The gliotransmitter S100β regulates synaptic plasticity in the visual cortex

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 S100β, have remained relatively underexplored despite their potential importance in regulating synaptic plasticity. S100β is a calcium-binding protein, allowing it to influence extracellular Ca²⁺ concentration and potentially all Ca ²⁺ -dependent plasticity processes. Building on our previous research in the visual cortex, where we examined the regulation of neuronal excitability by S100β, we chose to further investigate the role of astrocytes and S100β in synaptic plasticity at layer 2/3-layer 5 synapses in the visual cortex. We demonstrated that S100β is an important gliotransmitter to consider, capable of regulating long-term potentiation.