On day 43, the threshold intensity for a visually identifiable contraction of the abdominal wall and body arching were recorded during rectal distention. 5 mL at different times between postnatal days 8 and 21 to establish an animal model of visceral hypersensitivity. Neonatal male Sprague-Dawley rats received intracolonic injections of 0. The present study was designed to evaluate the expression of the 5- HT 4 receptor and the serotonin transporter (SERT as well as their roles in chronic visceral hypersensitivity using a rat model. These results indicate that both the 5- HT 4 receptor and SERT play a role in the pathogenesis of visceral hypersensitivity, and its mechanism may be involved in the local 5- HT levelĭirectory of Open Access Journals (Sweden)įull Text Available Visceral hypersensitivity plays an important role in motor and sensory abnormalities associated with irritable bowel syndrome, but the underlying mechanisms are not fully understood. day −1, day 43), or the combination of both, reduced visceral hypersensitivity and plasma 5- HT levels.As expected, transient colonic irritation at the neonatal stage led to visceral hypersensitivity, but no mucosal inflammation was later detected during adulthood. The 5- HT 4 receptor and SERT expression of the ascending colon were monitored using immunohistochemistry and Western blot analyses the plasma 5- HT levels were measured using an ELISA method. Histological evaluation and the myeloperoxidase activity assay were performed to determine the severity of inflammation.
5 mL at different times) between postnatal days 8 and 21 to establish an animal model of visceral hypersensitivity. The present study was designed to evaluate the expression of the 5- HT 4 receptor and the serotonin transporter (SERT) as well as their roles in chronic visceral hypersensitivity using a rat model. Visceral hypersensitivity plays an important role in motor and sensory abnormalities associated with irritable bowel syndrome, but the underlying mechanisms are not fully understood. International Nuclear Information System (INIS)Ĭhi, Yan Liu, Xin-Guang Wang, Hua-Hong Li, Jun-Xia Li, Yi-Xuan In contrast, several non-cholinergic cell populations within the basal forebrain and its target hippocampal and cortical areas express these receptors and are thus likely to mediate the enhancement of acetylcholine release elicited by 5- HT 4 agonists.Įffect of the 5- HT 4 receptor and serotonin transporter on visceral hypersensitivity in rats These results indicate that 5- HT 4 receptors are not synthesized by cholinergic cells, and thus would be absent from cholinergic terminals. Hippocampal and cortical glutamatergic neurons also express this receptor. In contrast, basal forebrain GABAergic, parvalbumin synthesizing, and glutamatergic cells contained 5- HT 4 receptor mRNA. 5- HT 4 receptor mRNA was not detected in the basal forebrain cholinergic cell population. 5- HT 4 receptor mRNA was visualized with isotopically labeled oligonucleotide probes, whereas cholinergic, glutamatergic, GABAergic and parvalbumin-synthesizing neurons were identified with digoxigenin-labeled oligonucleotide probes.
We have analyzed, using dual label in situ hybridization, the cellular localization of 5- HT 4 receptor mRNA in identified neuronal populations of the rat basal forebrain, which is the source of the cholinergic innervation to cortex and hippocampus. Although 5- HT 4 receptors are present in brain areas related to cognition, e.g., hippocampus and cortex, the cellular localization of the receptors that might modulate acetylcholine release is unknown at present. The proposed underlying neurochemical mechanism is the enhancement of acetylcholine release in frontal cortex and hippocampus elicited by 5- HT 4 agonists. Serotonin 5- HT 4 receptors and forebrain cholinergic system: receptor expression in identified cell populations.Īctivation of serotonin 5- HT 4 receptors has pro-cognitive effects on memory performance.
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