Expression of connexin genes in hippocampus of kainate-treated and kindled rats under conditions of experimental epilepsy. Brain Res. Mol. Brain Res. 83:44-51

Abteilung für Molekulargenetik, Institut für Genetik, Universität Bonn, 53117 Bonn, Germany
Molecular Brain Research (Impact Factor: 2). 12/2000; 83(1-2):44-51. DOI: 10.1016/S0169-328X(00)00195-9
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We have analyzed whether the expression of connexin genes is altered in the hippocampus of kindled and kainate-treated rats, i.e., animal models of human temporal lobe epilepsy. We have tested this hypothesis by analyzing mRNA, protein abundance and cellular location of connexins (Cx) 43, 36, 32 and 30. The expression of glial fibrillary acid protein and mRNA was also monitored both in kainate-treated and kindled rats, in order to take into account reactive gliosis under these conditions. We found significantly increased expression of GFAP mRNA (100%) and protein (178%) in kainate-treated rats 4 weeks after kainate application, whereas in kindled rats only moderate increases of GFAP mRNA and protein were detected 2–3 weeks (group 2) or 4–6 weeks (group 1) after the last stage 5 induced seizure. Under gliotic conditions, connexins 43 and 30 mRNA or protein expression in astrocytes of kainate-treated rats were nearly unaffected. Cx36 mRNA expression (presumably in neurons) was significantly reduced (44%), whereas abundance of Cx36 protein was only slightly reduced. In both groups of kindled rats, Cx30 and Cx43 mRNA or protein expression were either slightly decreased or unchanged. Again, Cx36 mRNA and protein expression were reduced by about half in group 2. Immunofluorescence analysis of Cx43, Cx36 and Cx30 expression revealed that 4 weeks after the last kainate administration or kindling, cellular localization of these connexins was indistinguishable from control animals.

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    • "Cx36 Principal cells Condorelli et al. (1998, 2000, 2003), Belluardo et al. (2000), Zoidl et al. (2002), Weickert et al. (2005) and Nagy (2012) Interneurons Kosaka and Hama (1985), Freund and Buzsáki (1996), Condorelli et al. (2000) (2003) and Baude et al. (2007) Cx43 Astrocytes Söhl et al. (2000), Nagy et al. (2001), Ohsumi et al. (2010), Abbasian et al. (2012) and Sayyah et al. (2012) Cx45 Oligonendrocytes Kunzelmann et al. (1997) and Condorelli et al. (2003) Principal cells Maxeiner et al. (2003) and Weickert et al. (2005) Cx47 Oligonendrocytes Weickert et al. (2005) Principal cells Teubner et al. (2001) Panexins 1 Principal cells Bruzzone et al. (2003), Ray et al. (2005), Vogt et al. (2005), Weickert et al. (2005), Zappala et al. (2006) and Zoidl et al. (2007) Panexins 2 Principal cells Bruzzone et al. (2003) and Vogt et al. (2005) The relevance of GJs to brain functions is evident in early brain development. It was earlier shown that there are numerous GJs in immature brain tissue, which decline rapidly as maturation progresses (Peinado et al., 1993; Perez-Velazquez and Carlen, 2000; Yuste et al., 1995). "
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    • "In contrast to Cx43, Cx30 levels were extremely low in the cortical hemispheres of wild-type mice. This is consistent with the previous demonstration of high levels of Cx43 and much lower levels of Cx30 within hippocampal and neocortical tissue by other groups [3] [13] [21]. As expected, Cx30 expression was virtually absent in Cx30−/− mice (Fig. 1). "
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    • ", reported no change in Cx43 mRNA expression in amygdala of the rats during development of amygdala kindling. Moreover, it has been found that hippocampal Cx43 expression at both mRNA and protein level is unchanged or slightly decreased in fully kindled rats 2–6 weeks after the last kindled seizures occurrence (Sohl et al., 2000 "
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