Journal of Applied Physiology, Vol 61, Issue 6 2067-2073, Copyright © 1986 by American Physiological Society
Effect of pressure on [3H]GABA release by synaptosomes isolated from cerebral cortex
S. C. Gilman, J. S. Colton and J. M. Hallenbeck
High hydrostatic pressure has been shown to produce neurological changes in
humans which manifest, in part, as tremor, myoclonic jerks,
electroencephalographic changes, and convulsions. This clinical pattern has
been termed high-pressure nervous syndrome (HPNS). These symptoms may
represent an alteration in synaptic transmission in the central nervous
system with the inhibitory neural pathways being affected in particular.
Since gamma-aminobutyric acid (GABA) transmission has been implicated in
other seizure disorders, it was of interest to study GABAergic function at
high pressure. Isolated synaptosomes were used to follow GABA release at
67.7 ATA of pressure. The major observation was a 33% depression in total
[3H]GABA efflux from depolarized cerebrocortical synaptosomes at 67.7 ATA.
The Ca2+-dependent component of release was found to be completely blocked
during the 1st min of [3H]GABA efflux with a slow rise over the subsequent
3 min. These findings lead us to conclude that high pressure interferes
with the intraterminal cascade for Ca2+-dependent release of GABA.
