Efferent, alpha motor neurons
What kind of neurons are signals which tel the muscle to contact, pass through?
No synaptobrevin>Ach cannot be released> no muscle contraction occurs.
What chops up synaptobrevin? What is the consequence of this?
Raising the Vm above the necessary threshold needed for an AP.
What is the basic function of nicotinic receptors?
Shorten: H zone and I band (thus the Z lines come closer)
Do not change: A bands
Which bands get shorter during contraction and which bands don't?
Sits under the P.M. and prevents contraction-induced injury of the membrane.
It also may serve as a scaffolding for cell signaling cascades that promote cell survival.
What is the purpose of the dystrophin-glycoprotein complex?
X-linked disease which causes progresive muscle wasting> pt's eventually wheel chair bound.
Due to a deffect in dystrophin gene resulting in a deficiency of the dystrophin protein in skeltal muscle, brain, retina, S.M.
Test: Use a western blot to look for dystrophin protein.
What is Duchenne's muscular dystrophy?
How do they test for it?
Invagination of the sarcolemma called T-Tubules
S.M.: Caveoli- rudimentary caveoli- not as dev.
What faciitates communication between the surface of the cell and it's interior in skeltal muscles? What about S.M.?
An AP comes to the SR and normally bound DHP from the T-tuble removes itself from the RH4 receptor on the sarcoplasmic reticulum> Ca++ can now come in> (Now actin-myosin interaction can take place and we can get contraction)
Explain what happens during the excitation-contractoin copuling of skeltal muscle
Cardiac muscle requires Extracellular Ca++ to come in which then stimulates the SR to release more Ca++.
Skeltal muscle's voltage from teh AP stimulates the release of Ca++ from the SR.
SO, the difference is that skeltal muscle is known as a "Voltage activated Ca++ release (VACR)" but the cardiac muscle is reffered to as a "Ca activated Ca release."
How are the initial stimulus' for contraction diff between Skeltal muscle and cardiac muscle?
The more troponin C binding to Ca++ keeping tropomyosin from blocking the binding= greater chance for contraction
The more Ca++ then....
When you die no more ATP coming in to release Myosin/Actin form their bound state so the body stays stiff/contracted!.. Eventually though after a few hours proteins denature so then myosin/actin are not stuck in their bound state.
What is rigor mortis?
1) Ca+-Na+ exchanger: using sodium pumps Ca+ back out into the extracellular space
2) SERCA: Puts Ca++ back into the SR and Calsequestrin binds it and keeps it inside
Rexlation: how do you put Ca++ back from where it came?
1) Pump Ca+ back into SR
**2) Dephosphorylation of the myosin light chain.
How do you terminate relaxatoin in smooth muscle cels?
Results from a defect in the SR Ca++ release channel (RYR) (activated by some anesthetics like Halothane)> too much Ca++ released)> muscle rigitidy, hyperthermia, etc.
______ is a disease causing disturbances n Ca++ homeostasis in skeletal muscle.
explain teh disease
What inheritance pattern does it have?
An autosomal dom disease resulting in muscle weakness and disintegration of contractile filaments, and loss of mitochondria due to excess Ca++
So defect in RYR> Excess Ca++ enters> Mitochondria have a Ca++ overload and some mitchondria lost.
What is central core disease?