Kaneko H, Taché Y
CURE:VA/UCLA Gastroenteric Biology Center, West Los Angeles Medical Center 90073, USA.
Brain Res. 1995 Nov 13;699(1):97-102. doi: 10.1016/0006-8993(95)00890-3.
The influence of excitation of the raphe pallidus neurons on gastric mucosal lesions was examined in urethane-anesthetized rats pretreated with indomethacin (5 mg/kg, i.p., -60 min). Kainic acid (12 ng/30 nl), delivered into the raphe pallidus, increased gastric acid secretion (94.8 +/- 15.9 mumol/60 min) and produced gastric lesions in 2.7 +/- 0.3% of the corpus mucosa. No gastric erosions were observed when kainic acid was injected nearby, but outside, of the raphe pallidus. The gastric lesions induced by microinjection of kainic acid into the raphe pallidus neurons were completely prevented by atropine (0.3 mg/kg, -30 min, s.c.) and bilateral microinjection of TRH antibody # 8964 (1.3 microgram/site) into the dorsal motor nucleus of the vagus (DMN). Microinjection of the TRH antibody into the hypoglossal nucleus or control antibody into the DMN did not modify the mucosal lesions induced by kainic acid into the raphe pallidus. These data suggest that activation of raphe pallidus induced vagal cholinergic mediated gastric erosion through TRH release in the DMN.