Disease relevance of Dimethyl acetamide

• Conditions causing these hallucinations include narcolepsy-cataplexy syndrome, peduncular hallucinosis, treated idiopathic Parkinson's disease, Lewy body dementia without treatment, migraine coma, Charles Bonnet syndrome (visual hallucinations of the blind), schizophrenia, hallucinogen-induced states and epilepsy [1].
• The concept that this drug is primarily a hallucinogen with mild toxicity is erroneous [2].
• The specific 5-HT2A agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) is a potent hallucinogen that also causes marked hyperthermia, suggesting the possibility that DOI, via stimulation of 5-HT2A receptors, might also cause sympathetically mediated cutaneous vasoconstriction [3].
• RESULTS: DMAC was useful as an additive in the donor vehicles, increasing the dissolved concentrations of poorly water-soluble HIV protease inhibitors, and enabling more reliable determination of P(app) values [4].
• On the 3 of 4-week schedule, 9-AC DMA infused at > or = 0.6 mg/m2 per day for 120 h weekly produced dose-limiting neutropenia, thrombocytopenia, and diarrhea, or resulted in 1-2-week treatment delays [5].

Psychiatry related information on Dimethyl acetamide

• In general, the evidence suggests that the prevalence of substance abuse in schizophrenia is comparable to that in the general population, with the possible exceptions of stimulant and hallucinogen abuse, which may be greater in patients with schizophrenia [6].
• CONCLUSIONS: While the prevailing view was that the activation of 5-HT(2) receptors is solely responsible for hallucinogenic drug effects, these results support a role for 5-HT(1A) receptors in the effects of the indoleamine hallucinogen 5-MeO-DMT on locomotor activity and PPI in rats [7].
• Among them, 83 had a diagnosis of alcohol dependence, 41 of heroin dependence and the remaining 17 cases of sedative, glue or hallucinogen dependence [8].
• Psychometric assessment of the Hallucinogen Rating Scale [9].
• Two variables were predictive of sexual risk-taking: higher level of hallucinogen use and sexual relationship with an IDU [10].

High impact information on Dimethyl acetamide

• Addition of the polar organic compounds, dimethylsulfoxide, N,N-dimethylformamide, N,N-dimethylacetamide, and butyric acid, to human lymphocyte cultures stimulated with the tumor-promoting agent, phorbol myristate acetate, results in greater than 90% inhibition of lymphocyte proliferation [11].
• Analyses of several sulfoxide complexes including rac-11 with N,N-dimethylacetamide (DMAC) or N-methyl-2-pyrrolidone (NMP) in a MeOH solution utilizing cold-spray ionization mass spectrometry provided, for the first time, direct information for intermolecular nonbonded S...O interactions between sulfoxides and amide (or lactam) in a solution [12].
• The activation of 5-HT(2A) receptors in medial prefrontal cortex (mPFC) by the hallucinogen DOI increases the firing activity of dorsal raphe (DR) 5-HT neurons and prefrontal 5-HT release [13].
• Coadsorption of smaller amounts of dimethylacetamide (PA = 217 kcal/mol) also produced no reaction, but with a higher loading, a proton was transferred from the carbenium ion to the base to leave 1,3-dimethylcyclopenta-1,3-diene in the zeolite as a neutral olefin [14].
• Therefore, these data indicate that the 5HT2 receptor gene product can produce a high affinity binding site for the phenylisopropylamine hallucinogen agonists as well as for the 5HT2 receptor antagonists [15].

Chemical compound and disease context of Dimethyl acetamide

• The administration of various doses of the phenylisopropylamine hallucinogen 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) to rats produced dose-related decreases in 1-hr food intake in a food-restricted paradigm and in locomotor activity [16].
• Posthallucinogen-like visual illusions (palinopsia) with risperidone in a patient without previous hallucinogen exposure: possible relation to serotonin 5HT2a receptor blockade [17].
• After controlling for sociodemographics, a significant association between any anxiety disorder diagnosis and lifetime stimulant use, cocaine use, and hallucinogen use was found in both surveys (OR approximately 1.5-3.0) [18].
• Acute and subchronic toxicity of dimethylformamide and dimethylacetamide following various routes of administration [19].
• The i.v. Bu dose was well tolerated and did not produce any acute toxicity reaction that could be attributed to the solvent system of dimethylacetamide and polyethylene glycol (PEG)-400 [20].

Biological context of Dimethyl acetamide

• Interaction of mescaline with phenothiazines: effect on behavior, body temperature, and tissue levels of hallucinogen in mice [21].
• This review examines aspects of that controversy, including the history of hallucinogens, epidemiology of current hallucinogen abuse, the association of LSD use with prolonged psychoses and hallucinogen persisting perception disorder, and the efforts to demonstrate the drug's therapeutic efficacy [22].
• Preclinical toxicology and pharmacology of dimethylacetamide, with clinical notes [23].
• Established immigrants more likely reported unprotected sex, hallucinogen or ecstasy use [24].
• This study was undertaken to investigate: (1) the effect of N,N-diethylacetamide (DEAC) and N,N-dimethylacetamide (DMAC) administration to rats on drug-metabolizing enzymes in the liver; (2) the in vitro dealkylation of DEAC and DMAC by hepatic microsomes from rats treated with various P450 inducers and purified P450 (2B1 and 2E1) [25].

Anatomical context of Dimethyl acetamide

• Number of surviving spermatozoa diminished progressively with increasing DMA concentrations in all species [26].
• A major role for thalamocortical afferents in serotonergic hallucinogen receptor function in the rat neocortex [27].
• CONCLUSION: It is discussed that ayahuasca-induced survival of binocular rivalry at high DSA rates may be related to slow visual processing and increased mean dominance periods may result from hallucinogen-induced alteration of gamma oscillations in the visual pathways [28].
• Consistent with a partial agonist action, LSD and DOI blocked the 5-HT excitation of piriform cortical interneurons only at the higher hallucinogen concentrations tested [29].
• The effects of the hallucinogen, harmaline (HME), and its congeners on human red blood cell (RBC) transport were studied [30].

Associations of Dimethyl acetamide with other chemical compounds

• DMSO, dimethylformamide (DMF) and dimethylacetamide (DMA) are similar solvents which are all very effective in their ability to suppress radiation-induced transformation in vitro (at concentrations in the cellular media down to 0.01%) [31].
• Theoretical conformational energy calculations were carried out for the (+) and (-) isomers of the hallucinogen 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM, STP) [32].
• Hallucinogen-induced UP states in the brain slice of rat prefrontal cortex: role of glutamate spillover and NR2B-NMDA receptors [33].
• The use of organic solvents in microfabricated capillary electrophoresis (CE) devices is demonstrated in connection with the separation of aliphatic amines in pure dimethylformamide, dimethylacetamide, dimethyl sulfoxide, or propylene carbonate media [34].
• RATIONALE: It has been suggested that the 5-HT1A receptor plays a significant modulatory role in the stimulus effects of the indoleamine hallucinogen lysergic acid diethylamide (LSD) [35].

Gene context of Dimethyl acetamide

• For example, 7b substituted for LSD in the drug discrimination assay with an ED50 of 61 nmol/kg and had Kj values in the nanomolar to subnanomolar range for the displacement of radioligand from rat and human 5-HT2 receptors, making it one of the most potent hallucinogen-like phenylalkylamine derivatives reported to date [36].
• 5-MeO-DIPT is thus effective in two rodent models of 5-HT2 agonist activity, and has affinity at receptors relevant to hallucinogen effects [37].
• In the present work, the effect of DMF and of the structurally related N,N-dimethylacetamide (DMAc) on the activating enzyme and the nature of the reactive species involved in the mechanism of P450 inactivation by the two chemicals were investigated in vitro [38].
• The paradox of 5-methoxy-N,N-dimethyltryptamine: an indoleamine hallucinogen that induces stimulus control via 5-HT1A receptors [39].
• Evidence for a common biological basis of the Absorption trait, hallucinogen effects, and positive symptoms: epistasis between 5-HT2a and COMT polymorphisms [40].

Analytical, diagnostic and therapeutic context of Dimethyl acetamide

• An hallucinogen analogue, trans-2-(2,5-dimethoxy-4-methylphenyl)cyclopropylamine (DMCPA), was resolved into ints two enantiomers by fractional crystallization of salts with d- or l-O,O-dibenzoyltartaric acid [41].
• Studies focused on spermatozoa tolerance to the following: 1) osmotic stress, 2) different extracellular concentrations of the cryoprotectant dimethylacetamide (DMA), 3) equilibration times of 1 versus 4 h, 4) equilibration temperature of 4 versus 21 degrees C, and 5) rapid versus slow cooling before cryopreservation and standard thawing [26].
• These findings are remarkable as structurally distinct serotonergic hallucinogen-like drugs do not maintain reliable self-administration in laboratory animals [42].
• RESULTS: Ayahuasca produced significant dose-dependent increases in five of the six subscales of the Hallucinogen Rating Scale, in the LSD, MBG, and A scales of the Addiction Research Center Inventory, and in the "liking", "good effects" and "high" visual analogue scales [43].
• Size-exclusion chromatography of technical lignins in dimethyl sulfoxide/water and dimethylacetamide [44].

References