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BIO254:Silent: Difference between revisions
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Several experiments demonstrate that excitatory synapses can effectively regulate their postsynaptic glutamate receptors. For instance, when some glutamatergic synapses are stimulate, no postsynaptic electrical signal is generated when the postsynaptic cell is at a normal resting membrane potential. In contrast, when these same postsynaptic cells are depolarized, these "silent synapses" are able to transmit strong postsynaptic responses that are detectable using electrophysiological methods (such as patch clamp). Because these silent synapses have the potential to be turned on or off in response to postsynaptic activity, this mechanism demonstrates a simple means for modifying and regulating neural activity. | Several experiments demonstrate that excitatory synapses can effectively regulate their postsynaptic glutamate receptors. For instance, when some glutamatergic synapses are stimulate, no postsynaptic electrical signal is generated when the postsynaptic cell is at a normal resting membrane potential. In contrast, when these same postsynaptic cells are depolarized, these "silent synapses" are able to transmit strong postsynaptic responses that are detectable using electrophysiological methods (such as patch clamp). Because these silent synapses have the potential to be turned on or off in response to postsynaptic activity, this mechanism demonstrates a simple means for modifying and regulating neural activity. | ||
Silent synapses are abundant in development and are found in several brain regions, including the hippocampus, the cerebral cortex, and the spinal cord. The "silence" of these synapses is the result of Mg++ blockade of NMDA receptors, which are voltage-dependent. Interestingly, glutamate released at silent synapses bind only to NMDA receptors, without binding to AMPA receptors. For years, this specificity has puzzles neurobiologists, but one explanation is that NMDA and AMPA receptors have significantly different affinities for binding the released glutamate neurotransmitter. Glutamate released onto neighboring neurons may diffuse only to synapses on the neuron from which the electrical recording is being taken. The concentration of glutamate may be sufficient enough to activate NMDA receptors (high-affinity), but not the low-affinity AMPA receptors. A second possibility states that both AMPA and NMDA receptors exist on the postsynaptic terminal, but only the NMDA are fully functional. Or, some specific excitatory synapses only have NMDA receptors; growing evidence tends to support this latter model. Immunocytochemical experiments perhaps provide the most compelling evidence for this explanation: staining done by Gomperts et al. show that select excitatory synapses only possess NMDA receptors. | |||
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==The iGluR channel== | ==The iGluR channel== | ||
