Anti-interleukin-1β antibody prevents the occurrence of repeated restraint stress-induced alterations in synaptic transmission and long-term potentiation in the rat frontal cortex

BackgroundThe mechanisms of the influence of prolonged stress on glutamatergic transmission and synaptic plasticity in the cerebral cortex remain poorly understood. The purpose of this study was to determine an involvement of interleukin-1β (IL-1β) in the effects of repeated restraint stress on excitatory synaptic transmission and long-term potentiation (LTP) in the rat frontal cortex.MethodsThe effects of restraint stress lasting for 10 min, repeated twice daily for 3 consecutive days were studied ex vivo in the rat frontal cortex slices prepared 24 h after the last stress session. Rats received intraperitoneal injections of interleukin-1β antibody. In a separate experimental group, rats received injections of IL-1β. Field potentials were recorded in the cortical layer II/III.ResultsIn slices originating from stressed animals, the amplitude of field potentials was increased. Consistent with the previous studies, restraint stress resulted in a reduced magnitude of LTP. Similar effects were evident after administration of IL-1β. Stress-induced modifications of the glutamatergic transmission and synaptic plasticity were prevented by interleukin-1β antibody, which was administered 15 min before each restraint session.ConclusionsThese data point to an involvement of peripherally produced IL-1β in mediating the influence of repeated restraint stress on the functions of the frontal cortex.