Interleukin-1 beta depresses calcium currents in CA1 hippocampal neurons at pathophysiological concentrations.

Interleukin-1 is present in the central nervous system (CNS) during acute and chronic pathological processes. In the present study, we examined the interaction between recombinant human interleukin-1 beta (rhIL-1 beta) and the voltage-dependent calcium (Ca2+) current using the whole-cell patch clamp technique. RhIL-1 beta depressed the voltage-gated Ca2+ current in acutely dissociated guinea pig hippocampal CA1 neurons. This depression is rapid and is observed at pathophysiological concentrations (greater than or equal to 1.97 pg/10 microliters). Concomitant application of rhIL-1 beta and rhIL-1 receptor antagonist had no effect indicating neuroactive specificity of rhIL-1 beta. The depression of the inward Ca2+ current by IL-1 beta may play a role in: 1) the regulation of neuronal excitability; 2) the induction of neurological manifestations during disease; and 3) in the induction and/or progression of neurodegenerative processes.