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-mu-1). 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.