CHOLINERGIC MODULATION OF THE PICROTOXIN-INDUCED ELECTROCORTICOGRAPHICAL EVENTS AND BEHAVIORAL PAIN-LIKE SYMPTOMS AT SOMATOMOTOR CORTICAL LEVEL IN THE RAT

In this study, we examined the modulation by acetylcholine of electroc orticographical (ECoG) ictal events and spontaneous pain-like behavior s following cortical application of the GABA(A) antagonist picrotoxin in the awake rat. Distilled water as vehicle, the cholinomimetic subst ance eserine, and the general muscarinic antagonist atropine were micr oinjected 10 min before the second microinjection of 2 mu g picrotoxin into the hind paw region of the somatomotor cortex (SmI). Under these conditions, we observed that eserine (physostigmine, 1 mu g, 10 mu g, and 20 mu g) did not consistently modify the number of the picrotoxin -induced ECoG spikes and bursts, but instead produced a massive enhanc ement of the number of hind paw licks compared with vehicle at 10 mu g and, to a lesser extent, the number of the stereotyped ''turn-in'' an d ''neglected'' paws following picrotoxin. In contrast, atropine (1 mu g, 10 mu g, and 20 mu g) increased the number of the picrotoxin-induc ed spikes and bursts at 10 mu g and, at all doses, decreased the numbe r of the picrotoxin-induced pain-like symptoms. Statistically signific ant changes for the number of paw lifts, licks, and ''turn-in'' paws w ere observed only with 10 Gig. These results tend to show that epileps y and pain are not strictly related to each other and also emphasize t he cortex as a target for interactions between GABA and acetylcholine relative to ''central'' pain.