Du bliver det som en god ven af mig kalder "Blank & Poleret", givet at du ryger noget tid efter efter MDMA'en er dampet af. Jeg har, som jeg har skrevet andetsteds, prøvet at se fjernsyn på et slukket fjernsyn mens jeg røg joints efter en ecstasy-rus. Man fatter virkelig ikke en meter, og har en 10-20 sekunders forsinkelse på alt der sker omkring én. I nogle tilfælde har jeg, som det udgår fra ovenstående, mistet korttidshukommelsen helt og aldeles. Og det gør ikke én friskere dagen efter.

F.eks hvis man kommer hjem fra byen, er meget beruset og ryger (bong evt.) så bliver man for det meste meget meget mere lam og ligger og siger mærkelige lyde ude på køkkengulvet. Hvad den videnskabelige forklaring er ved jeg ikke...

Det er også lækkert at ryge på mdma-comedownet (hash er desuden en glimrende antioxidant)

På den kombo har jeg to gange opløvet følelsen af at være ved at gå i bevidstløshed.

Den første gang blev jeg meget svimmel og derefter faldt jeg om på mit toilet og rystede uden at kunne styre min krop i nogle sekunder. Det holdt så op efter nogle minutter.

Anden gang var på roskilde festivallen her i år, hvor jeg stod og pissede og pludselig blev meget svimmel og havde det ligesom når man har lavet noget fysisk der er alt for hårdt så det sortner for øjnene og man får det skidt - det lykkedes mig at falde i søvn ret hurtigt efter heldigvis.

Det har ikke været skide morsomt... Pas lige på

Cannabidiol and other cannabinoids were examined as neuroprotectants in rat cortical neuron cultures exposed to toxic levels of the neurotransmitter, glutamate. The psychotropic cannabinoid receptor agonist delta 9-tetrahydrocannabinol (THC) and cannabidiol, (a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and kainate receptor mediated neurotoxicities. Neuroprotection was not affected by cannabinoid receptor antagonist, indicating a (cannabinoid) receptor-independent mechanism of action. Glutamate toxicity can be reduced by antioxidants. Using cyclic voltametry and a fenton reaction based system, it was demonstrated that Cannabidiol, THC and other cannabinoids are potent antioxidants. As evidence that cannabinoids can act as an antioxidants in neuronal cultures, cannabidiol was demonstrated to reduce hydroperoxide toxicity in neurons. In a head to head trial of the abilities of various antioxidants to prevent glutamate toxicity, cannabidiol was superior to both alpha-tocopherol and ascorbate in protective capacity. Recent preliminary studies in a rat model of focal cerebral ischemia suggest that cannabidiol may be at least as effective in vivo as seen in these in vitro studies.

Marijuana and related drugs (cannabinoids) have been proposed as treatments for a widening spectrum of medical disorders. R(+)-[2, 3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1, 4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate (R(+)-WIN 55212-2), a synthetic cannabinoid agonist, decreased hippocampal neuronal loss after transient global cerebral ischemia and reduced infarct volume after permanent focal cerebral ischemia induced by middle cerebral artery occlusion in rats. The less active enantiomer S(-)-WIN 55212-3 was ineffective, and the protective effect of R(+)-WIN 55212-2 was blocked by the specific central cannabinoid (CB1) cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2, 4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide-hydrochloride. R(+)-WIN 55212-2 also protected cultured cerebral cortical neurons from in vitro hypoxia and glucose deprivation, but in contrast to the receptor-mediated neuroprotection observed in vivo, this in vitro effect was not stereoselective and was insensitive to CB1 and CB2 receptor antagonists. Cannabinoids may have therapeutic potential in disorders resulting from cerebral ischemia, including stroke, and may protect neurons from injury through a variety of mechanisms.

Cannabinoids prevent the acute hyperthermia and partially protect against the 5-HT depleting effects of MDMA ("Ecstasy") in rats.

Morley KC, Li KM, Hunt GE, Mallet PE, McGregor IS.

School of Psychology, University of Sydney, Sydney, NSW 2006, Australia.

Abstract

Cannabinoid-MDMA interactions were examined in male Wistar rats.

MDMA ( [Formula: see text] mg/kg or [Formula: see text] mg/kg over 4 h on each of 2 days) was administered with or without Delta(9)-tetrahydrocannabinol (THC) ( [Formula: see text] mg/kg), the synthetic cannabinoid receptor agonist CP 55,940 ( [Formula: see text] or 0.2 mg/kg) or the cannabinoid receptor antagonist SR 141716 ( [Formula: see text] mg/kg).

Co-administered Delta(9)-THC and CP 55,940 but not SR 141716 prevented MDMA-induced hyperthermia, causing a powerful hypothermia.
Co-administered Delta(9)-THC, CP 55,940 and SR 141716 all tended to decrease MDMA-induced hyperactivity.

Co-administered Delta(9)-THC provided protection against the long-term increases in anxiety seen in the emergence test, but not the social interaction test, 6 weeks after MDMA treatment.

Co-administered Delta(9)-THC and CP 55,940, but not SR 141716, partly prevented the long-term 5-HT and 5-HIAA depletion caused by MDMA in various brain regions.

SR 141716 administered with CP 55,940 and MDMA prevented the hypothermic response to the CP 55,940/MDMA combination but did not alter the CP 55,940 attenuation of MDMA-induced 5-HT depletion.

These results suggest a partial protective effect of co-administered cannabinoid receptor agonists on MDMA-induced 5-HT depletion and long-term anxiety. This action appears to operate independently of cannabinoid CB1 receptors.

Braida D, Sala M (2002) Role of the endocannabinoid system in MDMA intracerebral self- administration in rats. Br J Pharmacol 136: 1089-1092.

Full text in PDF format

A possible role for the endocannabinoid system in modulating the rewarding effects of MDMA was investigated by comparing number of lever presses made to obtain i.c.v. injections of MDMA alone with number of responses made to obtain combinations of MDMA and an endocannabinoid agonist (CP 55,940) or an antagonist (SR141716A). After being trained to press a lever for water reinforcement, rats were trained to press levers for i.c.v injections of MDMA. The ICV dose producing maximal responses was 1 mcg MDMA, out of the tested doses of 0.01, 0.1, 1 and 2 mcg, with responses for MDMA decreasing at 2 mcg. Rats who had demonstrated 5 days of stable responses for 1 mcg MDMA were then tested with a combination of MDMA and cannabinoid agonist or MDMA and cannabinoid antagonist. Doses of cannabinoid agonist and antagonist were derived from findings in previous studies as producing maximal responding (for the agonist) or as completely blocking the effects of the agonist (for the antagonist). Rats pressed the MDMA (drug) lever less when given a combination of MDMA and cannabinoid agonist, and pressed the MDMA lever more when receiving a combination of MDMA and cannabinoid antagonist. Since the authors had pre-selected the dose of MDMA used in the drug combinations to be one producing maximal self-administration, they interpreted these findings as a reflection of a synergistic action of MDMA and the cannabinoid agonist that enhances the rewarding effects of MDMA. Likewise, the increase in response seen after the combination of MDMA and cannabinoid antagonist is interpreted as indicating that MDMA is less rewarding when cannabinoid receptors are not activated. The authors suggest that the cannabinoid system modulates dopamine release in specific brain areas. Since most ecstasy users use cannabis before or after ecstasy use, such findings might shed light on the popularity of this combination of substances. There are two different cannabinoid receptors, CB1 and CB2, and this report does not indicate whether the agonists and antagonists they used activate both receptors equally, or interact with one receptor more than another.