Abstract
Stress responses are highly plastic and vary across physiological states. The female estrous cycle is associated with a number of physiological changes including changes in stress responses, however, the mechanisms driving these changes are poorly understood. Corticotropin-releasing hormone (CRH) neurons are the primary neural population controlling the hypothalamic–pituitary–adrenal (HPA) axis and stress-evoked corticosterone secretion. Here we show that CRH neuron intrinsic excitability is regulated over the estrous cycle with a peak in proestrus and a nadir in estrus. Fast inactivating voltage-gated potassium channel (IA) currents showed the opposite relationship, with current density being lowest in proestrus compared to other cycle stages. Blocking IA currents equalized excitability across cycle stages revealing a role for IA in mediating plasticity in stress circuit function over the female estrous cycle.
Highlights
Stress responses are highly plastic and vary across physiological states
To assay Corticotropin-releasing hormone (CRH) neuron intrinsic excitability, neurons were held around − 60 mV in current clamp before injecting a family of current steps from 0 Peak amplitude (pA) to + 50 pA in 5 pA increments (Fig. 1C)
The total number of action potentials (APs) fired over all current steps was significantly different (one-way ANOVA, F(2,83 ) = 5.35, P = 0.006; Table 1) with post hoc tests showing higher numbers of spikes in proestrus compared to the estrus
Summary
The female estrous cycle is associated with a number of physiological changes including changes in stress responses, the mechanisms driving these changes are poorly understood. Corticotropin-releasing hormone (CRH) neurons are the primary neural population controlling the hypothalamic–pituitary–adrenal (HPA) axis and stress-evoked corticosterone secretion. Hypothalamic corticotropin-releasing hormone (CRH) neurons control both the HPA axis and behavioral responses to stress[11,12,13,14,15,16,17]. Plasticity of intrinsic excitability is mediated by changing levels of expression or function of ion channels in the cell m embrane[22,23,24]. In CRH neurons, plasticity of intrinsic excitability can be mediated via voltage-gated potassium channels[21]. We speculated that changes to potassium channels influences intrinsic excitability of CRH neurons over the estrous cycle
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
