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Diminished M Currents Contribute to Hyperactivity of Corticotrophin‐Releasing Hormone Neurons in Acute Stress

Corticosterone‐releasing hormone (CRH) neuron in the paraventricular nucleus (PVN) of hypothalamus is the essential component of hypothalamic‐pituitary‐adrenal (HPA) axis in regulating endocrine responses to stress. M‐current, generated through KCNQ2/3 channel, plays a key role in controlling neuronal excitability. In this study, we test a hypothesis that acute stress diminishes M currents to stimulate CRH neurons. The adeno‐associated viral (AAV) vector was microinjected into the PVN prior to acute stress, which carries sequence of green fluorescent protein (GFP) driven by CRH promoter. GFP‐tagged CRH neurons displayed positive immunoreactivity with a specific antibody against CRH. Compared to unstressed rats, acute restraint stress significantly elevated serum corticosterone levels; and the basal firing rate of GFP‐tagged CRH neurons was significantly higher in acute restraint rats. Meanwhile blocking KCNQ2/3 with XE991 induced greater depolarization and firing frequency in GFP‐tagged CRH neurons of unstressed rats, but not stressed rats. Furthermore, M‐currents were markedly decreased in PVN‐CRH neurons in acute restraint rats. Acute restraint stress significantly decreased protein and mRNA expression of KCNQ3, but not KCN2 in PVN. Collectively, our data suggest that diminished M current results in hyperactivity of CRH neuron in acute stress.