Understanding how the brain adapts to changes in activity is crucial for insights into neural health and disease. Homeostatic synaptic plasticity, a process by which neurons adjust synaptic strength to maintain stability, plays a key role in this adaptation. However, identifying the specific molecular players involved in this process remains challenging. Our recent study provides new insights by examining the effects of tetrodotoxin (TTX), a sodium channel blocker, on synaptic plasticity in hippocampal cultures.
Abstract
In this study, we investigated the mechanisms underlying TTX-induced homeostatic synaptic plasticity in organotypic entorhino-hippocampal cultures. Through electrophysiology, transcriptomics, and proteomics, we demonstrated that TTX treatment significantly enhances excitatory synaptic strength in both dentate granule cells and CA1 pyramidal neurons. This effect is accompanied by transcriptomic and proteomic shifts, particularly involving metabolic pathways. Novel targets identified include cytoglobin, SLIT-ROBO Rho GTPase Activating Protein 3, transferrin receptor, and HMG-CoA synthase. These findings provide a valuable resource for understanding the regulatory networks in homeostatic plasticity and open new avenues for research into neural adaptation mechanisms.
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