In: Anatomy and Physiology
Using bullet-point sentences, describe EVERY SINGLE action from the action potential moving down a motor neuron, to the synapse, and then all the way to contraction of the skeletal muscle cell.
Action Potential in motor Neuron
*Normal RMP ( Resting membrane potential ) of neuron is -70 .
Depolariation ---> Presynaptic membrane have Voltage sensitive sodium channels whose activation cause and entry of Na+ sodium inside So when membrane potential reaches -55 mv ,Action potential fires by opening sodium channels and allow entry of sodium channels inside and Membrane potential overshoots to + 55 mv.
Repolarisation ---> when depolarisation reaches to + 55 mv, K+ channel opens and Na channels become inactivated which causes repolarisation.
Hyperpolarisation ---> Unlike Na channels, K channels are slow, hence when action potential reaches resting level, continuous efflux of K+ causes more negativity inside cell membrane leading to hyperpolarisation
Neuromuscular transmission
Converting electrical signal into chemical signal .
Every neuron receives impulse in form of action potential
(Electrical signal)
Neuromuscular Junction
*The synapse that is formed between axons of an alpha-motor neuron acting as presynaptic neuron and a skeletal muscle fiber is called the neuromuscular junction (NMJ).
*The terminals of alpha-motor neurons contain vesicles containing acetylcholine (Ach), thus the synaptic transmission at the neuromuscular junction a type of cholinergic transmission.
Steps in Neuromuscular transmission
1.) The action potential travels down the motor neuron and
depolarizes the presynaptic membrane.
2) This depolarization opens voltage-gated Ca2+ channels in the presynaptic membrane, resulting in Ca2+ influx into the presynaptic terminal.
3) The rise in Ca2+ causes synaptic vesicles to release Acetylcholine. The amount of neurotransmitter release is directly related to the rise in cytosolic Ca2+, i.e., the more Ca2+ enters , more Acetylcholine released.
4. Ach binds to a nicotinic receptor located on the muscle membrane (NM receptor). The NM receptor is a non-selective monovalent cation channel (both Na+ and K+ can move). Now Na+ has a much greater net force depolarization occurs. This depolarization is called an end-plate potential (EPP). The magnitude of the EPP is directly related to the amount of Ach released.
5. The resulting depolarization opens fast Na+ channels on the muscle membrane (sarcolemma) causing an action potential to occur in the sarcolemma. An action potential in the motor neuron cause release of enough Ach to cause End Plate Potential that is at least threshold for the action potential in the skeletal muscle cell which occurs under normal circumstances . There is a one-to-one relationship between an action potential in the motor neuron and an action potential in the skeletal muscle cell.
6. The actions of Ach are terminated by acetylcholinesterase
(AchE), that breaks Acetylcholine into choline and acetate.
Acetylcholinesterase located on postsynaptic membrane . Choline is
taken back into the presynaptic terminal (reuptake), hence
providing substrate for re-synthesis of Acetycholine .
Excitation Contraction coupling steps
1) Action potential is transmitted along the sarcolemma of the muscle fiber and then down the T tubules
2) Depolarization of T-tubules causes conformation change in DHP receptors, opening the Ca++ release channels in the terminal cisternae of the sarcoplasmic reticulum.
3) This triggers release of Ca++ from the terminal cisterns of the L-tubule. Ca++ peaks at approximately 20 msec after the Action potential.
4) The released Ca++ binds to troponin-C Troponin-C facilitates movement of the associated tropomyosin molecule toward the actin filament The tropomyosin ‘moves away’, exposes the myosin binding site on the actin filament This triggers the cross-bridge cycling, including the powerstroke .
5) The active pumping of Ca++ back into the sarcoplasmic reticulum brings about relaxation.