Abstract
Sympathetic hyperactivity is a hallmark of hypertension, yet the cellular and network mechanisms that drive increased neuronal output remain incompletely understood. Here, I analyzed a large database of patch-clamp recordings using custom MATLAB and Python pipelines to investigate whether glial interactions modulate the frequency–current (F–I) relationship in sympathetic neurons. In parallel, I used RT-qPCR to quantify TMEM16A expression, which encodes a calcium-activated chloride channel (CaCC), to assess potential strain-dependent differences in intrinsic ion channel mechanisms. Our results suggest that sympathetic neuron firing output is shaped by glial modulation of network activity, while CaCCs represent a potential intrinsic mechanism contributing to the observed F–I curve properties.