The most common of such conditions is myasthenia gravis (MG), an autoimmune disorder in which an antibody-mediated, T-cell-dependent process targets acetylcholine receptors on the postsynaptic membrane
of the neuromuscular junction.
Subsequently, neurotransmitter is released into the synaptic cleft and diffuses to the postsynaptic membrane
to activate neurotransmitter receptors.
2010) mention that SNAP-23is involved in postsynaptic membrane
trafficking events and its alteration decreases expression of NMDA (non-natural aminoacid N-methyl-D-aspartate) receptors of glutamate surface and the amount of current receivers in dendritic spines from hippocampal neurons in culture.
This balance can be maintained by regulating the number of neurotransmitter receptors in the postsynaptic membrane
Sufficient depolarization of the postsynaptic membrane
reaches a threshold at which a second action potential is induced and the impulse is successfully transmitted to the next neuron.
Since weak depolarization of postsynaptic membrane
and activation of postsynaptic [G.
Glutamate then activates NMDA receptors [~50 NMDA receptors dispersed over a 400-nm-diameter postsynaptic density (1) at postsynaptic membrane
which further propagates excitatory impulse to cell body and also it activates calcium and calmodulin to bind with each other (2) and causes release of nitric oxide (NO) from nitric oxide synthetase (NOS) (One NOS molecule generates 20 NO molecules per second).
Additionally, LTP can be induced at lower frequencies if the postsynaptic membrane
is experimentally depolarized (Kelso and Brown, 1986; Wigstrom and Gustafsson, 1986; Meredith et al.
The depolarizing agents bind to acetylcholine receptors and cause a sustained postsynaptic membrane
synaptic development), the ability to detect and integrate signals that occur simultaneously at the presynaptic terminal and postsynaptic membrane
Following nerve impulse transmission, acetylcholine is released from the postsynaptic membrane
receptor and is broken down by acetylcholinesterase (AChE) to choline and acetic acid.
Research about the pathophysiology of MG reveals this immune dysfunction occurs in 3 ways, which primarily alter depolarization of muscle tissue at the postsynaptic membrane