• M Miampamba and K A Sharkey.
• Neuroscience Research Group, Department of Physiology and Biophysics, University of Calgary, Alberta, Canada.
• J. Auton. Nerv. Syst. 1999 Sep 24; 77 (2-3): 140-51.

AbstractFos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat. The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression. Tissues were removed 2 h after the injection of saline or formalin. Saline injected in the colon induced Fos in enteric glia in the myenteric plexus. The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin. Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin. Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem. Simultaneous administration of xylazine (8 mg/kg) and the alpha 2 adrenoceptor antagonist yohimbine (1 mg/kg) reversed the effects of xylazine in the spinal cord and brainstem, but not in the myenteric plexus. These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem. This may be due to the direct chemical stimulation of the innervation of the colon and/or the subsequent acute colitis. The observed neuronal Fos expression can be modulated by an alpha 2 adrenoceptor agonist through noradrenergic pathways and/or reduction of the excitability of the enteric neural circuitry.

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