• Fariba Karimzadeh, Mansoureh Soleimani, Mehdi Mehdizadeh, Maryam Jafarian, Maliheh Mohamadpour, Hadi Kazemi, Mohammad-Taghi Joghataei, and Ali Gorji.
• Tehran University of Medical Sciences, Tehran, Iran; Shefa Neuroscience Research Centre, Tehran, Iran.
• Synapse. 2013 Dec 1;67(12):839-46.

AbstractModulation of glutamatergic NMDA receptors affects the synchronization of spike discharges in in WAG/Rij rats, a valid genetic animal model of absence epilepsy. In this study, we describe the alteration of NR2B subunit of NMDA receptors expression in WAG/Rij rats in different somatosensory cortical layers and in hippocampal CA1 area. Experimental groups were divided into four groups of six rats of both WAG/Rij and Wistar strains with 2 and 6 months of age. The distribution of NR2B receptors was assessed by immunohistochemical staining in WAG/Rij and compared with age-matched Wistar rats. The expression of NR2B subunit was significantly decreased in different somatosensory cortical layers in 2- and 6-month-old WAG/Rij rats. In addition, the distribution of NR2B in hippocampal CA1 area was lower in 6-month-old WAG/Rij compared with age-matched Wistar rats. The reduction of NR2B receptors in different brain areas points to disturbance of glutamate receptors expression in cortical and subcortical areas in WAG/Rij rats. An altered subunit assembly of NMDA receptors may underlie cortical hyperexcitability in absence epilepsy.Copyright © 2013 Wiley Periodicals, Inc.

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