Plastic rearrangement of basal forebrain parvalbumin-immunoreactive neurons in the kainite model of epilepsy

• Published in: AIMS neuroscience Vol. 10; no. 4; pp. 300 - 314
• Main Authors: Carvalho, Ruben, Lukoyanova, Alisa N, Casalta-Lopes, João, Lukoyanov, Nikolay V, Soares, Joana Isabel
• Format: Journal Article
• Language: English
• Published: United States AIMS Press 01.01.2023
• Subjects: kainic-acid model; magnocellular preoptic nucleus; medial septum; neurophysiology; parvalbumin; temporal lobe epilepsy; magnocellular preoptic nucleus; temporal lobe epilepsy; medial septum; neurophysiology; kainic-acid model; parvalbumin
• ISSN: 2373-7972; 2373-7972
• DOI: 10.3934/NEUROSCIENCE.2023023

Temporal lobe epilepsy (TLE) is the most prevalent form of epilepsy, through the neuronal mechanisms of this syndrome remain elusive. In addition to the temporal lobe structures, it was found that the basal forebrain cholinergic cells are also involved in epileptogenesis. However, little is known about the involvement of the basal forebrain GABAergic neurons in epilepsy; despite this, they largely project to the temporal lobe and are crucial for the regulation of the hippocampal circuitry. In this study, we assessed epilepsy-induced changes in parvalbumin (PARV) immunoreactive neurons of the medial septum (MS) and of the magnocellular preoptic nucleus (MCPO) using the kainic acid (KA) model in rats. In addition, we estimated the respective changes in the cholinergic varicosities in the MS, where we observed a significant reduction in the PARV cell number (12849 ± 2715 vs. 9372 ± 1336, = .029) and density (16.2 ± 2.62 vs. 10.5 ± 1.00 per .001 mm , =.001), and an increase in the density of cholinergic varicosities (47.9 ± 11.1 vs. 69.4 ± 17.8 per 30,000 µm , =.036) in KA-treated animals. In the MCPO, these animals showed a significant increase in somatic volume (827.9 ± 235.2 µm vs. 469.9 ± 79.6 µm , = .012) and total cell number (2268.6 ± 707.1 vs. 1362.4 ± 262.0, =.028). These results show that the basal forebrain GABAergic cell populations undergo numerical and morphological changes in epileptic animals, which may contribute to an increased vulnerability of brain circuits to epilepsy and epilepsy-related functional impairments.