Corticotripin releasing hormone neurons in paraventricular hypothalamic nucleus participated in the modulation of gastric motility by electro-acupuncture

Objectives Acute gastric distension (GD) impairs gastric motility and engages central stress circuits. We tested whether electroacupuncture (EA) at RN12/BL21 restores motility and probed mechanisms in the paraventricular nucleus (PVN), focusing on corticotropin-releasing hormone (CRH) neurons. Methods Rats underwent graded gastric balloon distension (20, 40, 60 mmHg). Gastric motility and electrogastrography determined the dysmotility threshold. Animals were randomized to EA at RN12, BL21, RN12+BL21, or sham. PVN single-unit and local field potential activity were recorded at baseline, during GD, and after EA. c-Fos/CRH double labeling quantified PVN activation. To test causality, the CRH receptor antagonist Astressin was bilaterally microinjected into the PVN, alone or combined with EA. Results GD at 40 mmHg markedly suppressed gastric motility amplitude without altering slow-wave frequency, establishing this pressure as a reliable acute GD model. EA at RN12 and BL21 significantly enhanced gastric motility, with combined stimulation producing synergistic effects. GD robustly increased c-Fos expression in the PVN, including within CRH neurons, and elevated PVN neuronal firing rates and power spectral density. EA attenuated GD-induced PVN hyperactivity, reducing neuronal firing rates, power spectral energy, and local field potential activity. Immunofluorescence confirmed that EA suppressed GD-induced activation of PVN CRH neurons, with combined stimulation at RN12 and BL21 producing greater inhibition than either acupoint alone. PVN microinjection of Astressin restored gastric motility and reduced CRH neuronal activation, whereas the combination of EA and Astressin produced an additive effect on gastric motor function. Conclusions EA at RN12 and BL21 reverses GD-induced gastric dysmotility by dampening PVN hyperexcitability, particularly within CRH-expressing neurons. Dual-acupoint stimulation confers superior efficacy, and CRH blockade augments EA. These findings identify PVN CRH neurons as key substrates mediating EA’s central control of visceral function under acute stress. Graphical Abstract: http://links.lww.com/AHM/A191.