Department of Operational Environment, ERRSO, Institut de Recherches Biomédicales des Armées, Antenne Toulon, BP 20548, 83041, Toulon Cedex 9, France.
Neurochem Res. 2010 May;35(5):718-26. doi: 10.1007/s11064-010-0125-3. Epub 2010 Jan 29.
Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by nitrogen narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised nitrogen alone (-23.8%). The rate of dopamine decreased, which also occurred under pressurised nitrogen (-36.9 and -31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by nitrogen under pressure. This suggests that the nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.
先前在大鼠中进行的微透析研究表明，氮麻醉会导致纹状体多巴胺和谷氨酸的减少。我们试图确定谷氨酰胺能性的皮质纹状体通路的假设作用，因为在这种高压综合征中，基底神经节会出现谷氨酸缺乏。在常压下，用 1 mM 的 Saclofen 和 100 mM 的 KCl 在前额皮质进行逆行透析，导致纹状体谷氨酸水平增加 95.2%，而多巴胺水平没有变化。在 3 MPa 的氮气和输注下，纹状体谷氨酸的速率下降了 51.3%，比单独加压氮气下降的幅度更大（-23.8%）。多巴胺的速率也下降了，这也发生在加压氮气中（分别为-36.9%和-31.4%）。总之，在压力下，氮会影响皮质纹状体通路的功能。这表明，氮引起的转折点似乎位于谷氨酸能的纹状体向心性神经元。
