T Kiba1, K Tanaka, O Endo, S Inoue. 1. Third Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Abstract
BACKGROUND: It was recently reported that ventromedial hypothalamic (VMH) lesions produced an increase in gastrointestinal DNA content in rats. In the present study, the mechanism of this alteration was examined. METHODS: The DNA content and synthesis after VMH lesioning in rat gastrointestinal tracts were determined. RESULTS: Total content of DNA in stomach and small intestine began to increase at 3 days and continued to increase for 7 days, whereas DNA content in the large intestine began to increase at 3 days and maintained the same level until 7 days after VMH lesioning. DNA synthesis of these organs increased and reached maximum at 3 days and then decreased to the initial level 7 days following the lesions. This increase in DNA content and synthesis in these organs was largely inhibited by bilateral subdiaphragmatic vagotomy or the administration of atropine, a cholinergic blocker, but not by the administration of anti-insulin antibody. CONCLUSIONS: VMH lesions induce cell proliferation in the rat gastrointestinal tract by the firing of vagus nerve activity mainly through the cholinergic receptor mechanism.
BACKGROUND: It was recently reported that ventromedial hypothalamic (VMH) lesions produced an increase in gastrointestinal DNA content in rats. In the present study, the mechanism of this alteration was examined. METHODS: The DNA content and synthesis after VMH lesioning in rat gastrointestinal tracts were determined. RESULTS: Total content of DNA in stomach and small intestine began to increase at 3 days and continued to increase for 7 days, whereas DNA content in the large intestine began to increase at 3 days and maintained the same level until 7 days after VMH lesioning. DNA synthesis of these organs increased and reached maximum at 3 days and then decreased to the initial level 7 days following the lesions. This increase in DNA content and synthesis in these organs was largely inhibited by bilateral subdiaphragmatic vagotomy or the administration of atropine, a cholinergic blocker, but not by the administration of anti-insulin antibody. CONCLUSIONS: VMH lesions induce cell proliferation in the rat gastrointestinal tract by the firing of vagus nerve activity mainly through the cholinergic receptor mechanism.
Authors: Ghazaul Dezfuli; Richard A Gillis; Jaclyn E Tatge; Kimbell R Duncan; Kenneth L Dretchen; Patrick G Jackson; Joseph G Verbalis; Niaz Sahibzada Journal: Front Neurosci Date: 2018-03-01 Impact factor: 4.677