Previous studies performed in the laboratory have shown that
nitrogen narcosis induces a decrease in striatal
glutamate and
dopamine levels. Although we stimulated the
N-methyl-D-aspartate (
NMDA) receptor, an important
glutamate receptor required for motor and locomotor activity managed by the striatum, and demonstrated that the receptor was effective when exposed to
nitrogen at 3MPa, it was not possible to return the striatal
glutamate level to its base values. We conclude that it was the striatopetal neurons of the glutamatergic pathways that were mainly affected in this hyperbaric syndrome, without understanding the principal reasons. Hence we sought to establish what happens in the vicinity of the plasma membrane, downstream the
NMDA-Receptor, and we used the hypothesis that there could be
neuronal nitric oxide synthase (nNOS) disturbances. A microdialysis study was performed in rat striatum in order to analyse levels of
citrulline, the NO co-product, and
arginine, the NO precursor. Those both NO metabolites were detectable with an HPLC coupled to a fluorimetric detector. Exposure to pressurized
nitrogen induced a reduction in
citrulline (-18.9%) and
arginine (-10.4%) levels. Under the control normobaric conditions, the striatal
NMDA infusion enhanced the
citrulline level (+85.6%), whereas under 3 MPa of
nitrogen, the same
NMDA infusion did not change the
citrulline level which remains equivalent to that of the baseline. The level of
arginine increased (+45.7%) under normobaric conditions but a decrease occurred in pressurized
nitrogen (-51.6%). Retrodialysis with
Saclofen and KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of
citrulline (+30.5%) and a decrease in
arginine levels (-67.4%). There was no significant difference when
nitrogen at 3MPa was added. To conclude, the synthesis of
citrulline/NO is reduced in
nitrogen narcosis while it seems possible to activate it artificially by infusion. We have suggested that the low
glutamate levels recorded in
nitrogen narcosis induced these
dopamine and NO reductions in the striatum.