Gap junction plasticity can lead to spindle oscillations

TL;DR

This paper presents a computational model demonstrating that activity-dependent plasticity of gap junctions in the thalamic reticular nucleus can generate and modulate sleep spindle oscillations, providing insights into their neural mechanisms.

Contribution

The study introduces a novel computational model showing how gap junction plasticity can produce and regulate sleep spindles in thalamocortical networks.

Findings

Gap junction plasticity influences TRN-TC network synchrony.

The model reproduces pharmacologically induced spindle activity.

Plasticity mechanisms can generate sleep spindles in simulations.

Abstract

Patterns of waxing and waning oscillations, called spindles, are observed in multiple brain regions during sleep. Spindle are thought to be involved in memory consolidation. The origin of spindle oscillations is ongoing work but experimental results point towards the thalamic reticular nucleus (TRN) as a likely candidate. The TRN is rich in electrical synapses, also called gap junctions, which promote synchrony in neural activity. Moreover, gap junctions undergo activity-dependent long-term plasticity. We hypothesized that gap junction plasticity can modulate spindle oscillations. We developed a computational model of gap junction plasticity in recurrent networks of TRN and thalamocortical neurons (TC). We showed that gap junction coupling can modulate the TRN-TC network synchrony and that gap junction plasticity is a plausible mechanism for the generation of sleep-spindles. Finally, our results are robust to the simulation of pharmacological manipulation of spindles, such as the administration of propofol, an anesthetics known to generate spindles in humans.