what happens at the neuromuscular junction
Motor neurons release acetylcholine (ACh) which is a neurotransmitter
Ach is ALWAYS excitatory in skeletal muscle
ACh binds to ionotropic cholinergic receptors
These ionotropic cholinergic receptors open Na+ channels
Na+ influx causes the depolarization
what happens at muscle excitation
- unidirectional transmission of a nerve impulse to the muscle fiber
- axon terminal neurotransmitter ACh is involved which difusses through the synaptic clef and binds receptors on the motor endplate of the sarcolemma
explain the step by step NMJ transmission of action potential
- Action potential arrives at motor neuron terminal
- ACh is released at the synaptic cleft
- ACh binds receptors on motor end plate
- Na+ enters the cell
- Muscle depolarizes
- Voltage gated Na channels open
- Action potential spreads across sarcolemma
- ACh is broken down by acetylcholinesterase (AChE)
what is a MUST need intracellular thing in muscle contraciton
For muscles to contract, they depend on intracellular Ca
Calcium regulates the interactions between actin and myosin
Tropomyosine is rope like and obstructs myosin binding sites/ blocks them at rest (on actin)
Troponin has TnC which is a ca binding site and 2 other binding sites
what are the basic steps of muscle contraction to occur/cross bridge interaction
- Action potential triggers ACh release to synaptic cleft
- Sarcolemma depolarizes and allows for Na+ entry
- Cytosolic Ca increases
- Ca binds to troponin and tropomyosin undergoes conformational change when troponin binds and shifts off myosin binding site
- Myosin head binds tightly and makes power stroke (cross bridge interaction)
t-tubules vs sarcoplasmic reticulum
Transverse tubules are the extensive part of the sarcolemma and allow for uniform contraction. Also, action potentials penetrate inner myofibrils and these carry action potentials deep into the muscle.
Sarcoplasmic reticulum stores Ca, surrounds each myofibril and has a Ca-ATPase pump
Terminal cisternae is enlarged SR regions, close to T-tubules (makes triad), and primary Ca release site.
DHPR vs RyR
DHPR = dihydropyridine receptor
This is a volage sensitive receptor and located in t-tubule membrane
RyR (ryanodine receptor)
This is the Ca release channel and located in SR membrane
what is the mechanism of DHPR and RyR
Mechanism
1. Action potential travels down T-tubule
2. DHPR senses voltage change
3. DHPR activates RyR
4. RyR releases Ca from SR
5. Ca floods sarcoplasm
6. Ca binds troponin
7. Contraction can occur
explain the simplified cross bridge cycle
ATP binds myosin and the cross bridge is severed, where myosin detaches from actin
ATP hydrolysis causes ADP+Pi to attach and myosin to reach forward to a new actin molecule
Power stroke where Pi is released and myosin jerks, actin pulled toward center and the conformational change is what allows the myosin neck to pull actin toward the tail
ADP is released and myosin remained attached, myosin is bound to G-actin monomer
Completion of power stroke releases ADP and cross bridge remains rigor
why is atp significant
ATP is required for myosin detachment, myosin head re cocking, and Ca2+ pumping back into SR
Without ATP myosin cannot detach.
what does cross bridge remain rigor mean
ADP is released and myosin remained attached, myosin is bound to G-actin monomer
Completion of power stroke releases ADP and cross bridge remains rigor
so its basically when myosin is still bound to the g-actin when the adp is released and cross bridge interaction remains
what is rigor mortis
Rigor mortis:
After death:
No atp produced
Myosin head remains attached with no ADP or Pi
Sustained contraction
Muscle stiffness
Rigor mortis = lack of ATP
the absense of ATP prevents myosin head from detatching from actin filaments and leads to a sustained muscle contraction and rigidity
