The N-methyl-D-aspartate receptor's neglected subunit - GluN1 matters under normal and hyperbaric conditions

Alice Bliznyuk, Ben Aviner, Hava Golan, Michael Hollmann, Yoram Grossman

Research output: Contribution to journalArticlepeer-review


Professional deep-water divers exposed to hyperbaric pressure (HP) above 1.1 MPa develop high-pressure neurological syndrome, which is associated with central nervous system 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 the two-electrode voltage-clamp technique, of eight specific NMDAR subtypes generated by the co-expression of GluN1-1a or GluN1-1b 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 (5.1 MPa). 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 central nervous system, may offer a partial explanation for the mechanism governing the complex signs and symptoms of high-pressure neurological syndrome, and an explanation for the suspected long-term HP health decrement due to repetitive deep dives by professional divers.

Original languageAmerican English
Pages (from-to)2577-2584
Number of pages8
JournalEuropean Journal of Neuroscience
Issue number8
StatePublished - 1 Oct 2015


  • Central nervous system hyperexcitability
  • Diving physiology
  • High-pressure neurological syndrome
  • Oocyte
  • Pressure
  • Xenopus laevis

All Science Journal Classification (ASJC) codes

  • General Neuroscience


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