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 microg
picrotoxin into the hind paw region of the somatomotor cortex (SmI). Under these conditions, we observed that
eserine (
physostigmine, 1 microg, 10 microg, and 20 microg) 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 microg and, to a lesser extent, the number of the stereotyped "turn-in" and "neglected" paws following
picrotoxin. In contrast,
atropine (1 microg, 10 microg, and 20 microg) increased the number of the
picrotoxin-induced spikes and bursts
at 10 microg 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 microg. 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.