Sound Danger Signals Activate the Nitrergic System of the Medial Prefrontal Cortex

Abstract

Studies on Sprague–Dawley rats using in vivo intracerebral microdialysis showed that presentation of animals with a conditioned sound signal previously combined with pain stimulation (execution of a conditioned reflex fear response) was accompanied by an increase in the extracellular citrulline (a coproduct of NO synthesis) level in the medial prefrontal cortex. Presentation of a differential sound signal (not associated with electrocutaneous stimulation) to the same animals led to no more than a small increase in this measure. The increase in the citrulline level induced by the conditioned signal was prevented by administration of the neuronal NO synthase inhibitor Nω-propyl-L-arginine (1 mM) into the medial prefrontal cortex and was not seen in rats of the control group (same procedure but no pain stimulation). These data provide the first evidence that danger-associated sound signals but not safe differential signals activate the nitrergic system of the medial prefrontal cortex.