γ‐aminobutyric acid‐mediated neurotransmission in cerebellar–hypothalamic circuit attenuates gastric mucosal injury induced by ischemia‐reperfusion

• DOI: 10.1111/nmo.12062
• Publication Date: 2012-12-24T03:24:52Z
• Authors: D. S. Du; T. Zhu; S. T. Ren; G. L. Xie; S. B. Li; D. C. Chu; X. T. Liu; M. Liu; X. B. Ma; M. H. Zhou; D. N. Zhu; Z. X. Deng; J. Wang
• Keywords: Fastigial nucleus

Abstract Background Excessive greater splanchnic nerve (GSN) activation contributes to the progression of gastric ischemia‐reperfusion (GI‐R) injury. This study was designed investigate protective mechanism cerebellar fastigial nucleus (FN) stimulation against GI‐R Methods The injury model induced in rats by clamping celiac artery for 30 min, and then reperfusion 1, 3, 6, or 24 h, respectively. Key Results Microinjection l ‐Glu (3, 12 μ g) into FN dose‐dependently attenuated GSN activity. In addition, there an enhancement mucosal blood flow rats. Pretreatment with glutamic acid decarboxylase antagonist FN, GABA A receptor lateral hypothalamic area lesion superior peduncle all reversed effects stimulation. Furthermore, reduced TUNEL‐positive cell Bax‐positive Conclusions & Inferences These results indicate that may be mediated attenuation excessive activation, apoptosis, Bax expression