Cholinergic modulation of the picrotoxin-induced electrocorticographical events and behavioral “pain-like” symptoms at somatomotor cortical level in the rat

Abstract 

In this study, we examined the modulation by acetylcholine of electrocorticographical (ECoG) ictal events and spontaneous pain-like behaviors following cortical application of the GABA_A antagonist picrotoxin in the awake rat. Distilled water as vehicle, the cholinomimetic substance eserine, and the general muscarinic antagonist atropine were microinjected 10 min before the second microinjection of 2 μg picrotoxin into the hind paw region of the somatomotor cortex (SmI). Under these conditions, we observed that eserine (physostigmine, 1 μg, 10 μg, and 20 μg) did not consistently modify the number of the picrotoxin-induced ECoG spikes and bursts, but instead produced a massive enhancement of the number of hind paw licks compared with vehicle at 10 μg and, to a lesser extent, the number of the stereotyped “turn-in” and “neglected” paws following picrotoxin. In contrast, atropine (l μg, 10 μg, and 20 μg) increased the number of the picrotoxin-induced spikes and bursts at 10 μg and, at all doses, decreased the number of the picrotoxin-induced pain-like symptoms. Statistically significant changes for the number of paw lifts, licks, and “turn-in” paws were observed only with 10 μg. These results tend to show that epilepsy and pain are not strictly related to each other and also emphasize the cortex as a target for interactions between GABA and acetylcholine relative to “central” pain.