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J Neurophysiol (March 16, 2005). doi:10.1152/jn.01342.2004
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Submitted on December 30, 2004
Accepted on March 8, 2005

Changes in mIPSCs and sIPSCs after Kainate Treatment: Evidence for Loss of Inhibitory Input to Dentate Granule Cells and Possible Compensatory Responses

Li-Rong Shao1 and F. Edward Dudek1*

1 Department of Biomedical Sciences, Anatomy and Neurobiology Section, Colorado State University, Fort Collins, CO, USA

* To whom correspondence should be addressed. E-mail: ed.dudek{at}colostate.edu.

How inhibition is altered after status epilepticus and the role of inhibition during epileptogenesis remain unsettled issues. The present study examined acute (4-7 days) and chronic (>3 months) changes of GABAA-receptor-mediated inhibitory synaptic input to dentate granule cells after kainate-induced status epilepticus. Whole-cell patch-clamp techniques were used to record spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) in the presence of 6,7-dinitroquinoxaline-2,3-dione (DNQX) and DL-2-amino-5-phosphonopentanoic acid (AP-5) to block glutamatergic excitatory synaptic transmission. In both groups, mean sIPSC frequency of dentate granule cells from the saline- and kainate-treated rats was not significantly different. However, mIPSC frequency from the kainate-treated rats of both groups was about 30% lower than that of the respective saline controls. The mean amplitude of sIPSCs and mIPSCs from kainate-treated rats was not reduced in either the acute or chronic groups. The mean 10-90% rise time of IPSCs was not altered in kainate-treated rats, but the decay time constant was slightly longer than in controls, and the charge transfer 4-7 days after kainate treatment was significantly larger. The similar reduction of mIPSC frequency (i.e., ~30%) in the two groups of kainate-treated rats suggests a decreased inhibitory input to dentate granule cells (presumably due to a partial loss of inhibitory interneurons that innervate them), without recovery during epileptogenesis. The lack of effect on sIPSC frequency and the decreased mIPSC frequency in both groups suggests a possible compensatory increase in firing rate of interneurons, which may involve a hypothetical reduction of inhibitory input to the remaining interneurons.




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