Table of Contents
ISRN Neurology
Volume 2013, Article ID 875834, 48 pages
http://dx.doi.org/10.1155/2013/875834
Review Article

Neurochemical and Behavioral Features in Genetic Absence Epilepsy and in Acutely Induced Absence Seizures

1Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Science, Russian Federation, 5A Butlerov Street, Moscow 117485, Russia
2Biological Psychology, Donders Centre for Cognition, Donders Institute for Brain, Cognition and Behavior, Radboud University Nijmegen, P.O. Box 9104, 6500 HE Nijmegen, The Netherlands

Received 21 January 2013; Accepted 6 February 2013

Academic Editors: R. L. Macdonald, Y. Wang, and E. M. Wassermann

Copyright © 2013 A. S. Bazyan and G. van Luijtelaar. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.