For instance HSA has been used as a model protein for numerous studies investigating protein/drug binding and protein/nano-particle interactions. Lot-to-lot variability may make any conclusions drawn from these or future studies using OsrHSA difficult to interpret. Furthermore, altered drug binding could be significant for the future consideration of heavily glycated OsrHSA with regards to individuals receiving large doses of recombinant albumin expressed in O. sativa. We also demonstrated that Sigma-Aldrich sourced OsrHSAs have dramatically improved thermal stability, due to the presence of FAs, when compared to other OsrHSAs, which could impact their function as biotherapeutics. However, the source and composition of these FAs or the potential for lot-to-lot variability in their composition have yet to be determined. These channels are composed by a multigene family of integral membrane proteins called connexins. So far, at least 20 Cx genes were identified in the mouse and human genome. Notably, communication through GJ channels has been recognized as an important mechanism for synchronizing neuronal networks in both physiological and pathological conditions. In fact, several evidences from animal models and human slices from epileptic patients indicate the participation of GJ channels in the generation and maintenance of epileptic seizures. Moreover, specific alterations of Cx expression have been described in tissue from epileptic patients and in experimental models. The aim of this study was to determine the involvement of GJ channels in the Talazoparib epileptiform activity induced by pilocarpine by examining the changes in electrophysiological patterns produced by uncoupling of these channels with carbenoxolone. After we established the participation of GJ in the ictal discharges, we thoroughly analyzed the regulation of gene expression, changes in protein levels, phosphorylation profile and distribution of the neuronal Cx36 and Cx45 and the glial Cx43, three of the most highly expressed Cxs in the rat hippocampus, during acute seizures and the epileptogenic process. We observed that pharmacological blockade of GJ channels decreases the epileptiform activity, which in turn regulates Cx gene expression, protein levels and phosphorylation. Thus, our results revealed a reciprocal, mutual regulation of Cx-mediated communication and the epileptiform phenomenon. The main purposes of this work were to demonstrate the involvement of GJ communication in the epileptiform activity and the possible alterations in Cx gene expression, protein levels, phosphorylation profile and distribution in the hippocampus triggered by pilocarpine. Indeed, our results showed that blockade of Cx channels produced antiepileptiform effects, indisputably correlating the GJ coupling with the epileptiform activity induced by pilocarpine. In spite of previous evidences in the literature regarding the anticonvulsant effects of GJ blockers, based on both in vitro and in vivo models, this is the first report addressing this issue in the pilocarpine model, which reproduces most of the characteristics of human temporal lobe epilepsy.