| First Author | Wang J | Year | 2019 |
| Journal | J Integr Neurosci | Volume | 18 |
| Issue | 2 | Pages | 173-179 |
| PubMed ID | 31321958 | Mgi Jnum | J:294380 |
| Mgi Id | MGI:6456240 | Doi | 10.31083/j.jin.2019.02.145 |
| Citation | Wang J, et al. (2019) Protein kinase C-epsilon contributes to a chronic inhibitory effect of IL-1beta on voltage-gated sodium channels in mice with febrile seizure. J Integr Neurosci 18(2):173-179 |
| abstractText | This study aimed to understand the role of Interleukin-1beta in mouse febrile seizures. To investigate the chronic effects of raised Interleukin-1beta on seizures, the sodium currents of hippocampal neurons were recorded by whole-cell voltage clamp. Interleukin-1beta inhibited sodium currents in mouse hippocampal neurons and verified that protein kinase C epsilon contributed to the effect of Interleukin-1beta exposure. The inhibitory effect was also identified in neurons from a protein kinase C epsilon null mutant mouse. Action potentials were recorded using a ramp depolarizing current. Peak spike depolarization was significantly reduced by Interleukin-1beta treatment, and was abolished following the administration of a protein kinase C epsilon inhibitor, epsilonV1-2. However, neither Interleukin-1beta nor epsilonV1-2 had any significant effect on spike threshold. Interleukin-1beta reduced the amplitude of action potentials due to its inhibitory effect on sodium channels. This is hypothesised to decrease the release of presynaptic transmitters of neuroexcitability, thus exerting a neuroprotective role in excitotoxicity. To ascertain the role of protein kinase C epsilon on febrile seizures in vivo, a heated water-bath model was used to identify susceptible mice. It was found that protein kinase C epsilon reduced susceptibility to, and frequency of, febrile seizure onset. This may be related to the neuroprotective effect of Interleukin-1beta on hippocampal neurons. |
