| First Author | Zhang R | Year | 2008 |
| Journal | Biochem Biophys Res Commun | Volume | 372 |
| Issue | 4 | Pages | 816-20 |
| PubMed ID | 18519030 | Mgi Jnum | J:137765 |
| Mgi Id | MGI:3802859 | Doi | 10.1016/j.bbrc.2008.05.128 |
| Citation | Zhang R, et al. (2008) Inhibition of NMDA-induced outward currents by interleukin-1beta in hippocampal neurons. Biochem Biophys Res Commun 372(4):816-20 |
| abstractText | There is increasing evidence that a functional interaction exists between interleukin-1beta (IL-1beta) and N-methyl-D-aspartate (NMDA) receptors. The present study attempted to elucidate the effect of IL-1beta on the NMDA-induced outward currents in mechanically dissociated hippocampal neurons using a perforated patch recording technique. IL-1beta (30-100 ng/ml) inhibited the mean amplitude of the NMDA-induced outward currents that were mediated by charybdotoxin (ChTX)-sensitive Ca(2+)-activated K(+) (K(Ca)) channels. IL-1beta (100 ng/ml) also significantly increased the mean ratio of the NMDA-induced inward current amplitudes measured at the end to the beginning of a 20-s application of NMDA. In hippocampal neurons from acute slice preparations, IL-1beta significantly inhibited ChTX-sensitive K(Ca) currents induced by a depolarizing voltage-step. IL-1 receptor antagonist antagonized effects of IL-1beta. These results strongly suggest that IL-1beta increases the neuronal excitability by inhibition of ChTX-sensitive K(Ca) channels activated by Ca(2+) influx through both NMDA receptors and voltage-gated Ca(2+) channels. |
