Nitrogen pressure exposure, in rats, resulted in a decreased
dopamine (DA) level by the striatal terminals of the substantia nigra pars compacta (SNc) dopaminergic neurons, due to the
narcotic potency of
nitrogen. In the SNc, the nigrostriatal pathway is under glutamatergic and GABAergic control mediated by
ion-channel NMDA and
GABA(A) receptors, main targets of volatile
anesthetics. The aim of this study was to investigate the role of these receptors in the regulation of striatal
dopamine level under
nitrogen narcosis. Under
general anesthesia, male Sprague-Dawley rats were bilaterally implanted in the striatum with
dopamine-sensitive
electrodes and, in the SNc, with guide
cannulae for
drug injections. After recovery from surgery, the striatal
dopamine level was quantified using differential pulse voltammetric measurements in freely moving rats. Focal
injections of agonists (
NMDA/
muscimol) and antagonists (AP7/
gabazine) of
NMDA/
GABA(A) receptors were made within SNc. Both normobaric condition and 3 MPa
nitrogen pressure were studied. Control experiments confirmed a direct glutamatergic control on the striatal DA level through
NMDA receptors. Both direct and indirect GABAergic control through two different types of
GABA(A) receptors located on GABAergic interneurons and on DA cells were indicated. Under
nitrogen pressure, the decrease in
dopamine level (20%) was suppressed by both
NMDA and
GABA(A) agonist infusion. There was an unexpected increasing DA level, induced by AP7 (about 10%) and
gabazine (about 30%). These results indicate that
NMDA receptors remain functional and suggest a decreased
glutamate release. The findings also describe an increase of
GABA(A) receptor-mediated inhibition on DA cells under
nitrogen pressure exposure.