Earlier studies from this laboratory have indicated that CNS exerts a modulatory influence over acute
inflammation in rats. The present study examines the existence of a similar modulatory effect of CNS on a subacute inflammatory paradigm, the
croton oil-induced
granuloma pouch in rats. The inflammatory exudate, collected on 6th day after
croton oil administration, was found to be substantially less in intracerebroventricular (icv) cannulated and artificial cerebrospinal fluid administered rats as compared to their uncannulated saline (ip) administered counterparts. This effect may be due to stress induced by cannulation. Centrally administered pharmacological agents which attenuate central monoaminergic,
cholinergic or
prostaglandin systems had insignificant effects on the inflammatory exudate. However, induced increase in central noradrenergic activity was found to attenuate the
inflammation when the treatment was done before, but not 48 hr after, the induction of the
inflammation. In contrast, induced increase in central serotonergic activity had no effect on the volume of the inflammatory exudate at either time period. Steady state levels of rat brain
noradrenaline and
serotonin, but not
dopamine, were enhanced by the inflammatory procedure. However, these effects may be attributed to the stress induced by
croton oil inflammation. The investigation indicates that the modulatory influence of CNS remains limited to the acute phase of
inflammation, being exerted mainly by the central noradrenergic system. Once the
inflammation has progressed, this modulatory influence of CNS is no longer apparent.