Lateral hypothalamic area mediated the aggravated effect of microinjection of Baclofen into cerebellar fastigial nucleus on stress gastric mucosal damage in rats.

Cerebellum, primarily believed as a subcortical somatic motor center, is increasingly considered to be implicated in visceral activities. However, little is known about its regulation on gastrointestinal organs. In this research, we investigated the aggravated effect of microinjection of gamma-aminobutyric acid receptor subtype B (GABA(B)R) agonist, Baclofen into cerebellar fastigial nucleus (FN) on stress gastric mucosal damage (SGMD) and its possible regulatory mechanism. The gastric mucosal damage index was chosen to indicate the severity of gastric mucosal injure. Immunohistochemistry and transferase-mediated dUTP-biotin nick-endlabeling (TUNEL) methods were used to detect the variations of lateral hypothalamic area (LHA) and gastric mucosa. It had been demonstrated that FN participates in regulation of SGMD via its GABA(B)R and GABA neural pathway, which passes through the decussation of superior cerebellar peduncle and projects to the GABA receptors in LHA. Meanwhile, celiac sympathetic nerve involves in this process via mediating neural discharge, which results in the decrease of gastric mucosal blood flow. Additionally, apoptosis, proliferation and oxidation in gastric mucosa, and gastric acid contribute in the mechanism. It could be expected that these results might suggest insights to the cerebellar and hypothalamic function, and the treatment of gastrointestinal diseases.