Although interleukin-1β (IL-1β) is well known to modulate synaptic transmission and plasticity of the hippocampus, no study has yet evaluated how this cytokine affects long-term depression (LTD), one of the major forms of hippocampal synaptic plasticity. Here we report that at Schaffer collateral-CA1 synapses, bath application of IL-1β induces a long-lasting decrease in synaptic strength in intact slices, but not in disinhibited slices in the presence of bicuculline, a γ-aminobutyric acid receptor antagonist. The IL-1β-induced synaptic depression efficiently foreclosed the subsequent induction of LTD in response to a 1-Hz tetanus and, conversely, it was also prevented by preexisting LTD. These results suggest that IL-1β-induced, persistent depression of synaptic efficacy is required for GABAergic activation and shares, at least in part, a common cellular mechanism for LTD.
- Hippocampus synaptic plasticity
- Knockout mouse
- Long-term potentiation