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

Safiye Çavdar,Mazhar Özkan,İlknur Sur-Erdem,Büşra Köse

doi:10.1007/s00429-021-02310-y

Safiye Çavdar, Mazhar Özkan + Show 2 more

Open Access

https://doi.org/10.1007/s00429-021-02310-y

Copy DOI

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 quantified astrocyte GJ protein connexin (Cx) 30 and 43 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 per unit area were quantified for each region of the three animal strains. Furthermore, 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 significant 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 significant increase in SSCx, VB and TRN. The protein expression was increased in both Cx30 and Cx43 in the two epileptic strains compared to control Wistar animals. The significant increase in the astrocytic GJ proteins Cx30 and Cx43 and the differences in the co-expression of Cx30 and Cx43 in the genetically absence epileptic strains compared to control Wistar 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 and/or development of absence seizures.

Highlights

Astrocytes are not a simple supporting cell of the central nervous system; play a more active role in higher neural processing than previously recognized
The present study showed an increase in the number of connexin 30 (Cx30) immunopositive astrocytes in all regions studied in genetic absence epilepsy rats from Strasbourg (GAERS) and Wistar albino glaxo rats from Rijswijk (WAG/Rij) compared to control Wistar animals, except lateral geniculate (LGN) of WAG/Rij
The Western Blot results highly correlated with the immunohistochemistry results showing significant increase in Cx30 and Cx43 protein expression of GAERS and WAG/Rij compared to Wistar control animals in all brain regions studied

Summary

Introduction

Astrocytes are not a simple supporting cell of the central nervous system; play a more active role in higher neural processing than previously recognized. The knowledge related to the heterogeneity and complexity of astrocytes and its association with neurons has significantly increased in the last 20 years (Nedergaard et al 2003; Pannasch et al 2011; Dallérac and Rouach 2016). Astrocytes play a key role in large spectrum of complex and essential functions of the central nervous system (CNS). These include synaptic function, regulation of blood flow and fluid, ion, pH and transmitter homeostasis and development of the CNS (Barres 2008; Araque et al 2014; Dallérac and Rouach 2016). Astrocytes respond to all forms of CNS insults through a process referred to as reactive astrogliosis, which has become a pathological verification of CNS structural lesions (De Keyser et al 2008)

Methods

Results

Discussion

Conclusion