Abstract

Vital intracerebral microdialysis studies in Sprague–Dawley rats showed that placing the animal in a conditioned reflex chamber in which a conditioned reflex fear response to a sound signal (combination of a tone and an unavoidable electric shock) had previously been acquired led to an increase in the extracellular citrulline (a coproduct of NO synthesis) level in the medial prefrontal cortex and induced freezing of the animal (an expression of fear). This increase was not seen in animals of the control group (same procedure, but without pain stimulation) and it was prevented by administration of the neuronal NO synthase inhibitor Nω-propyl-L-arginine (1 mM) into the medial prefrontal cortex. Administration of this substance decreased freezing induced by being placed in the conditioned reflex chamber without any effect on the rats’ mobility. These data provide evidence of the involvement of the nitrergic system of the medial prefrontal cortex in regulating the expression of fear induced by contextual danger signals.

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