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The structure of cocaine with relevant structural motifs for activity at the dopamine transporter highlighted. While it was originally thought that the 2β-carbomethoxy moiety interacted with the DAT through hydrogen bonding, subsequent research has indicated that electrostatic (ionic) interactions are the primary means of interactions with the DAT.
[1] [2] Besides subjective effects, (R)-MDMA increased heart rate, blood pressure, and body temperature similarly to MDMA and (S)-MDMA, though it was less potent in producing these effects. [2] Body temperature was notably increased to the same extent with ( R )-MDMA 250 mg as with MDMA 125 mg and ( S )-MDMA 125 mg. [ 2 ]
Cocaine's desired euphoric effects are delayed when snorted through the nose by about five minutes. This occurs because cocaine's absorption is slowed by its constricting effect on the blood vessels of the nose. [12] Insufflation of cocaine also leads to the longest duration of its effects (60–90 minutes). [12]
Cocaine is a relatively "balanced" inhibitor, although facilitation of dopaminergic neurotransmission is what has been linked to the reinforcing and addictive effects. In addition, cocaine has some serious limitations in terms of its cardiotoxicity [188] due to its local anesthetic activity. Thousands of cocaine users are admitted to emergency ...
It is a primary metabolite of cocaine, [1] and is pharmacologically inactive. [2] It is the corresponding carboxylic acid of cocaine, its methyl ester. It is formed in the liver by the metabolism of cocaine by hydrolysis, catalysed by carboxylesterases, and subsequently excreted in the urine. It is readily synthesised by boiling cocaine ...
Normally, metabolism of cocaine produces two primarily biologically inactive metabolites—benzoylecgonine and ecgonine methyl ester. The hepatic enzyme carboxylesterase is an important part of cocaine's metabolism because it acts as a catalyst for the hydrolysis of cocaine in the liver, which produces these inactive metabolites.
This receptor had been seen to modulate the rewarding effects of cocaine, and receptor antagonists had blocked the acute locomotor stimulating effect and lowered behavioral sensitization. Changes in the sigma 1 receptor have been shown to modulate dopamine release, so shifts in its expression can change the behavioral responses to cocaine with ...
Methylecgonidine (anhydromethylecgonine; anhydroecgonine methyl ester; AEME) is a chemical intermediate derived from ecgonine or cocaine.. Methylecgonidine is a pyrolysis product formed when crack cocaine is smoked, making this substance a useful biomarker to specifically test for use of crack cocaine, as opposed to powder cocaine which does not form methylecgonidine as a metabolite. [1]