Psychedelia.dk

Abstract

Gammahydroxybutyric acid (GHB) is an endogenous constituent of the central nervous system that has acquired great social relevance for its use as a recreational ‘club drug’. GHB, popularly known as ‘liquid ecstasy’, is addictive when used continuously. Although the symptoms associated with acute intoxication are well known, the effects of prolonged use remain uncertain. We examined in male rats the effect of repeated administration of GHB (10 and 100 mg/kg) on various parameters: neurological damage, working memory and spatial memory, using neurological tests, the Morris water maze and the hole-board test. The results showed that repeated administration of GHB, especially at doses of 10 mg/kg, causes neurological damage, affecting the ‘grasping’ reflex, as well as alteration in spatial and working memories. Stereological quantification showed that this drug produces a drastic neuronal loss in the CA1 hippocampal region and in the prefrontal cortex, two areas clearly involved in cognitive and neurological functions. No effects were noted after quantification in the periaqueductal grey matter (PAG), a region lacking GHB receptors. Moreover, NCS-382, a putative antagonist of GHB receptor, prevented both neurological damage and working- memory impairment induced by GHB. This suggests that the effects of administration of this compound may be mediated, at least partly, by specific receptors in the nervous system. The results show for the first time that the repeated administration of GHB, especially at very low doses, produces neurotoxic effects. This is very relevant because its abuse, especially by young persons, could produce considerable neurological alterations after prolonged abuse.

Neurotoxicity

In multiple studies, GHB has been found to impair spatial and working learning and memory in rats with chronic administration.[57][58][59][60] These effects are associated with decreased NMDA receptor expression in the cerebral cortex and possibly other areas as well.[57]

Pedraza et al. (2009) found that repeated administration of GHB to rats for 15 days drastically reduced the number of neurons and non-neuronal cells in the CA1 region of the hippocampus and in the prefrontal cortex. With doses of 10 mg/kg of GHB, they were decreased by 61% in the CA1 region and 32% in the prefrontal cortex, and with 100 mg/kg, they were decreased by 38% and 9%, respectively. It is interesting to note that GHB has biphasic effects on neuronal loss, with lower doses (10 mg/kg) producing the most neurotoxicity, and higher doses (100 mg/kg) producing less.

Pretreatment with NCS-382, a GHB receptor antagonist, prevents both learning/memory deficits and neuronal loss in GHB-treated animals, suggesting that GHB's neurotoxic actions are mediated via activation of the GHB receptor.[60] In addition, the neurotoxicity appears to be caused by oxidative stress.[61][60][62]

GHB efterlader ingen toksiske metabolitter i kroppen og brænder derfor ingen hjerneceller af som opløsningsmidler som eks. alkohol og vist også GBL, da dette jo netop også er et opløsningsmiddel.

GHB efterlader ingen toksiske metabolitter i kroppen og brænder derfor ingen hjerneceller af som opløsningsmidler som eks. alkohol og vist også GBL, da dette jo netop også er et opløsningsmiddel.

Ethanol er ikke skadeligt fordi det er et opløsningsmiddel... - Eller jo, det er derfor det kan give mavesår med mere. Den primære skadelighed i ethanol, er at det bliver nedbrudt til ethanal/acetaldehyd. - som er meget kræftfremkaldende, skadende osv.