The pivotal role played by
ion-channel dysregulations in the pathogenesis of
epilepsy has always garnered much attention. Since mutation of
ion-channel proteins CACNA1A and GABRD have been associated with
epilepsy, it is important to determine the
post-traumatic epilepsy-associated changes in expression levels of these
ion channel proteins. Additionally,
curcumin is already known for its
antiepileptic and neuroprotective potential in FeCl3-induced model of
post-traumatic epilepsy. Thus, we investigated FeCl3-induced
epilepsy mediated differential expression of CACNA1A and GABRD in the cortical region of the rat brain. Furthermore, we investigated the effect of
curcumin on the expression of both
proteins. For this,
epilepsy was induced by intracortical FeCl3 injection (5 μl of 100 mM). Additionally,
curcumin (conc. 1000 ppm; 75 mg/kg of b.wt.; for 14 and 28 days) was administered, mixed with normal food pellets. Results obtained from EEG-MUA and Morris water maze assay demonstrate the progression of
epilepsy after FeCl3 injection. Additionally, western blotting and histological studies show the downregulation of CACNA1A and GABRD during epileptogenesis. It was observed that
epilepsy-associated decline in learning and memory of animals might be linked with the dysregulation of both
proteins. Results also demonstrated that
curcumin administration ameliorated
epilepsy-associated change in expression of both CACNA1A and GABRD
proteins. In conclusion, the
neuroprotective effect of
curcumin against
iron-induced
epilepsy might be accompanied by the alleviated upregulation of these channel
proteins.