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Intracisternal Antisense Oligodeoxynucleotides to the Thyrotropin-Releasing Hormone Receptor Blocked Vagal-Dependent Stimulation of Gastric Emptying Induced by Acute Cold in Rats¹

CURE: Digestive Diseases Research Center, West Los Angeles Veterans Administration Medical Center, and the Department of Medicine, Digestive Disease Division, and Brain Research Institute, University of California School of Medicine, Los Angeles, California 90073

Address all correspondence and requests for reprints to: Y. Taché, Ph.D., CURE: Digestive Diseases Research Center, Veterans Administration Medical Center, Building 115, Room 203, 11301 Wilshire Boulevard, Los Angeles, California 90073. E-mail: ytache{at}ucla.edu

Cold exposure increases TRH gene expression in hypothalamic and raphe nuclei and results in a vagal activation of gastric function. We investigated the role of medullary TRH receptors in cold (4–6 C, 90 min)-induced stimulation of gastric motor function in fasted conscious rats using intracisternal injections of TRH receptor (TRHr) antisense oligodeoxynucleotides (100 µg twice, -48 and -24 h). The gastric emptying of a methyl-cellulose solution was assessed by the phenol red method. TRH (0.1 µg) or the somatostatin subtype 5-preferring analog, BIM-23052 (1 µg), injected intracisternally increased basal gastric emptying by 34% and 47%, respectively. TRHr antisense, which had no effect on basal emptying, blocked TRH action but did not influence that of BIM-23052. Cold exposure increased gastric emptying by 64%, and the response was inhibited by vagotomy, atropine (0.1 mg/kg, ip), and TRHr antisense (intracisternally). Saline or mismatched oligodeoxynucleotides, injected intracisternally under similar conditions, did not alter the enhanced gastric emptying induced by cold or intracisternal injection of TRH or BIM-23052. These results indicate that TRH receptor activation in the brain stem mediates acute cold-induced vagal cholinergic stimulation of gastric transit, and that medullary TRH may play a role in the autonomic visceral responses to acute cold.

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