Journal
BRAIN RESEARCH
Volume 1200, Issue -, Pages 116-131Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2008.01.017
Keywords
pilocarpine; epilepsy; presynaptic; granule cell; mossy fiber
Categories
Funding
- NIGMS NIH HHS [SC1 GM081109, SC1 GM081109-01, 1R25GM06592501A1, 1SC1GM081109-01] Funding Source: Medline
- NIMHD NIH HHS [P20MD001091] Funding Source: Medline
- NINDS NIH HHS [R21 NS056160, 1R21NS056160-01A2, R21 NS056160-01A2] Funding Source: Medline
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In the hippocampus, BK channels are preferentially localized in presynaptic glutamatergic terminals including mossy fibers where they are thought to play an important role regulating excessive glutamate release during hyperactive states. Large conductance calcium -activated potassium channels (BK, MaxiK, Slo) have recently been implicated in the pathogenesis of genetic epilepsy. However, the role of BK channels in acquired mesial temporal lobe epilepsy (MTLE) remains unknown. Here we used immunohistochemistry, laser scanning confocal microscopy (LSCM), Western immunoblotting and RT-PCR to investigate the expression pattern of the alpha-pore-forming subunit of BK channels in the hippocampus and cortex of chronically epileptic rats obtained by the pilocarpine model of MTLE. All epileptic rats experiencing recurrent spontaneous seizures exhibited a significant down-regulation of BK channel immunostaining in the mossy fibers at the hilus and stratum lucidum of the CA3 area. Quantitative analysis of immunofluorescence signals by LSCM revealed a significant 47% reduction in BK channel immunofluorescent signals in epileptic rats when compared to age-matched non-epileptic control rats. These data correlate with a similar reduction in BK channel protein levels and transcripts in the cortex and hippocampus. Our data indicate a seizure-related down-regulation of BK channels in chronically epileptic rats. Further functional assays are necessary to determine whether altered BK channel expression is an acquired channelopathy or
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