TY - JOUR
T1 - Changes in mIPSCs and sIPSCs after kainate treatment
T2 - Evidence for loss of inhibitory input to dentate granule cells and possible compensatory responses
AU - Shao, Li Rong
AU - Dudek, F. Edward
PY - 2005/8
Y1 - 2005/8
N2 - 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 mo) 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 and DL-2-amino-5-phosphonopentanoic acid 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 ∼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.
AB - 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 mo) 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 and DL-2-amino-5-phosphonopentanoic acid 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 ∼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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U2 - 10.1152/jn.01342.2004
DO - 10.1152/jn.01342.2004
M3 - Article
C2 - 15772233
AN - SCOPUS:23044442127
SN - 0022-3077
VL - 94
SP - 952
EP - 960
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 2
ER -