ESI TALKS: Carmen Canavier

At this bi-weekly event, we invite speakers from Neuroscience and related fields to share their current research in an informal and casual environment. The ESITALKS last around 45 minutes, followed by discussions.

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Using the phase response curves to understand synchronization of theta nested gamma oscillations in the MEC

Theta-nested gamma in the medial entorhinal cortex (MEC) is thought to encode episodic information and to convey that information to hippocampal area CA1. Optogenetically-Driven Theta-nested Gamma in the MEC in vitro is a putative analogue for theta-nested gamma in vivo. Parvalbumin positive (PV+) inhibitory interneurons are thought to contribute to gamma synchrony via their synapses with each other (interneuronal network gamma ING) and/or via their reciprocal connectivity with excitatory neurons (pyramidal interneutonal gamma PING). Optogenetic stimulation of the PV cells alone produces nested oscillations that are faster and weaker than those observed when both cell populations are stimulated. A model of a network of PV+ neurons was calibrated to closely match biophysical data from the MEC. At biophysical levels of heterogeneity and at the measured values of synaptic delays, gap junctions of physiological strength were required for synchrony. We found that simply changing the bias current of neurons with identical f/I curves does not fully capture the effects of intrinsic heterogeneity. Simulated optogenetic stimulation of the calibrated ING network evoked high frequency nested gamma ~150 Hz in agreement with data. Synaptic depression causes nested gamma in strongly driven networks with hyperpolarizing synapses to favor early theta phases. PRC analysis suggests that at physiological delays, inhibition with Erev =-75 mV synchronizes and -55 desynchronizes. Uniformly distributing the synaptic reversal largely preserved the synchrony observed with Erev=-75 mV. New results are presented for synchronization of one and two clusters of neurons using the phase resetting curve under the pulsatile couple assumption. Adding excitation to the network can slow the frequency by recruiting inhibition, but only for hyperpolarizing inhibition. Adding reciprocal excitation to an ING network can synchronize interneurons that cannot synchronize on their own if the PRCs have the correct slope at the locking point.

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