Neurophysiological interactions between the competitive
N-methyl-D-aspartate (
NMDA) preferring receptor antagonist,
CPP (3-((+-)-2-carboxypiperazine-4-yl)-propyl-1-
phosphonate) and the
high pressure neurological syndrome (
HPNS) have been investigated in the non-human primate Papio anubis. Eight animals were exposed on two occasions to environmental pressures of 81 atmospheres absolute (ATA) in a hyperbaric chamber, using
helium and
oxygen. One exposure followed pretreatment with
CPP (either 5 or 10 mg/kg i.v. plus 5 mg/kg/hr infusion), the other a saline control. Pretreatment with
CPP delayed moderate signs of face
tremor and
myoclonus and abolished severe signs of whole body
tremor and seizure activity. By 81 ATA, scores representing severity of
HPNS were significantly reduced by
CPP to a mean score, reflecting a level of just mild to moderate limb tremoring (P less than 0.001). Changes in the EEG were observed in channels associated with the frontal, parietal and occipital regions of the left cortex. Amplitude and frequency spectra were calculated and changes with pressure in the 4 conventional wavebands were analysed. The most striking change was the complete prevention by
CPP of the 100% increase in the amplitude of alpha waves at 81 ATA in the frontal region (P less than 0.001). It is concluded that
NMDA transmission has a major role in the expression of
HPNS.