The whole concept of "dopamine rebound" is not exactly true. GHB has (relevant) affinities for two receptor classes: the GABA(B) receptor (inhibitory) and the GHB receptor (excitatory). GHBs affinity for the GABA(B) receptor is substantially lower than than that of the GHB receptor. Hence, at the lower end of the dosage spectrum you primarily see activation of the excitatory GHB receptor, while at higher doses the GABA(B) receptor is activated, resulting in the compounds obvious sedative/hypnotic effects.
When plasma concentrations of GHB decrease, allosteric modulation/activation of the inhibitory GABA(B) receptor are minimal compared to the excitatory stimulation of the GHB receptor. So, as the drug wears off, the GABA(B)-mediated sedation is effectively lost and the excitatory GHB-receptor activation becomes the predominant effect. This is the mechanism behind the so-called "dopamine rebound."
I do not believe it is possible to circumvent this excitatory phase w/out further pharmacologic intervention. As others have stated, using GHB/GBL to sleep can quickly turn into 24/7 dosing and dependence. From what I have read/seen, GHB withdrawal is HELL and to complicate matters the vast majority of MDs do NOT know how to effectively treat acute GHB withdrawals as it is not a very common drug of abuse. The GABA(B) agonist baclofen is supposedly the most effective means of managing GHB abstinence syndrome, as even heroic doses of benzos (GABA(A) agonists) are marginally effective.
When plasma concentrations of GHB decrease, allosteric modulation/activation of the inhibitory GABA(B) receptor are minimal compared to the excitatory stimulation of the GHB receptor. So, as the drug wears off, the GABA(B)-mediated sedation is effectively lost and the excitatory GHB-receptor activation becomes the predominant effect. This is the mechanism behind the so-called "dopamine rebound."
I do not believe it is possible to circumvent this excitatory phase w/out further pharmacologic intervention. As others have stated, using GHB/GBL to sleep can quickly turn into 24/7 dosing and dependence. From what I have read/seen, GHB withdrawal is HELL and to complicate matters the vast majority of MDs do NOT know how to effectively treat acute GHB withdrawals as it is not a very common drug of abuse. The GABA(B) agonist baclofen is supposedly the most effective means of managing GHB abstinence syndrome, as even heroic doses of benzos (GABA(A) agonists) are marginally effective.
Last edited:
