State of peripheral catecholaminergic systems during pharmacologic correction of immobilization stress by sodium hydroxybutyrate

Effect of sodium hydroxybutyrate in pain syndromes

“…Presynaptic, reciprocal, and descending inhibition of the segmental apparatus in the spinal cord is boosted by GHBA [1], bringing about a decrease of GPEE activity. In the first hours of development of the pathological process GHBA prevents increased release of norepinephrine and conserves a large depot of this transmitter [5]; it also boosts the synthesis and release of norepinephrine and serotonin, thereby enhancing descending monoaminergic inhibition [4,8,12 ]. During the development of a pain syndrome, after an initial compensatory elevation of opioids disadaptive processes evolve in the spinal cord, causing a drop of the level of opioid peptides in it [7]; GHBA increases the level of dinorphin and [3-endorphin in various brain regions, and boosts the synthesis and hastens the release of opioids [10].…”