%0 Journal Article
%T Neurochemical and Behavioral Features in Genetic Absence Epilepsy and in Acutely Induced Absence Seizures
%A A. S. Bazyan
%A G. van Luijtelaar
%J ISRN Neurology
%D 2013
%R 10.1155/2013/875834
%X The absence epilepsy typical electroencephalographic pattern of sharp spikes and slow waves (SWDs) is considered to be due to an interaction of an initiation site in the cortex and a resonant circuit in the thalamus. The hyperpolarization-activated cyclic nucleotide-gated cationic Ih pacemaker channels (HCN) play an important role in the enhanced cortical excitability. The role of thalamic HCN in SWD occurrence is less clear. Absence epilepsy in the WAG/Rij strain is accompanied by deficiency of the activity of dopaminergic system, which weakens the formation of an emotional positive state, causes depression-like symptoms, and counteracts learning and memory processes. It also enhances GABAA receptor activity in the striatum, globus pallidus, and reticular thalamic nucleus, causing a rise of SWD activity in the cortico-thalamo-cortical networks. One of the reasons for the occurrence of absences is that several genes coding of GABAA receptors are mutated. The question arises: what the role of DA receptors is. Two mechanisms that cause an infringement of the function of DA receptors in this genetic absence epilepsy model are proposed. 1. Introduction Absence seizures, typical for many different patients with absence epilepsy, principally differ from convulsive seizures. To illustrate, a number of widely used and efficient anticonvulsant drugs enhance absence seizures in patients and in the genetic absence models and ethosuximide is only effective in suppressing absence seizures and completely ineffective in other types of seizures [1¨C3]. Absence epilepsy is characterized by the occurrence of spontaneous occurring spike-wave discharges (SWDs) and periods of reduced alertness or responsiveness. The SWDs are induced by hyperpolarization and they appear on an otherwise normal EEG. The spike of the SWD represents an excitatory postsynaptic potential and bursts of action potentials (Figure 1(b)) of thalamocortical and corticothalamic cells, the wave a slow wave in the EEG, is the subsequent inhibitory phase [4, 5]. The generalized and widespread bilaterally synchronous SWDs are the result of highly synchronized oscillations in corticothalamocortical networks. SWDs, as can be found in WAG/Rij rats, have a local cortical origin in the perioral region of the somatosensory cortex [6¨C12], which is now confirmed in GAERS [13, 14], another well validated and often used strain of rats with absence epilepsy [15, 16]. Local injections in the perioral region of the somatosensory cortex of the T-type Ca2+ channel blocker ethosuximide was rather effective in suppressing
%U http://www.hindawi.com/journals/isrn.neurology/2013/875834/