Molecular mechanism of emotional fever--the role of nitric oxide.

The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N(5) - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 microg and 10 microg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in T(b) and it was accompanied with an increase of motor activity. Both inhibitors significantly suppressed the stress fever. vL-NIO did not influence stress-induced rise in locomotor activity as well as did not change T(b) in unstressed rats. Since aminoguanidine caused a transient fall in T(b) below the baseline in rats exposed or not to open field and because this inhibitor suppressed stress-induced rise in locomotor activity, we concluded that nNOS expression inside the brain is critically involved in the rise in T(b) due to exposure to psychological stress.