GHB drug question- for health project!?

how does the drug GHB enter the body?

its for a project for health..
thanks!

GHB: Gamma hydroxy butyrate or Gamma hydroxybutyric acid, Sodium Oxybate

Description: A clear liquid. Looks just like water. Can be mistaken for water because it is usually found in a small (30ml) clear plastic bottle, a water bottle, or even Gatorade bottles, which contains several doses. One quick taste, and you'll know it's not water. Not as common, but also found as a white powder. In fact powder use is on the rise!

Effects: Intoxication, increased energy, happiness, talking, desire to socialize, feeling affectionate and playful, mild dis inhibition, sensuality, enhanced sexual experience, muscle relaxation, loss of coordination due to loss of muscle tone, possible nausea, difficulty concentrating, loss of gag reflex.

Many people have bad reactions. These can include nausea, headaches, drowsiness, dizziness, amnesia, vomiting, loss of muscle control, respiratory problems, loss of consciousness, being conscious but unable to move, and death- Especially when combined with alcohol or other drugs.
GHB has at least two distinct binding sites in the central nervous system, the newly characterized GHB receptor which is excitatory and the GABAB receptor which is inhibitory. GHB exists endogenously at concentrations high enough to activate the GHB receptor but not at concentrations high enough to activate the GABAB receptor. This means that endogenous GHB has all the characteristics of an excitatory neurotransmitter.

However, at pharmacological doses, GHB reaches much higher concentrations in the brain and activates GABAB receptors, which is responsible for its sedative effects. GHB's sedative effects are blocked by GABAB antagonists.

The role of the GHB receptor in the behavioral effects induced by GHB is more complex. GHB receptors are densely expressed in many areas of the brain, including the cortex and hippo campus, and these are the receptors that GHB displays the highest affinity for. There has been somewhat limited research into the GHB receptor - however, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate - the principle excitatory neurotransmitter. Drugs which selectively activate the GHB receptor receptor cause absent seizures in high doses, as do GHB and GABA(B) agonists.

Activation of both the GHB receptor and GABA(B) is responsible for the addictive profile of GHB. GHB's effect on dopamine release is biphasic, low concentrations stimulate dopamine release via the GHB receptor. Higher concentrations inhibit dopamine release - via GABA(B) receptors (as to other GABA(B) agonists - Baclofen, Phenibut) - after the initial phase of inhibition, dopamine release is then increased via the GHB receptor. Both the inhibition and increase of dopamine release by GHB are inhibited by opioid antagonists (Naloxone, Naltrexone). Dynorphin may play a role in the inhibition of dopamine release via Kappa opioid receptor.