Effects of rosiglitazone and GW9662 on UCP2 expression in hippocampal CA3 neurons following experimental temporal lobe status epilepticus Our fourth series of experiments further explored a causal role for PPAR�� and UCP2 in Sorafenib Tosylate experimental temporal lobe status epilepticus. Bilateral microinjection of the PPAR�� agonist, rosiglitazone into the hippocampal CA3 region significantly increased the expression of UCP2 in the mitochondrial fraction from the CA3 sub field 24 h after the elicitation of sustained hippocampal seizure discharges. On the other hand, bilateral micro injection of the PPAR�� antagonist, GW9662 reduced the elicited UCP2 expression. Similar observations were obtained from double immunofluores cence staining coupled with laser scanning confocal mi croscopy.

Compared to sham Inhibitors,Modulators,Libraries control, there was an increase in UCP2 immunoreactivity in neurons from the hippocampal CA3 subfield on the right side 24 h after KA induced status epilepticus. Moreover, Inhibitors,Modulators,Libraries whereas Inhibitors,Modulators,Libraries pretreatment with rosiglitazone increased, GW9662 pre treatment decreased UCP2 immunoreactivity in the hippocampal CA3 neurons. We also verified Inhibitors,Modulators,Libraries the localization of UCP2 immunoreactiv ity in mitochondria by co immunofluorescence staining with the mitochondrial membrane protein, COX IV of hippocampal CA3 neurons on the right side, 24 h after KA induced status epilepticus compared with sham control. Additionally, pretreatment with rosiglitazone increased, and GW9662 pretreatment decreased UCP2 immunoreactivity in the mitochondria of hippocampal CA3 neurons.

However, the immunoreactivity for UCP2 was not significantly changed in hippocampal cells that were immunoreactive Inhibitors,Modulators,Libraries to the astrocyte marker GFAP 24 h following experimental status epilepticus. Effects of rosiglitazone and GW9662 on superoxide production and oxidized protein expression in the hippocampal CA3 subfield following experimental temporal lobe status epilepticus To strengthen a pivotal role of the PPAR�� UCP2 signal ing pathway in oxidative stress damage in the hippocam pus following experimental status epilepticus, we observed that bilateral microinjection of rosiglitazone into the hippocampal CA3 region, at a dose that enhanced UCP2 expression, also decreased the levels of O2 or oxidized protein in the CA3 subfield 24 h after KA induced experimental status epilepticus. On the other hand, pretreatment with GW9662 increased the levels of O2 or oxidized protein.

Effects of rosiglitazone and GW9662 on the activity of mitochondrial respiratory enzymes in the hippocampal CA3 subfield following experimental temporal lobe status epilepticus Our laboratory reported previously that depression of mitochondrial complex I and preservation of INCB-018424 complex IV enzyme activity in the hippocampus takes place in our experimental model of temporal lobe status epilepticus.