Interneuron and Pyramidal Cell Interplay During In Vitro Seizure-like Events
Interneuron and Pyramidal Cell Interplay During In Vitro Seizure-like Events
Excitatory and inhibitory (EI) interactions shape network activity. However, little is known about the EI interactions in pathological conditions such as epilepsy. To investigate EI interactions during seizure-like events (SLEs), we performed simultaneous dual and triple whole cell and extracellular recordings in pyramidal cells and oriens interneurons in rat hippocampal CA1. We describe a novel pattern of interleaving EI activity during spontaneous in vitro SLEs generated by the potassium channel blocker 4-aminopyridine in the presence of decreased magnesium. Interneuron activity was increased during interictal periods. During ictal discharges, interneurons entered into long-lasting depolarization block (DB) with suppression of spike generation; simultaneously, pyramidal cells produced spike trains with increased frequency (6-14 Hz) and correlation. After this period of runaway excitation, interneuron postictal spiking resumed and pyramidal cells became progressively quiescent. We performed correlation measures of cell-pair interactions using either the spikes alone or the subthreshold postsynaptic interspike signals. EE spike correlation was notably increased during interneuron DB, whereas subthreshold EE correlation decreased. EI spike correlations increased at the end of SLEs, whereas II subthreshold correlations increased during DB. Our findings underscore the importance of complex cell-type-specific neuronal interactions in the formation of seizure patterns.
Control of Traveling Waves in Mammalian Cortex
Neural activity can propagate as waves in the brain. Such waves of activity may be important in processing of sensory information when awake, are present during deep sleep, and may be involved with spread of epileptic seizures. In this present paper, we predicted from a mathematical model of wave propagation, then confirmed experimentally, that externally applied electrical fields can slow such waves sufficiently to stop them. Specifically, we demonstrated that by using electric fields to modulate neuronal excitability, we can speed up, slow down and even halt propagation of seizure-like waves of activity in rat brain slices. An important application of such control over the propagation of waves of activity in human brain would allow for the development of implantable seizure control electrical devices that can be used to contain seizure activity within a small localized region and thereby prevent such seizures from spreading throughout the brain.
Abstract: We experimentally confirmed predictions that modulation of neuronal threshold with electrical fields can speed up, slow down, and even block traveling waves in neocortical slices. The predictions are based on a Wilson-Cowan type integrodifferential equation model of propagating neocortical activity. Wave propagation could be modified quickly and reversibly within targeted regions of the network. To the best of our knowledge, this is the first example of direct modulation of threshold to control wave propagation in a neural systems.
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