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Lecture 9

BIO270H1 Lecture Notes - Lecture 9: Gap Junction, Futile Cycle, Autonomic Nervous System


Department
Biology
Course Code
BIO270H1
Professor
Chris Garside
Lecture
9

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Lecture 9 (November 18, 2015): Movement and Muscle Part 2
troponin
otrimer composed of 3 polypeptide subunits
TnI
binds to actin, inhibits of cross-bridges
TnC
binds Ca2+ leading to a conformational change
there are 4 binding sites
at the C-terminus
ohigh affinity sites
ostructure Ca2+ binding sites
ocan always bind Ca2+ no matter what concentration of Ca2+
there is which allows the trimer to stay attached
at the N-terminus
olow affinity, regulatory binding sites
owhen the concentration of Ca2+ increases, Ca2+ can be
bound, leading to conformational change, which uncovers
the hydrophobic region of the TnC and can then interact
with TnI and weaken the interaction of TnI with actin,
which pulls troponin/tropomyosin off the myosin binding
sites, then when ATP is present, cross-bridges can be
formed
TnT
tightly bound to tropomyosin (blocks actin binding sites)
orelaxation
sarcolemma repolarizes and Ca2+ returns to resting levels
thin filament proteins in skeletal muscles are what confer Ca2+ sensitivity
in striated muscle
can be thin and thick filaments for smooth muscle
ostrength of contraction is dependent on concentration of Ca2+
oduration of contraction is dependent on how long the Ca2+ levels are elevated
SKELETAL MUSCLE AND CARDIAC MUSCLE
general information
otime course of action potential: doing contractions at different rates due to the
density of ion channels and their activity on the sarcolemma
oeffective refractory period: cannot stimulate another action potential on the
sarcolemma
ensures no summation of tetanus (maximum sustained contraction)
opropagation and EC (excitation-contraction) coupling
big muscles with thousands of fibers

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conductance is facilitated by transverse tubules (T-tubules)
oenhances penetration of depolarization
omore developed in twitching muscles
oT-tubules are less developed in cardiac muscles
sarcoplasmic reticulum (SR)
modified endoplasmic reticulum of muscle cells
stores massive amounts of Ca2+
oCa2+ is bound to calsequestrin
oterminal cisternae localize Ca2+ to T-tubules
important for SR to retain a high concentration of Ca2+
odepolarization leads to an increase in the Ca2+ concentration
Ca2+ channel is membrane
dihydropyridine receptor (DHPR) responds to depolarization
(voltage gates)
Ca2+ channels in the SR
ryanodine receptors (RyR) allow Ca2+ to move down it's
concentration gradient
transporters remove Ca2+ from the cytoplasm
in cell membrane
oCa2+ ATPase
oNa+/ Ca2+ exchanger (NaCaX)
in SR
oCa2+ ATPase (SERCA)
is Ca2+ that enter DHPR enough to cause contraction?
no is most cases
omaybe in slow contraction muscles
cardiac
omyogenic
starts in muscle
ospontaneous
opacemaker cells depolarize the fastest because they have an unstable resting
membrane potential
slowly depolarize on its own, reaches threshold, action potential does not
need external influences to happen
ofunny channel
cation specific
Na+ has a strong driving force and K+ is not as strong, which leads to the
depolarization of the sarcolemma
otime course
AP has rapid depolarization
slow repolarization due to voltage fates Ca2+ channels which keep the cell
depolarized for a long time
orefractory period
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can increase the rate of contraction , but force does not increase
if heart is stimulated at rapid rates, it's arrhythmia
heart is not pumping as it should
opropagation and EC coupling
diad
T-tubule with one terminal cisternae
doesn't need as much release of Ca2+
at the Z-disk
ocellular origins of Ca2+
" Ca2+ induced, Ca2+ release"
DHPR opens, Ca2+ moves in, binds to allosteric site on RyR receptors,
RyR opens and Ca2+ is released
Ca2+ functions as the ligand for RyR
EGTA is a Ca2+ chelator (binds them all)
if bound to cardiac and skeletal, only skeletal will contract when
stimulates because it does not require Ca2+ outside of the cell to
function
skeletal
orequires stimulus from motor neurons
oneurogenic (starts in neuron)
opassive spread of depolarization and has to reach the entire muscle cell
to enhance the passive movement, there can be multiple innervation sites
from the motor neuron (tonic), but most are single (twitch) innervation
sites
ojunctional folds
high concentraiton of nicotinic acetlycholine receptors
foldings of sarcolemma to get a rapid response
motor end plate
oexcitation (action potential) moves down the pre synaptic terminal, stimulates
opening of voltage gates Ca2+ channels, Ca2+ comes in the pre synaptic neuron,
Ca2+ binds SNARE proteins, triggers fusion of vesicles with acetylcholine,
acetylcholine diffuses across the synapse and binds to the post synapse (muscle),
opens a ligand gated ion channel, Na+ rushes in the muscle cell and triggers an
action potential
omotor neurons of invertebrates release other neurotransmitters other than
acetlycholine
otime course
fast skeletal
fast depolarization and repolarization
fast contraction
slow skeletal
slow, sustained contraction
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