Intercellular coupling via gap junction channels is vital for astrocytic function.
The role of gap junctional communication under ischemic conditions is discussed controversely.
In our model of focal cerebral ischemia, we studied the expression of connexin 43,
one of the major gap junction proteins in astrocytes. Connexin 43 mRNA is elevated
in cells surrounding the lesion site which was shown by RNA/RNA in situ hybridization. The hybridization signal in pericarya around the lesion was much higher
than in the remaining brain areas. This upregultion was further investigated by semiquantitative
RT-PCR. Biopsies were taken from the lesion site as well as from the corresponding
area in the intact hemisphere and from sham-operated animals. In each analyzed animal
(n=6) with a focal cerebral ischemia the amount of specific PCR product was higher
in the sample from the operated site than in the intact. Sham-operated animals (n=5)
showed no variation between sides. Real-time RT-PCR analysis confirmed the results
obtained in semiquantitative RT-PCR studies. Our results affirm that gap junctions
composed of connexin 43 play a role after ischemia. Whether this upregulation of connexin
43 mRNA after an ischemic insult contributes to neuroprotection or propagation of
the cell needs to be determined.
