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Updated: Jul 4, 2026
Horizontal Hippocampal Slices of the Mouse Brain
Published on: September 22, 2020
Inhibition of NMDA-induced outward currents by interleukin-1beta in hippocampal neurons
Ruoyu Zhang1, Jun Yamada, Yoshinori Hayashi
1Laboratory of Oral Aging Science, Faculty of Dental Sciences, Kyushu University, Maidashi 3-1-1, Fukuoka 812-8582, Japan.
Insights
Interleukin-1beta (IL-1beta) inhibits calcium-activated potassium channels (KCa) in hippocampal neurons. This action increases neuronal excitability by affecting N-methyl-D-aspartate (NMDA) receptor function.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- A functional interaction between interleukin-1beta (IL-1beta) and N-methyl-D-aspartate (NMDA) receptors is increasingly recognized.
- IL-1beta is a key inflammatory cytokine implicated in various neurological processes.
Purpose of the Study:
- To investigate the effect of IL-1beta on NMDA receptor-mediated currents in hippocampal neurons.
- To elucidate the specific ion channels involved in the IL-1beta and NMDA receptor interaction.
Main Methods:
- Perforated patch-clamp recording technique in mechanically dissociated hippocampal neurons and acute slice preparations.
- Application of IL-1beta and measurement of NMDA-induced outward and inward currents.
- Utilized charybdotoxin (ChTX) to identify specific potassium channels.
Main Results:
- IL-1beta (30-100 ng/ml) significantly inhibited NMDA-induced outward currents mediated by ChTX-sensitive Ca(2+)-activated K(+) (KCa) channels.
- IL-1beta increased the ratio of NMDA-induced inward current amplitudes, suggesting altered channel kinetics.
- IL-1beta also inhibited ChTX-sensitive KCa currents in acute hippocampal slices, an effect antagonized by IL-1 receptor antagonist.
Conclusions:
- IL-1beta enhances neuronal excitability in the hippocampus.
- This effect is mediated through the inhibition of ChTX-sensitive KCa channels.
- The inhibition affects Ca(2+) influx through both NMDA receptors and voltage-gated Ca(2+) channels.
Abstract:
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.
