Toggling between gamma-frequency activity and suppression of cell assemblies

Abstract

Gamma (30–80 Hz) rhythms in hippocampus and neocortex resulting from the interaction of excitatory and inhibitory cells (E- and I-cells), called Pyramidal-Interneuronal Network Gamma (PING), require that the I-cells respond to the E-cells, but don't fire on their own. In idealized models, there is a sharp boundary between a parameter regime where the I-cells have weak-enough drive for PING, and one where they have so much drive that they fire without being prompted by the E-cells. In the latter regime, they often de-synchronize and suppress the E-cells; the boundary was therefore called the “suppression boundary” by Börgers and Kopell (2005). The model I-cells used in the earlier work by Börgers and Kopell have a “type 1” phase response, i.e., excitatory input always advances them. However, fast-spiking inhibitory basket cells often have a “type 2” phase response: Excitatory input arriving soon after they fire delays them. We study the effect of the phase response type on the suppression transition, under the additional assumption that the I-cells are kept synchronous by gap junctions. When many E-cells participate on a given cycle, the resulting excitation advances the I-cells on the next cycle if their phase response is of type 1, and this can result in suppression of more E-cells on the next cycle. Therefore, strong E-cell spike volleys tend to be followed by weaker ones, and vice versa. This often results in erratic fluctuations in the strengths of the E-cell spike volleys. When the phase response of the I-cells is of type 2, the opposite happens: strong E-cell spike volleys delay the inhibition on the next cycle, therefore tend to be followed by yet stronger ones. The strengths of the E-cell spike volleys don't oscillate, and there is a nearly abrupt transition from PING to ING (a rhythm involving I-cells only).

Input-dependent modulation of MEG gamma oscillations reflects gain control in the visual cortex

“…This, in turn, may be a crucial factor that mitigates excessive excitation while suppressing gamma oscillations 21,36,37 .…”

Neurosystems: brain rhythms and cognitive processing

“…Thus, gamma rhythms may be modulated by the addition of inhibition to the FS cells [e.g. by another class of interneurons, such as low‐threshold spiking (LTS) cells], which can increase the gamma power by preventing this ‘suppression transition’ (Börgers & Kopell, ; Börgers et al ., ; Börgers & Walker, ).…”

Effects of Neuromodulation on Excitatory–Inhibitory Neural Network Dynamics Depend on Network Connectivity Structure

“…Computational studies probing oscillatory synchronous activity in E-I networks, and in particular the intricacies of PING rhythms, are prevalent in the literature (Traub et al 1997;Kopell et al 2010;Whittington et al 2000;Ermentrout and Kopell 1998;Börgers and Kopell 2003;Börgers et al 2012;Börgers and Kopell 2005;Borgers and Walker 2013;Krupa et al 2014;Olufsen et al 2003). These studies pay less attention to the role of intrinsic cellular properties or the impact of more varied network structures, as the conceptual PING mechanism assumes strong E-I and I-E inter-connectivity as well as strong I-I intra-connectivity and burst frequencies are presumed to be dictated by properties of synaptic currents.…”