Often in parallel to the demonstration of its uncoupling properties. Indeed, the effects of CBX and its analogous on neuronal coupling and synchronization convincingly recapitulated Cx KO models. Taken together, these independent evidences from distinct groups allows for the use of CBX in GJ studies. In addition to the participation of GJ communication in the epileptiform activity, we also determined several changes in Cx expression during the acute and latent periods. Although there are studies pointing to the participation of Cx36 in epileptiform discharges, we were not able to detect changes in Cx36 mRNA and protein levels. Furthermore, the spatial pattern distribution of Cx36 throughout acute and latent periods remains constant, in conditions of epileptiform discharges and subsequent epileptogenesis. However, considering that pilocarpine model induces neuronal loss, Cx36 stability might reflect an important role of GJ communication in the networks of GABAergic interneurons and principal cells that express this protein. Moreover, it is possible that even small differences in Cx expression play a significant role in the network coupled by electrical synapses, which in turn could participate in the seizure activity and the following process of epileptogenesis. In agreement with previous studies, we detected the presence of Cx45 in hippocampal neurons. Moreover, we detected changes in Cx45 distribution in the SO in the latent phase, which is consistent with the enhanced Cx45 transcript levels. Indeed, electronic coupling via GJ was reported between SO interneurons presumably in dendrites. Additionally, the typical low pass filter feature imposed by GJ coupling over of the signal conductance could support synchronization of slow oscillations in the distal dendrites between SO interneurons. Also, it was reported the possible involvement of GABAergic interneurons presumably coupled by GJ in the slow oscillations recorded in hippocampal pyramidal cells. Thus, our data regarding increase of Cx45 in SO could Tofacitinib indicate the enhancement of coupling between the interneurons, which might intensify the occurrence of slow oscillations that, in turn, are noticed in a variety of epileptic activities. Furthermore, the expression of Cx45 in the SO hippocampal region, as pointed out in our work, could represent a substrate for the GJ coupling between axons of principle cells previously reported in the hippocampus. During the latent period, we observed an increased amount of Cx45 in this region. Interestingly, collateral connections from CA3 to CA1 are located within SO, and this is probably the site of occurrence of GJ connections. Taking together, if the axo-axonal coupling that possibly takes place at SO involves Cx45, the upregulation of this protein could account for the generation of high frequency oscillations and the increased excitability observed in epileptic conditions. Contrasting the increased levels in the SO, we noticed a decrease of Cx45 in the SLM during the latent period. It is well established that interneuron-mediated GABAergic synchronous potentials might play an important role in epilepsy, and that the mechanisms underlying these responses could be mediated by electrical coupling.