Previous neurochemical studies performed in rats have revealed a decrease of striatal
dopamine and
glutamate induced by
inert gas narcosis. We sought to establish the hypothetical role of
glutamate and its main receptor, the
N-methyl-d-aspartate (
NMDA) receptor, in this syndrome. We aimed to counteract the
nitrogen narcosis-induced
glutamate and
dopamine decreases by stimulating the
NMDA receptor in the striatum. We used bilateral retrodialysis on awake rats, submitted to
nitrogen under pressure (3 MPa). Continuous infusion of 2 mM of
NMDA under normobaric conditions (0.01 MPa) (n = 8) significantly increased extracellular average levels of
glutamate,
aspartate,
glutamine, and
asparagine by 241.8%, 292.5%, 108.3%, and 195.3%, respectively. The same infusion conducted under
nitrogen at 3 MPa (n = 6) revealed significant lower levels of these
amino acids (n = 8/6, P > 0.001). In opposition, the
NMDA-induced effects on
dopamine, dihydrophenylacetic
acid (
DOPAC), and
homovanillic acid (HVA) levels were statistically not affected by the
nitrogen at 3 MPa exposure (n = 8/6, P > 0.05).
Dopamine was increased by >240% on average. HVA was decreased (down to 40%), and there was no change in
DOPAC levels, in both conditions. Results highlight that the
NMDA receptor is not directly affected by
nitrogen under pressure as indicated by the elevation in
NMDA-induced
dopamine release under hyperbaric
nitrogen. On the other hand, the
NMDA-evoked
glutamate increase is counteracted by
nitrogen narcosis. No improvement in motor and locomotor disturbances was observed with high striatal concentration in
dopamine. Further experiments have to be done to specify why the striatal
glutamate pathways, in association with the inhibition of its metabolism, only are affected by
nitrogen narcosis in this study.