fused along in the inner leaflet of membrane in parallel rows
acetylcholine (ACh)
neurotransmitter, each vesicle contains 100mM of ACh
curare
competitive antagonist to ACh
alpha bugarotoxin
non-competitive antagonist to ACh
basal lamina
space between the pre and post-synaptic clefts
acetylcholinesterase (AChE)
cleaves ACh into choline and acetate; found int he basal lamina
myastemia gravis
autoimmune disease where antibodies block the AChR
junctional folds
located on post-synaptic membrane, 1.) membrane invaginations increase the surface area of the post synaptic membrane, therefore, more space for AChR receptors 2) also decrease distance between pre and post synaptic membrane, increase speed at which signal travels
development and innervation
with development, polyneural innervation ends; each muscle fiber is contacted by a single axon, but a single motor axon can innervate several muscle fibers
dystrophin
links muscle membrane to actin cytskeleton, giving structure to the NMJ; gene defects can result in muscular dystrophy
agrin
tells muscle membrane to form new NMJ
steps at the NMJ
1.) action potential reaches presynaptic membrane and sodium rushes in, causing depolarization 2.) current of Ca2+ rushes into cell 3.) as presynaptic cell repolarizes, calcium influx stops 4.) NT released in synaptic cleft and binds to postsynaptic membrane 5.) activation of AChR causes EPP 6.) EPP results in new action potential in muscle cell
synaptic delay
time delay between the arrival of the action potential and production of the post synaptic response
calcium
in the nanometer scale inside the cell, 4 orders of magnitude lower than the outside; most calcium immediately sequestered upon entering the cell
calmodulin
binds Ca2+ in the cell
calcinerurin
binds Ca2+ in the cell
calreticulin
binds Ca2+ in the cell
smooth ER and Ca2+
brings Ca2+ into the organelles
IP3
membrane phospholipid PLA2 cleaved into IP3 and DAG, IP3 binds to IP3 receptor on smooth ER causing calcium release from smooth ER and increasing cytosolic Ca2+ levels.
ryanodine
present in SER membrane, responsible for calcium release related to muscle contraction; caffeine is a stimulator–releases INTRACELLULAR Ca2+ levels
mitochondria
controls Ca2+ homeostasis with a Na+/Ca2+ antiport system but smooth ER plays a much bigger role in Ca2+ homeostatsis than mitochondria
calcium sequestration
into smooth ER and mitochondria; smooth ER has ATP pump, and mitochondria has Na+/Ca2+ antiport system
calcium release
IP3 receptors and ryanodine receptors
calcium expulsion
Ca2+/ATPase on plasma membrane and Na+/Ca2+ antiport system (3 to 1 system)
L type calcium channel
voltage gated, activated at higher membrane potentials, open slower and remain open longer than T-type…..play a role in sustaining action potential
T type calcium channel
voltage gated, activated a lower voltages, open more quickly and remain open shorter that L type channels, respond well to rhythmic stimulation, play an important role in hearth beat, walking, etc.
N type calcium channel
voltage gated, involved in NT release from presynaptic cleft, slow to activate, require strong depolarization
P/Q and R type calcium channels
slow to activate, require strong depolarization, P channel also in presynaptic area and control release of ACh
dihydropyridines (DHPs)
block L-type channels, do not affect synaptic calcium channels, used to treat angina and hypertension
conotoxin
blocks N type voltage gated calcium channels
life of ACh
1ms at room temperature, either diffuses, binds or is enzymatically destroyed once release from presynaptic cleft
rate determining step for synaptic transmission
how long the AChR receptor stays open
