Benassi SK, Blanco MM, Mello LE (2004) Electrophysiological profile of IgG192saporin-lesioned rats in the pilocarpine model of epilepsy. Neuroscience 2004 Abstracts 452.14. Society for Neuroscience, San Diego, CA.
Summary: In order to investigate the importance of the basal forebrain cholinergic reorganization to the epileptogenesis process, adult male Wistar EPM-1 rats (180-220g) were subjected to status epilepticus (SE) induction by pilocarpine injection (320mg/kg, i.p.), after cholinergic lesion through IgG192-saporin (5μg/5μL, i.c.v.). Two months after SE induction animals were deeply anesthetized (choral hydrate 400 mg/kg, i.p.) and subjected to the electrical stimulation of the right CA3 and recorded (3M NaCl, 1MΩ) in the contralateral (left) CA1 region. Histological analysis included Nissl staining for the location of stimulating and recording electrodes and histochemistry for acetylcholinesterase (AChE) for the assessment of IgG192-induced lesions. The administration of the IgG192-saporin consistently and specifically diminished AChE staining in the hippocampus and neocortex while not affecting other brain areas (e.g., amygdala, striatum, etc). As compared to naive control animals, pilocarpine-treated animals generally showed loss of paired-pulse inhibition and the presence of multiple population spikes. Epileptic animals that were pre-treated with the cholinergic toxin did not differ from untreated epileptic animals in terms of paired-pulse inhibition or the presence of multiple population spikes. Large paired-pulse facilitation (P2>10 P1) for interstimulus intervals varying from 20 to 200 ms was encountered for both groups of epileptic animals with no distinction between each other. We suggest that the basal forebrain cholinergic system does not have a major role in defining the hyperexcitability of hippocampal circuits in the pilocarpine model of epilepsy.
Related Products: 192-IgG-SAP (Cat. #IT-01)