Neurogastroenterology and motility · 2026
Possible Involvement of Descending Monoaminergic Pathways in Colorectal Dysmotility Using a Rat Model of Colitis.
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Yuki Natsufu, Hiroki Yuuno, Sawamura Tomoya, Mori Ayuna, Takashima Kazuya, Horii Yuuki, Shiina Takahiko, Shimizu Yasutake
Аннотация
BACKGROUND: Colonic inflammation is known to cause intestinal dysmotility. We examined the possible involvement of descending monoaminergic neurons projecting to the lumbosacral spinal cord in colorectal dysmotility using a rat model of colitis.
METHODS: Colitis was induced in rats by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid. Motility in inflamed and noninflamed colorectal regions was assessed in vivo under anesthesia.
KEY RESULTS: Colonic inflammation suppressed colorectal motility responses to noxious stimulus applied on inflamed colonic regions. The suppressed responses recovered as inflammation improved. In a subset of rats with colitis, basal motility in noninflamed regions was significantly enhanced, and this was abolished by intrathecal administration of serotonergic and dopaminergic receptor antagonists to the lumbosacral spinal cord. In some rats, enhanced basal motility spontaneously subsided then returned to a hyperactive state. The re-enhanced basal motility was also suppressed by monoaminergic receptor antagonists, suggesting intermittent activity of the descending monoaminergic neurons.
CONCLUSIONS AND INFERENCES: This study suggested that persistent noxious input from an inflamed colon activates descending monoaminergic neurons, leading to enhanced basal motility in noninflamed regions. Our findings provide important insights into the pathophysiology of inflammation-associated dysmotility.
METHODS: Colitis was induced in rats by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid. Motility in inflamed and noninflamed colorectal regions was assessed in vivo under anesthesia.
KEY RESULTS: Colonic inflammation suppressed colorectal motility responses to noxious stimulus applied on inflamed colonic regions. The suppressed responses recovered as inflammation improved. In a subset of rats with colitis, basal motility in noninflamed regions was significantly enhanced, and this was abolished by intrathecal administration of serotonergic and dopaminergic receptor antagonists to the lumbosacral spinal cord. In some rats, enhanced basal motility spontaneously subsided then returned to a hyperactive state. The re-enhanced basal motility was also suppressed by monoaminergic receptor antagonists, suggesting intermittent activity of the descending monoaminergic neurons.
CONCLUSIONS AND INFERENCES: This study suggested that persistent noxious input from an inflamed colon activates descending monoaminergic neurons, leading to enhanced basal motility in noninflamed regions. Our findings provide important insights into the pathophysiology of inflammation-associated dysmotility.