The gliotransmitter S100β regulates synaptic plasticity in the visual cortex

Abstract

Synaptic plasticity is a fundamental mechanism of memory storage in the brain. Among the various rules governing changes in synaptic strength, Spike Timing-Dependent Plasticity (STDP) stands out for its strong physiological relevance in vivo. Ubiquitous across brain regions and neuronal types, STDP is a complex and multifactorial process influenced by factors such as neuromodulation, extracellular calcium levels, and activity patterns. However, one relatively understudied factor is the role of astrocytes, despite their well-established involvement in regulating synaptic transmission and neuronal excitability through gliotransmitter release. While some factors have garnered significant attention, others, like S100{beta}, have remained relatively underexplored despite their potential importance in regulating synaptic plasticity. S100{beta} is a calcium-binding protein, allowing it to influence extracellular Ca{superscript 2} concentration and potentially all Ca2+-dependent plasticity processes. Building on our previous research in the visual cortex, where we examined the regulation of neuronal excitability by S100{beta}, we chose to further investigate the role of astrocytes and S100{beta} in synaptic plasticity at layer 2/3-layer 5 synapses in the visual cortex. We demonstrated that S100{beta} is an important gliotransmitter to consider, capable of regulating long-term potentiation.