Anja R. Müller, Hiroshi Saito, Fatima El-Raziq
Synaptic plasticity, a fundamental mechanism underlying learning and memory, is modulated by a variety of cellular and molecular processes. Recent studies suggest that astrocytes, through calcium signaling, play a crucial role in regulating synaptic plasticity. This study aims to elucidate the role of astrocytic calcium signaling in modulating synaptic plasticity in cortical neurons. Using a combination of two-photon calcium imaging and electrophysiological recordings, we observed that astrocytic calcium transients precede and potentially modulate synaptic plasticity events. Inhibiting astrocytic calcium signaling with BAPTA disrupted long-term potentiation (LTP) with a significant decrease in amplitude (p < 0.01, n=10). In contrast, pharmacological elevation of astrocytic calcium levels resulted in enhanced synaptic efficacy, as indicated by a 25% increase in LTP magnitude (p < 0.05, n=10). These results underscore the importance of astrocytic activity in synaptic modulation and suggest a bidirectional communication between neurons and astrocytes. Our findings provide novel insights into the cellular mechanisms of synaptic plasticity and highlight potential therapeutic targets for cognitive dysfunctions. Future research should focus on the molecular pathways linking astrocytic calcium dynamics with synaptic changes.