RETRACTED ARTICLE: Comparing astrocytic gap junction of genetic absence epileptic rats with control rats: an experimental study

Abstract

The synchronization of astrocytes via gap junctions (GJ) is a crucial mechanism in epileptic conditions, contributing to the synchronization of the neuronal networks. Little is known about the endogenous response of GJ in genetic absence epileptic animal models. We evaluated and quanti ed astrocyte GJ protein connexin 30 (Cx30) and 43 (Cx43) in the somatosensory cortex (SSCx), ventrobasal (VB), centromedian (CM), lateral geniculate (LGN) and thalamic reticular (TRN) nuclei of thalamus of genetic absence epilepsy rats from Strasbourg (GAERS), Wistar albino glaxo rats from Rijswijk (WAG/Rij) and control Wistar animals using immunohistochemistry and Western Blot.The Cx30 and Cx43 immunopositive astrocytes in per unite area were quanti ed for each region of the three animal strains. Further, Cx30 and Cx43 Western Blot was applied to the tissue samples from the same regions of the three strain.The number of Cx30 immunopositive astrocytes showed signi cant increase in both GAERS and WAG/Rij compared to control Wistar in all brain regions studied except LGN of WAG/Rij animals. Furthermore, Cx43 in both GAERS and WAG/Rij showed signi cant increase in SSCx, VB and TRN. The percentage of dual expression of Cx30 and Cx43 in the same astrocyte ranged between 17-100% for the 5 brain regions of the 3 animal strains studied. The protein expression of both Cx30 and Cx43 in the two epileptic strain showed an increase compared to Wistar control animals.The signi cant increase in the astrocytic GJ proteins Cx30 and Cx43 and the differences in the dual expression of Cx30 and Cx43 in the genetically absence epileptic strains compared to control animals may suggest that astrocytic Cx's may be involved in the mechanism of absence epilepsy. Increased number of astrocytic Cx's in GAERS and WAG/Rij may represent a compensatory response of the thalamocortical circuitry to the absence seizures or may be related to the production of absence seizures.

Does astrocyte gap junction protein expression differ during development in absence epileptic rats?

“…Early studies reported that the expression of Cx43 starts around embryonic day 12, whereas Cx30 was detectable from postnatal day 16 (Kunzelmann et al, 1999). Our developmental immunohistochemical and western blot results showed the presence of Cx30 expression at P10 of both GAERS and evidence of nonspecific binding (Arun et al, 2016;Jothi et al, 2020;Çavdar et al, 2021).…”