NUCLEUS-RETICULARIS THALAMI AND NEOCORTICAL PAROXYSMS IN THE RAT

Citation
G. Marini et al., NUCLEUS-RETICULARIS THALAMI AND NEOCORTICAL PAROXYSMS IN THE RAT, European journal of neuroscience, 7(11), 1995, pp. 2301-2307
Citations number
32
Categorie Soggetti
Neurosciences
ISSN journal
0953816X
Volume
7
Issue
11
Year of publication
1995
Pages
2301 - 2307
Database
ISI
SICI code
0953-816X(1995)7:11<2301:NTANPI>2.0.ZU;2-X
Abstract
The role of the nucleus reticularis thalami in spike-wave discharges i n rats with genetic absence epilepsy has already been demonstrated. Th is study further investigated the role of the nucleus reticularis thal ami in paroxysmal synchronizations in Sprague-Dawley rats; this strain shows no propensity to epileptic activity. Electroencephalographic pa tterns were followed in chronically implanted, unrestrained rats. Afte r both electrolytic and chemical unilateral lesions, stereotaxically p laced in the anterolateral sectors of this nucleus (verified post mort em), abnormal electroencephalographic rhythms (high-voltage polyspikes and spike-wave complexes) were recorded from the frontoparietal corte x, primarily in the contralateral hemisphere. Stereotyped discharges a t 3 Hz developed progressively from multiple spikes within the alpha f requency range through the lengthening of the wave component. The exce ssive synchronized activity recorded from the intact hemisphere was of greater amplitude and occurred slightly earlier than from the lesione d hemisphere. These EEG patterns were associated with behavioural mani festations closely resembling those seen during absence seizures in hu mans. Bilateral lesions did not induce paroxysmal activity, both hemis pheres being characterized by dominant delta/theta activity without si gns of EEG-synchronized sleep. The seizures may thus have been due to disinhibition of the contralateral reticularis nucleus, recently shown to project to the reticularis nucleus of the other side in rats. This working hypothesis is supported by callosal cuts. The results indicat e that the reticular neurons exert a control over neocortical paroxysm al activity even in animals which do not present genetic absence epile psy.