R. Schuligoi et al., DIFFERENTIAL EXPRESSION OF C-FOS MESSENGER-RNA IN THE RAT SPINAL-CORDAFTER MUCOSAL AND SEROSAL IRRITATION OF THE STOMACH, Neuroscience, 72(2), 1996, pp. 535-544
Expression of the immediate early gene c-fos is considered to be a mar
ker for neuronal activation in the spinal cord in response to afferent
input. Since the stomach is continually exposed to injurious chemical
s, the present study examined whether application of acid (0.15 M HCl)
and formalin (5%) to the gastric mucosa or serosal surface of the sto
mach stimulates c-fos transcription in the caudal thoracic spinal cord
of anaesthetized rats. The spinal cord was removed 15, 45 or 120 min
after exposure of the stomach to the noxious chemicals and processed f
or quantitative in situ hybridization autoradiography of c-fos messeng
er RNA. Exposure of the gastric mucosa to acid or formalin failed to i
ncrease the expression of c-fos messenger RNA in the thoracic spinal c
ord. Application of acid to the serosal surface of the stomach was als
o unable to stimulate c-fos transcription, whereas serosal application
of formalin led to substantial expression of c-fos messenger RNA in t
he superficial bur also deeper laminae of the spinal dorsal horn when
examined 45 min, but not 15 or 120 min, post-stimulation. The highest
expression of c-fos messenger RNA was seen when formalin was injected
subcutaneously into one hindpaw and c-fos transcription was examined i
n the lumbar spinal cord. These data indicate that acute exposure of t
he gastric mucosa to chemical injury does not provide the afferent inp
ut which is necessary to cause appreciable c-fos transcription in seco
nd order neurons within the spinal cord. Stimulation of the gastric mu
cosa by acid and formalin was followed, however, by gastric hyperaemia
in which spinal afferents releasing vasodilator peptides have been im
plicated. It is concluded, therefore, that acute stimulation of nocice
ptive afferents in the stomach causes local homoeostatic reactions but
does not necessarily provide afferent input sufficient to recruit spi
nal nociceptive circuits.