| Synaptic Plasticity |
Article Index for Synaptic |
Information AboutSynaptic Plasticity |
| CATEGORIES ABOUT SYNAPTIC PLASTICITY | |
| neurophysiology | |
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Two known molecular mechanisms for synaptic plasticity were revealed by research in laboratories such as that of Eric Kandel . The first mechanism involves modification of existing synaptic proteins (typically Protein Kinase s) resulting in altered synaptic function (Shi et al., 1999). The second mechanism depends on Second Messenger neurotransmitters regulating Gene Transcription and changes in the levels of key proteins at synapses. This second mechanism can be triggered by protein phosphorylation but takes longer and lasts longer, providing the mechanism for long-lasting memory storage. Long-lasting changes in synaptic connectivity ( Long-term Potentiation , or LTP), between two neurons can involve the making and breaking of synaptic contacts. A synapse's strength also depends on the number of ion channels it has (Debanne et al., 2003). Several facts suggest that neurons change the density of receptors on their Postsynaptic Membranes as a mechanism for changing their own excitability in response to stimuli. In a dynamic process that is maintained in equilibrium, NMDA and AMPA Receptor s are added to the membrane by Exocytosis and removed by Endocytosis (Shi et al., 1999; Song and Huganir, 2002; Pérez-Otaño and Ehlers, 2005). These processes, and by extension the number of receptors on the membrane, can be altered by synaptic activity (Shi et al., 1999; Pérez-Otaño and Ehlers, 2005). Experiments have shown that AMPA receptors are delivered to the membrane due to repetitive NMDAR activation (Shi et al., 1999; Song and Huganir, 2002). If the strength of a synapse is only reinforced by stimulation or weakened by its lack, a positive feedback loop will develop, leading some cells never to fire and some to fire too much. But two regulatory forms of plasticity, called scaling and metaplasticity, also exist to provide negative feedback (Pérez-Otaño and Ehlers, 2005). Synaptic scaling serves to maintain the strengths of synapses relative to each other, lowering amplitudes of small excitatory Postsynaptic Potential s in response to continual excitation and raising them after prolonged blockage or inhibition (Pérez-Otaño and Ehlers, 2005). This effect occurs gradually over hours or days, by changing the numbers of NMDA Receptor s at the synapse (Pérez-Otaño and Ehlers, 2005). Metaplasticity, another form of negative feedback, reduces the effects of plasticity over time (Pérez-Otaño and Ehlers, 2005). Thus, if a cell has been affected by a lot of plasticity in the past, metaplasticity makes future plasticity less effective. Since LTP and LTD rely on the influx of Ca2+ through NMDA channels, metaplasticity may be due to changes in NMDA receptors, for example changes in their subunits to allow the concentration of Ca2+ in the cell to be lowered more quickly (Pérez-Otaño and Ehlers, 2005). SEE ALSO REFERENCES
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