Professional deep-water divers exposed to hyperbaric pressure (HP) above 1.1MPa develop High Pressure Neurological Syndrome (HPNS), which is associated with CNS hyperexcitability. It was previously reported that HP augments N-methyl-D-aspartate receptor (NMDAR) synaptic responses, increases neuronal excitability, and potentially causes irreversible neuronal damage. In addition, we have reported that HP (10.1 MPa) differentially affects ionic currents, measured by two-electrode voltage clamp technique, of eight specific NMDAR subtypes generated by co-expression of GluN1-1a or -1b with one of the four GluN2(A–D) subunits in Xenopus laevis oocytes. We now report that eight GluN1 splice variants, when co-expressed with GluN2A, mediate different ionic currents at normal and HP (5.1MPa). These data in conjunction with our previous results indicate that both GluN1 and GluN2 subunits play a critical role in determining NMDAR currents under normal and HP conditions. These data, given the differential spatial distribution of the different NMDAR subtypes in the CNS, may offer a partial explanation for the mechanism governing the complex HPNS signs and symptoms and an explanation for the suspected long-term HP health decrement due to repetitive deep dives by professional divers.
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