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γ‐aminobutyric acid‐mediated neurotransmission in cerebellar–hypothalamic circuit attenuates gastric mucosal injury induced by ischemia‐reperfusion
Author(s) -
Du D. S.,
Zhu T.,
Ren S. T.,
Xie G. L.,
Li S. B.,
Chu D. C.,
Liu X. T.,
Liu M.,
Ma X. B.,
Zhou M. H.,
Zhu D. N.,
Deng Z. X.,
Wang J.
Publication year - 2013
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12062
Subject(s) - medicine , stimulation , fastigial nucleus , reperfusion injury , anesthesia , pharmacology , endocrinology , lesion , ischemia , pathology
Background Excessive greater splanchnic nerve (GSN) activation contributes to the progression of gastric ischemia‐reperfusion (GI‐R) injury. This study was designed to investigate the protective mechanism of cerebellar fastigial nucleus (FN) stimulation against GI‐R injury. Methods The GI‐R injury model was induced in rats by clamping the celiac artery for 30 min, and then reperfusion for 30 min, 1, 3, 6, or 24 h, respectively. Key Results Microinjection of l ‐Glu (3, 6, 12 μ g) into the FN dose‐dependently attenuated GI‐R injury and GSN activity. In addition, there was an enhancement of gastric mucosal blood flow in GI‐R rats. Pretreatment with the glutamic acid decarboxylase antagonist into the FN, the GABA A receptor antagonist into the lateral hypothalamic area or lesion of superior cerebellar peduncle all reversed the protective effects of the FN stimulation. Furthermore, the FN stimulation reduced the TUNEL‐positive gastric mucosal cell and Bax‐positive gastric mucosal cell in GI‐R rats. Conclusions & Inferences These results indicate that the protective effects of the FN stimulation against GI‐R injury may be mediated by attenuation of the excessive GSN activation, gastric mucosal cell apoptosis, and Bax expression in GI‐R rats.