ABSTRACT
Excitatory amino acid antagonists have been shown to protect against the hyperexcitability associated with exposure to high pressure. This suggests that these excitatory neurotransmitter substances may play a role in the development of the symptoms of high pressure nervous syndrome (HPNS). Using a superfusion technique, we investigated the effect of exposure to 67.7 ATA of pressure on the release of aspartate and glutamic acid by isolated presynaptic nerve terminals from the guinea pig cerebral cortex. Pressure exposure was found to significantly increase the depolarization-induced release of aspartate by these synaptosomes. On the other hand, compression to 67.7 ATA had no effect on glutamic acid release. These findings suggest that increased aspartate release may be a contributing factor in the etiology of HPNS.
