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Misuse, Recreational Use, and Addiction in Relation to Prescription Medicines
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Francesco S. Bersani, Claudio Imperatori
Gamma-hydroxybutyric acid (GHB) (and its prodrug gamma-butyrolactone), clinically used for a range of conditions including narcolepsy, alcohol withdrawal syndrome, and fibromyalgia (Busardo, Kyriakou, Napoletano, Marinelli, & Zaami, 2015), is also one of the most commonly misused GABAergic drugs (Davidson & Schifano, 2016). GHB is an agonist at the newly characterized GHB receptor and a weak agonist at the GABAB receptor (Brennan & Van Hout, 2014). As reviewed by Corkery et al. in 2015, at low to moderate doses, the most detected psychological effects of GHB include euphoria, calmness, disinhibition, and increased libido, while very high doses of 50–70 mg/kg lead to convulsions, amnesia, hypotonia, and coma (Corkery et al., 2015). GHB is highly addictive in both general and clinical populations, and it has been associated with many side effects and fatalities (Corkery et al., 2015). Of relevance, GHB is primarily known to the general public as a ‘rape drug’, as the drug has been used in 0.2–4.4% of reported sexual assaults to numb the other person and facilitate the rape (Nemeth, Kun, & Demetrovics, 2010).
Flumazenil partially reverses gamma-hydroxybutyrate (GHB)-induced coma: a case report
Published in The American Journal of Drug and Alcohol Abuse, 2022
Shiao-Yu Chen, Feng-Yuan Chu, Chih-Yu Yang, Der-Cherng Tarng
Although GHB primarily interacts with GABA-B receptors (1), GHB may also interact with GABA-A receptors (3). Although others have suggested that GHB also acts on several receptors other than GABA-A and GABA-B receptors (4), we suggest that the flumazenil responsiveness in the present case is through GABA-A receptor modulation since both GHB and flumazenil act on this receptor (5). This is consistent with previous work demonstrating flumazenil of antagonism of the GHB-anxiolytic effects via indirect interaction at GABA-A receptors, though the sedative and cataleptic effects of a high dose of GHB via GHB receptor were not affected in this rodent model (6).