Skeletal Muscle Physiology DSA Flashcards
voltage gated sodium channel
closed but capable of opening RMP -70
open - activated -50 to +30
closed and not capable of opening +30 to -70
h gate
inactivation gate
m gate
activation gate
voltage gated potassium gate
closed but capable of opening at RMP
- delayed opening triggered at threshold**
- remains closed to peak potential
- 70 to +30
open from peak polarization to after hyperpolarization
+3- to -80
resting membrane potential depends on
extracellular K concentrations**
increased K uptake by cell - insulin, epinephrine, aldosterone - hyperkalemia
increased K conductance
hyperpolarization
hypokalemia
hyperpolarization
hyperkalemia
depolarization
changes in Na and K conductance
Na - rapid rise and fall
K - slow rise and fall
neurotransmitter release
AP at axon terminal - trigger voltage gated Ca channel opening
influx of Ca - release of synaptic vesicles
AP at NMJ vs. synapse
synapse - summation of EPSPs brings to threshold
-excitatory or inhibitory
NMJ - one to one transmission of APs
-always excitatory
postjunctional fold
at NMJ
-increase surface area
receptors for ACh at NMJ
nicotinic AChR
acetylcholinesterase
terminates synaptic transmission at NMJ
breaks down to choline + acetate
synthesis of ACh
choline acetyltransferase
-choline + acetyl CoA
ACh-H exchanger
uptake of ACh into vesicles
-driven by proton gradient
positive voltage and low pH inside vesicle
vesicle fusion at NMJ
synaptbrevin - v-SNARE
complex with snap-25 and syntaxin (t-SNAREs)
detects rise in Ca at NMJ and trigger exocytosis of bound ACh vesicles
synaptomagmin
Ca receptor**
syntaxin and SNAM-25
t-SNAREs
presynaptic membrane of nerve terminal
bind with synaptobrevin**
bring vesicles closer to presynaptic membrane
tetanus
synaptobrevin
botulinum A and E
cleave SNAP-25
botulinum C1
cleave syntaxin
botulinum B, D, F, G
act on synaptobrevin
ACh receptor
permeable to cations
weak ionic selectivity - functions to raise Vm above threshold
AP at -50
opening of AChR at NMJ
Na and K equally permeable
- increases normally low resting permeability
- large movement of Na into cell
- small movement of K out of cell
- results in graded end plate potential
Vm shifts to between E-K and E-Na
sarcomere
Z line to Z line
A band
myosin thick filaments
partial overlap with actin thin filaments
H zone
middle of A band
part of myosin where actin does not overlap
I band
part of actin not overlapping myosin
H zone
middle of A band
-part of myosin where actin does not overlap
Z line
thin filament attachment
thick filament
bipolar assembly of multiple myosin molecules
2 myosin heavy chains
-rod, hinge, head
4 light chains - 2 alkali, 2 regulatory
binding sites on heavy chains
actin binding - for cross bridging
ATPase site - for binding ATP
thin filaments
actin - F-actin
alpha helical polymer of actin is backbone
13 actin monomers makes 1 helical turn - F-actin
tropomyosin
blocks actin binding to myosin at rest
interacts with 7 actin monomers
troponin
interacts with 1 tropomyosin and 1 actin
troponin T
TnT, TNNT
binds single tropomyosin molecule
troponin C
TnC, TNNC
binds Ca
troponin I
TnI, TNNI
binds actin and inhibits contraction
Ca combines with troponin
tropomyosin slips away from blocking position between actin and myosin
myosin binding site on actin forms cross bridge - contraction can occur
excitation contraction coupling
AP of sarcolemma (excitation)
increased Ca allows actin and myosin binding (coupling)
increased Ca
intracellular signal to trigger and sustain contraction**
AP propagate fro sarcolemma to interior of muscle fibers via transverse tubules
Ca released from SR
Ca binds troponin - allows cross bridging
triad
t tubule and 2 associated cisternae
propagate AP into t tubule - depolarizes triad
Ca release from lateral sacs of SR
DHPR and RyR important
DHPR
dihydropyridine receptor
-L type Ca channel
voltage sensor**
associated with T tubule
tetrads - groups of 4
RyR
ryanodine receptor
-Ca release
release stored Ca from SR**
cluster at portion of SR opposite the T tubule
continued force through cross bridge cycling
depends on Ca supply
relaxation
reuptake of Ca fro sarcoplasm back to SR
requires ATP
- Ca pumps
- ATPase binding site on myosin head
pumps removing Ca for relaxation
Na-Ca exchanger
Ca pump
MAJOR - SERCA pump
-most important mechanism for returning resting Ca levels in skeletal m
high Ca
inhibits activity of SERCA
Ca binding proteins in SR
delay inhibition of SERCA pump
buffer increased Ca during Ca reuptake and can increase Ca storage capacity of SR
calsequestrin
major Ca binding protein in skeletal m
localized in SR at triad
-form complex with Ca RyR
facilitate muscle relaxation by buffering Ca and unbinds Ca near Ca release channel
calreticulin
Ca binding protein in smooth m