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Effect of Pressure on the Release of Radioactive Glycine and γ‐Aminobutyric Acid from Spinal Cord Synaptosomes
Author(s) -
Gilman Sara C.,
Colton Joel S.,
Dutka Andrew J.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb01029.x
Subject(s) - aminobutyric acid , glycine , chemistry , spinal cord , biochemistry , neuroscience , biology , amino acid , receptor
Exposure to high hydrostatic pressure produces neurological changes referred to as the high‐pressure nervous syndrome (HPNS). Manifestations of HPNS include tremor, EEG changes, and convulsions. These symptoms suggest an alteration in synaptic transmission, particularly with inhibitory neural pathways. Because spinal cord transmission has been implicated in HPNS, this study investigated inhibitory neurotransmitter function in the cord at high pressure. Guinea pig spinal cord synaptosome preparations were used to study the effect of compression to 67.7 atmospheres absolute on [ 3 H]glycine and [ 3 H]γ‐aminobutyric acid ([ 3 H]GABA) release. Pressure was found to exert a significant suppressive effect on the depolarization‐induced calcium‐dependent release of glycine and GABA by these spinal cord presynaptic nerve terminals. This study suggests that decreased tonic inhibitory regulation at the level of the spinal cord contributes to the hyperexciltability observed in animals with compression to high pressure.

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