TY - JOUR
T1 - Inhibition of NMDA-induced outward currents by interleukin-1β in hippocampal neurons
AU - Zhang, Ruoyu
AU - Yamada, Jun
AU - Hayashi, Yoshinori
AU - Wu, Zhou
AU - Koyama, Susumu
AU - Nakanishi, Hiroshi
N1 - Funding Information:
This study was supported by Grants-in-Aid for Scientific Research (No. 17390495 to H.N.; No. 18613010 to Z.W.) and a Grant-in-Aid for Scientific Research on Priority Area (No. 15082204 to H.N.) from the Ministry of Education, Science and Culture, Japan.
PY - 2008/8/8
Y1 - 2008/8/8
N2 - There is increasing evidence that a functional interaction exists between interleukin-1β (IL-1β) and N-methyl-d-aspartate (NMDA) receptors. The present study attempted to elucidate the effect of IL-1β on the NMDA-induced outward currents in mechanically dissociated hippocampal neurons using a perforated patch recording technique. IL-1β (30-100 ng/ml) inhibited the mean amplitude of the NMDA-induced outward currents that were mediated by charybdotoxin (ChTX)-sensitive Ca2+-activated K+ (KCa) channels. IL-1β (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-1β significantly inhibited ChTX-sensitive KCa currents induced by a depolarizing voltage-step. IL-1 receptor antagonist antagonized effects of IL-1β. These results strongly suggest that IL-1β increases the neuronal excitability by inhibition of ChTX-sensitive KCa channels activated by Ca2+ influx through both NMDA receptors and voltage-gated Ca2+ channels.
AB - There is increasing evidence that a functional interaction exists between interleukin-1β (IL-1β) and N-methyl-d-aspartate (NMDA) receptors. The present study attempted to elucidate the effect of IL-1β on the NMDA-induced outward currents in mechanically dissociated hippocampal neurons using a perforated patch recording technique. IL-1β (30-100 ng/ml) inhibited the mean amplitude of the NMDA-induced outward currents that were mediated by charybdotoxin (ChTX)-sensitive Ca2+-activated K+ (KCa) channels. IL-1β (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-1β significantly inhibited ChTX-sensitive KCa currents induced by a depolarizing voltage-step. IL-1 receptor antagonist antagonized effects of IL-1β. These results strongly suggest that IL-1β increases the neuronal excitability by inhibition of ChTX-sensitive KCa channels activated by Ca2+ influx through both NMDA receptors and voltage-gated Ca2+ channels.
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U2 - 10.1016/j.bbrc.2008.05.128
DO - 10.1016/j.bbrc.2008.05.128
M3 - Article
C2 - 18519030
AN - SCOPUS:45449113531
SN - 0006-291X
VL - 372
SP - 816
EP - 820
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -