Cortical gamma rhythms modulate NMDAR-mediated spike timing dependent plasticity in a biophysical model
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Citation (published version)Lee S, Sen K, Kopell N (2009) Cortical Gamma Rhythms Modulate NMDAR-Mediated Spike Timing Dependent Plasticity in a Biophysical Model. PLoS Comput Biol 5(12): e1000602. https://doi.org/10.1371/journal.pcbi.1000602
Spike timing dependent plasticity (STDP) has been observed experimentally in vitro and is a widely studied neural algorithm for synaptic modification. While the functional role of STDP has been investigated extensively, the effect of rhythms on the precise timing of STDP has not been characterized as well. We use a simplified biophysical model of a cortical network that generates pyramidal interneuronal gamma rhythms (PING). Plasticity via STDP is investigated at the excitatory pyramidal cell synapse from a gamma frequency (30–90 Hz) input independent of the network gamma rhythm. The input may represent a corticocortical or an information-specific thalamocortical connection. This synapse is mediated by N-methyl-D-aspartate receptor mediated (NMDAR) currents. For distinct network and input frequencies, the model shows robust frequency regimes of potentiation and depression, providing a mechanism by which responses to certain inputs can potentiate while responses to other inputs depress. For potentiating regimes, the model suggests an optimal amount and duration of plasticity that can occur, which depends on the time course for the decay of the postsynaptic NMDAR current. Prolonging the duration of the input beyond this optimal time results in depression. Inserting pauses in the input can increase the total potentiation. The optimal pause length corresponds to the decay time of the NMDAR current. Thus, STDP in this model provides a mechanism for potentiation and depression depending on input frequency and suggests that the slow NMDAR current decay helps to regulate the optimal amplitude and duration of the plasticity. The optimal pause length is comparable to the time scale of the negative phase of a modulatory theta rhythm, which may pause gamma rhythm spiking. Our pause results may suggest a novel role for this theta rhythm in plasticity. Finally, we discuss our results in the context of auditory thalamocortical plasticity.
RightsCopyright: © 2009 Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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