postsynaptic membrane

post·syn·ap·tic mem·brane

that part of the plasma membrane of a neuron or muscle fiber with which an axon terminal forms a synaptic junction; in many instances, at least part of such a small postsynaptic membrane patch shows characteristic morphologic modifications such as greater thickness and higher electron density, believed to correspond to the transmitter-sensitive receptor site of such synapses.

post·syn·ap·tic mem·brane

(pōst'si-nap'tik mem'brān)
That part of the plasma membrane of a neuron or muscle fiber with which an axon terminal forms a synaptic junction.

postsynaptic membrane

the excitable membrane of the DENDRITE next to the AXON at a synapse, that receives the nerve impulse.
References in periodicals archive ?
This tends to promote the formation of new neronal circuits that allow the formation of new movement patterns by axonal growth and sprouting and an increase in the number of postsynaptic membrane receptors [2, 3].
Regulation of postsynaptic membrane potential represents a significant part of oxytocin's contribution to the modulation of synaptic function.
Myasthenia gravis (MG) is an autoimmune disease characterized by muscle weakness which results from blockade of the acetylcholine receptors (AChR) by antibodies and destruction of the receptors on the postsynaptic membrane. In 10 to 15 percent of patients with MG, thymic tumors occur, while in 65 percent lymphofollicular hyperplasia of the thymic medulla is found.
It is characterized by decrease in the number of available nicotinic acetylcholine receptors at postsynaptic membrane due to presence of pathogenic autoantibodies [1, 2].
Postsynaptic neurotoxins can bind to the postsynaptic membrane and acetylcholine receptors [4].
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.
In addition, the numbers of synapses and synaptic vesicles were significantly reduced, synaptic structure was interrupted, postsynaptic membrane was swelling, and synaptic cleft was blurred or even disappeared (Figure 3(B2)).
The model we have proposed is fundamentally probabilistic because not all of the neurotransmitters leaving presynaptic neuron arrive the adjacent postsynaptic membrane. Some are lost in the synaptic cleft due to various reasons including the level of concentration of ions, reactions with other ions in the cleft as well as diffusion out of the cleft.
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.sub.q/11]-coupled receptors can be achieved by synaptic activity, [Ca.sup.2+]-assisted RER appears to be most relevant for synaptically-driven eCB-STD (see below) among CaER, RER and [Ca.sup.2+]-assisted RER.