Endogenous Production
Cells produce GHB by reduction of succinic semialdehyde via the enzyme succinic semialdehyde dehydrogenase. This enzyme appears to be induced by cAMP levels, meaning substances that elevate cAMP, such as forskolin and vinpocetine, may increase GHB synthesis and release. People with the disorder known as succinic semialdehyde dehydrogenase deficiency, also known as gamma-hydroxybutyric aciduria, have elevated levels of GHB in their urine, blood plasma and cerebrospinal fluid.
The precise function of GHB in the body is not clear. It is known, however, that the brain expresses a large amount of receptors that are activated by GHB. These receptors are excitatory and not responsible for the sedative effects of GHB – they have been shown to elevate the principle excitatory neurotransmitter—glutamate. The benzamide antipsychotics—amisulpride, sulpiride—have been shown to bind to this receptor in vivo. Other antipsychotics were tested and were not found to have an affinity for this receptor.
It is a precursor to GABA, glutamate, and glycine in certain brain areas.
GHB has neuroprotective properties and has been found to protect cells from hypoxia.
Read more about this topic: gamma-Hydroxybutyric Acid
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