someone misinformed you. lol. All of the GABA B agonists HAVE short half-lives, yes. But they take
forever to kick in. And the GABA B receptor, given it's very nature, can take up 260 to even elicit a response to GABA or an exogenous ligand.
GHB, phenibut, lyrica, neurontin, baclofen can all last around 24 hours, depending on dose, OP
^It may not be an enzyme deficiency kleinerkiffer.
I'm deffiecient in cyp3a4 and cyp2a6, yet I am hugely tolerant to everything, everything barely everything effects me, has any duration, etc.
And Burn Out, MDMA is supposed to make you sweat.
And GHB is supposed to feel like MDMA. Everybody says it does! It IS called LIQUID ECSTACY after all. I don't know who you have been talking to who has been comparing it to alcohol...
I have never compared it to alcohol.
It's pharmacology - GHB/GABA B agonism has nothing in common with alcohol...except the GIRK agonism...
And maybe you are doing to much GHB wich can precipitate sweating sometimes...
Alcohol is also an NMDA antagonist, like ketamine. So it should cause a mild dissociation, that, if anything, should be
slightly like
alcohol's
I think when the people you have talked to have compared the two, they were probably finding similarities in the activation between ethanol's effects on Ki channels and GHB's on GABA B GIRK channels.
GHB makes you sweat for the same reason that phenibut would or baclofen would - simlar drugs - both GABA B agonists, just not GHB agonists (also alpha 2 delta calcium channel negative allosteric modulators, and both drugs have been compared to MDMA, as well).
1. It presynaptically binds to what is known as the GABA B autoreceptor. Autorecptors are receptor proteins that exists on the presynaptic proteins that control outgoing neurotrnasmitter release.
If too much GABA is released from the neuron, it will be able to detect this via the autoreceptors, and shut off GABA release via activation of these receptors. If there is not enough releases, not enough of these autoreceptors will get activated, and GABA release will henceforth continue.
Now when GHB is artificially agonizing these presynaptic receptors, it artificially shuts off GABA release, regardless of synaptic level. Hence a reason for the sweating.
2. Second reason. When postsynaptic GABA B receptors are activated, they cause intense hyperpolaraziations (
a change in a cell's membrane potential that makes it more negative. It is the opposite of a depolarization. It inhibits action potentials by increasing the stimulus required to move the membrane potential to the action potential threshold.) which bring the subseqent presynaptic membrane potential just low enough to elict the burst and repetitive firing of what are known as low voltage gated t-type calcium channels
https://en.wikipedia.org/wiki/T-type_calcium_channel
Now this is going to increase depolarizations and NT, especially dopamine, norepinephrine, and glutamate.
Combined with the GABA inhibition
*along*
with the GHB agonism - which induces glutamate and dopamined release BTW (glutamate is the major excitotoxin in the brain that causes chemical damage and releases all other neurotransmitter and ions).
This is responsible for the sweating.
As for it feeling like MDMA. That's just been a consensus. Lyrica, Neurontin, baclofen, phenibut, GBL, GHB have been all combared to MDMA, benzos, etc.
