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Sybaptic Plasticity

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  1. Introduction
  2. Long term depression
  3. Long term potentiation
  4. The role of phosphorylation
  5. Actions of psychotropic drugs
  6. Conclusion
  7. References

In its simplest form, the postsynaptic response to neurotransmitter release can be mediated by a single protein complex. For example, nicotinic acetylcholine receptors are self-contained stimulus-response modules that both detect a stimulus, acetylcholine, and generate a response, passage of ion currents. In a similar vein, other members of this superfamily of ionotropic receptors, including g-aminobutyric acid (GABA) and glutamate receptors, have the ability to function in a manner that is independent of the intracellular signaling pathways discussed. Thus, in contrast to growth factor or G-protein?coupled receptors, which often recruit elaborate cascades to elicit a response, the simplicity of self-sufficient ionotropic receptor complexes represents an optimal design for achieving reliability, precision, and speed. However, this view of ionotropic receptors as insulated from their social environment has had to be abandoned in the face of overwhelming evidence that this class of receptors is dynamically regulated by intraneuronal signaling pathways. Although these receptors do not rely on intraneuronal signaling pathways to operate ion channels, because these channels are an intrinsic feature of the receptor complex the linkage between ligand binding and ion channel gating is nevertheless subject to regulation by the network of intraneuronal signaling pathways just described. For example, phosphorylation of the GABA or glutamate receptors modulates their response to ligand exposure.

[...] Role of Phosphorylation The associative property of this model of synaptic plasticity has focused attention on deciphering the intraneuronal signaling pathways that mediate the long-term change in synaptic transmission triggered by NMDA receptor stimulation. NMDA receptor activation leads to transient rises in intracellular levels of calcium making this second messenger an attractive candidate. Experiments demonstrating that intracellular calcium chelators block this form of long-term potentiation corroborated the critical role of calcium in this process. Subsequent studies investigated whether either of the calcium-sensitive kinases that are highly enriched in neuronal dendrites, calcium/calmodulin-dependent kinase II and protein kinase were critical for this process. [...]

[...] Although the formal similarities between the associative properties of long- term potentiation and classical conditioning have provided compelling support for the hypothesis that this form of synaptic plasticity underlies associative learning, it has been difficult to gain experimental support linking this electrophysiological response to the behavioral phenomena. An important breakthrough in this area has been the utilization of transgenic animals with targeted mutations in genes encoding signaling molecules involved in long-term potentiation. The ability to examine the effect of these genetic alterations on behavior in the intact animal as well as on long-term potentiation in vitro has provided a means of bridging the gap between intraneuronal signaling pathways and behavior. [...]

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