Objective: To study the expression of Cx32 and Cx43 in medically intractable temporal lobe epilepsy in human and investigate the pathogenic relationship between gap junctions and seizures.
Methods: The expression of Cx32 and Cx43 was detected by Western blot and immunohistochemistry in 14 consecutive samples of hippocampus from epileptic patients undergoing an amygdalohippocampectomy for the treatment of intractable seizures. During postmortem dissection, 8 samples of hippocampus in nonepileptic patients dying of other diseases were taken as control group.
Results: The expression of Cx32 and Cx43 was at a low level in the control group [Cx32: count of positive cell (9.4 +/- 1.1), ratios of gray scale (0.2 +/- 0.1); Cx43: count of positive cell (9.2 +/- 4.7), ratios of gray scale (0.5 +/- 0.2)], but Cx43 and Cx32 appeared to be expressed at a higher level in epileptic patients compared with that of the control group by immunohistochemistry [Cx32: count of positive cell (14.6 +/- 3.4), Cx43: count of positive cell (16.5 +/- 3.1)] (P < 0.01), and their expression significantly increased by Western blot [Cx32: ratios of gray scale (1.5 +/- 0.2), Cx43: ratios of gray scale (1.4 +/- 0.3)] (P < 0.01). Over-expression of Cx32 and Cx43 was found in 14 consecutive samples of hippocampus from epileptic patients.
Conclusion: Gap junctions play an important role in the occurrence and progression of intractable seizures.
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