<unk>  has at least two distinct binding sites in the central nervous system.<unk>  acts as an agonist at the inhibitory<unk>  receptor and as a weak agonist at the inhibitory GABAB receptor.<unk>  is a naturally occurring substance that acts in a similar fashion to some neurotransmitters in the mammalian brain.<unk>  is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire.<unk>  has been found to activate oxytocinergic neurons in the supraoptic nucleus. If taken orally, GABA itself does not effectively cross the blood–brain barrier.<unk>  induces the accumulation of either a derivative of tryptophan or tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood–brain barrier. The blood content of certain neutral amino-acids, including tryptophan, is also increased by peripheral<unk>  administration.<unk> -induced stimulation of tissue serotonin turnover may be due to an increase in tryptophan transport to the brain and in its uptake by serotonergic cells. As the serotonergic system may be involved in the regulation of sleep, mood, and anxiety, the stimulation of this system by high doses of<unk>  may be involved in certain neuropharmacological events induced by<unk>  administration. However, at therapeutic doses,<unk>  reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects.<unk> 's sedative effects are blocked by GABAB antagonists. The role of the<unk>  receptor in the behavioural effects induced by<unk>  is more complex.<unk>  receptors are densely expressed in many areas of the brain, including the cortex and hippocampus, and these are the receptors that<unk>  displays the highest affinity for. There has been somewhat limited research into the<unk>  receptor; however, there is evidence that activation of the<unk>  receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter. Drugs that selectively activate the<unk>  receptor cause absence seizures in high doses, as do<unk>  and GABAB agonists. Activation of both the<unk>  receptor and GABAB is responsible for the addictive profile of<unk> .<unk> 's effect on dopamine release is biphasic. Low concentrations stimulate dopamine release via the<unk>  receptor. Higher concentrations inhibit dopamine release via GABAB receptors as do other GABAB agonists such as baclofen and phenibut. After an initial phase of inhibition, dopamine release is then increased via the<unk>  receptor. Both the inhibition and increase of dopamine release by<unk>  are inhibited by opioid antagonists such as naloxone and naltrexone. Dynorphin may play a role in the inhibition of dopamine release via kappa opioid receptors. This explains the paradoxical mix of sedative and stimulatory properties of<unk> , as well as the so-called "rebound" effect, experienced by individuals using<unk>  as a sleeping agent, wherein they awake suddenly after several hours of<unk> -induced deep sleep. That is to say that, over time, the concentration of<unk>  in the system decreases below the threshold for significant GABAB receptor activation and activates predominantly the<unk>  receptor, leading to wakefulness. Recently, analogs of<unk> , such as 4-hydroxy-4-methylpentanoic<unk>  (UMB68) have been synthesised and tested on animals, in order to gain a better understanding of<unk> 's mode of action. Analogues of<unk>  such as 3-methyl-GHB, 4-methyl-GHB, and 4-phenyl-GHB have been shown to produce similar effects to<unk>  in some animal studies, but these compounds are even less well researched than<unk>  itself. Of these analogues, only 4-methyl-GHB (γ-hydroxyvaleric<unk> , GHV) and a prodrug form γ-valerolactone (GVL) have been reported as drugs of abuse in humans, and on the available evidence seem to be less potent but more toxic than<unk> , with a particular tendency to cause nausea and vomiting. Other prodrug ester forms of<unk>  have also rarely been encountered by law enforcement, including 1,4-butanediol diacetate (BDDA/DABD), methyl-4-acetoxybutanoate (MAB), and ethyl-4-acetoxybutanoate (EAB), but these are, in general, covered by analogue laws in jurisdictions where<unk>  is illegal, and little is known about them beyond their delayed onset and longer duration of action. The intermediate compound γ-hydroxybutyraldehyde <unk> AL) is also a prodrug for<unk> ; however, as with all aliphatic aldehydes this compound is caustic and is strong-smelling and foul-tasting; actual use of this compound as an intoxicant is likely to be unpleasant and result in severe nausea and vomiting. Metabolic pathway of<unk>  Both of the metabolic breakdown pathways shown for<unk>  can run in either direction, depending on the concentrations of the substances involved, so the body can make its own<unk>  either from GABA or from succinic semialdehyde. Under normal physiological conditions, the concentration of<unk>  in the body is rather low, and the pathways would run in the reverse direction to what is shown here to produce endogenous<unk> . However, when<unk>  is consumed for recreational or health promotion purposes, its concentration in the body is much higher than normal, which changes the enzyme kinetics so that these pathways operate to metabolise<unk>  rather than producing it.
Gamma-Hydroxybutyric acid
Gamma-Amino-beta-hydroxybutyric acid
Choline
Beta-Hydroxy beta-methylbutyric acid
Phenylacetic acid
Butyric acid
Arachidonic acid
Glutamate 