M. Miampamba et Ka. Sharkey, c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall, J AUTON NER, 77(2-3), 1999, pp. 140-151
Fos expression induced by injection of dilute formalin (50 mu l, 5% in phys
iological saline) into the colonic wall was examined in the myenteric plexu
s, 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 resp
onse to the injection of formalin into the colon and (ii) to examine whethe
r administration of an alpha 2 adrenoceptor agonist modulates Fos expressio
n. Tissues were removed 2 h after the injection of saline or formalin. Sali
ne injected in the colon induced Fos in enteric glia in the myenteric plexu
s. The number of Fos immunoreactive nuclei significantly increased in both
myenteric neurons and enteric glia after the injection of formalin. Similar
ly, Fos immunoreactive neuronal nuclei were significantly increased in the
spinal cord, area postrema and nucleus of the solitary tract after the inje
ction of formalin. Pretreatment of rats with the alpha 2 adrenoceptor agoni
st xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dos
e-dependently reduced the number of Fos immunoreactive neuronal and glial n
uclei in the myenteric plexus, and neuronal nuclei in the spinal cord and b
rainstem. Simultaneous administration of xylazine (8 mg/kg) and the alpha 2
adrenoceptor antagonist yohimbine (1 mg/kg) reversed the effects of xylazi
ne 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 ex
pression in myenteric neurons and enteric glia, and neurons in the spinal c
ord and brainstem. This may be due to the direct chemical stimulation of th
e innervation of the colon and/or the subsequent acute colitis. The observe
d neuronal Fos expression can be modulated by an alpha 2 adrenoceptor agoni
st through noradrenergic pathways and/or reduction of the excitability of t
he enteric neural circuitry. (C) 1999 Elsevier Science B.V. All rights rese
rved.