Subdiaphragmatic vagotomy prevents restraint stress-induced alternations in glutamatergic transmission and LTP in the rat frontal cortex

BACKGROUNDANDAIMS: Repeated exposure of experimental animalsto stressinduces a spectrumof depression-like symptomsincluding anorexia, weight loss, anhedonia, fatigue, impaired social interactions and memory dysfunctions. However, the mechanisms of the influence of stress on glutamatergic transmission and synaptic plasticity in the cerebral cortex remain poorly understood. The vagus nerve appears to be an important neural pathway for communicating immune signals originating in the periphery to the brain. Subdiaphragmatic vagotomy (SV) had earlier been shown to inhibit behavioral and neural effects of peripheral interleukin-1beta (IL-1β). We have previously demonstrated that peripherally produced IL-1β may mediate the influence of repeated restraintstress on the functions of the frontal cortex. The purpose of this study was to determine whether the vagus nerve mediates the effects of repeated restraint stress on excitatory synaptic transmission and longterm potentiation (LTP) in the rat frontal cortex. METHODS: Subdiaphragmatic vagotomy or sham surgery was performed 10 days before restraint stress and electrophysiological measurements. The effects of 10 min restraint stress, 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. RESULTS: In slices originating from stressed animals, the amplitude of field potentials was increased, compared to control preparations. Consistent with the previous studies, restraint stress resulted in a reduced magnitude of LTP. Stress-induced modifications of the glutamatergic transmission and synaptic plasticity were prevented by SV procedure. CONCLUSION: These data suggest that the vagus nerve may mediate the influence of repeated restraint stress on the rat frontal cortex.