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  • 1
    Electronic Resource
    Electronic Resource
    Cannabinoid CB1 receptor knockout mice exhibit markedly reduced voluntary alcohol consumption and lack alcohol-induced dopamine release in the nucleus accumbens (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 84 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mechanisms underlying predisposition to alcohol abuse and alcoholism are poorly understood. In this study, we evaluated the role of cannabinoid (CB1) receptors in (i) voluntary alcohol consumption, and (ii) acute alcohol-induced dopamine (DA) release in the nucleus accumbens, using mice that lack the CB1 receptor gene (CB1–/–). CB1–/– mice exhibited dramatically reduced voluntary alcohol consumption, and completely lacked alcohol-induced DA release in the nucleus accumbens, as compared to wild-type mice. The gender difference, with female mice consuming significantly more alcohol than wild-type male mice, was observed in wild-type mice, whereas this gender difference was nonexistent in CB1 mutant male and female mice. There was also a significant gender difference, with the wild-type, heterozygous, and mutant females consuming significantly more liquid and food than wild-type, heterozygous and mutant males. However, the total volume of fluid consumption and food intake did not differ between wild-type, heterozygous, and mutant mice. These results strongly suggest that the CB1 receptor system plays an important role in regulating the positive reinforcing properties of alcohol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01576.x
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  • 2
    Electronic Resource
    Electronic Resource
    Chronic Ethanol Increases the Cannabinoid Receptor Agonist Anandamide and Its Precursor N-Arachidonoylphosphatidylethanolamine in SK - N - SH Cells (1999)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 72 (1999), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : In an earlier study, we demonstrated that chronic ethanol(EtOH) exposure down-regulated the cannabinoid receptors (CB1) in mouse brainsynaptic plasma membrane. In the present study, we investigated the effect ofchronic EtOH on the formation of anandamide (AnNH), an endogenouscannabimimetic compound, and its precursorN-arachidonoylphosphatidylethanolamine (N-ArPE) in SK-N-SH cells thatwere prelabeled with [3H]arachidonic acid. The results indicatethat exposure of SK-N-SH cells to EtOH (100 mM) for 72 hsignificantly increased levels of [3H]AnNH and[3H]N-ArPE (p 〈 0.05) (1.43-fold for[3H]AnNH and 1.65-fold for [3H]N-ArPE). Exposure ofSK-N-SH cells to EtOH (100 mM, 24h) inhibited initially the formationof [3H]AnNH at 24 h, followed by a progressive increase, reaching astatistical significance level at 72 h (p 〈 0.05).[3H]N-ArPE increased gradually to a statistically significant levelafter 48 and 72 h (p 〈 0.05). Incubation with exogenousethanolamine (7 mM) and EtOH (100 mM, 72 h) did not resultin an additive increase in the formation of [3H]AnNH. The formationof [3H]AnNH and [3H]N-ArPE by EtOH was enhanced by theCa2+ ionophore A23187 or by the depolarizing agent veratridine andthe K+ channel blocker 4-aminopyridine. Further, the EtOH-inducedformation of [3H]AnNH and [3H]N-ArPE was inhibited byexogenous AnNH, whereas only [3H]AnNH formation was inhibited bythe CB1 receptor antagonist SR141716A and pertussis toxin, suggesting that theCB1 receptor and Gi/o protein mediated the regulation of AnNH levels. The observed increase in the levels of these lipids in SK-N-SH cells may be a mechanism for neuronal adaptation and may serve as a compensatory mechanism to counteract the continuous presence of EtOH. The present observation taken together with our previous results indicate the involvement of the endocannabinoid system in mediating some of the pharmacological actions of EtOH and may constitute part of a common brain pathway mediating reinforcement of drugs of abuse including EtOH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1999.0720522.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of acute and chronic ethanol exposure on fatty acid ethyl ester synthases in mouse cerebellar membranes (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Addiction biology 3 (1998), S. 0 
    Details
    ISSN: 1369-1600
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Fatty acid ethyl esters (FAEE), the products of esterification of fatty acids with ethanol (EtOH), are shown to cause organ injury in chronic alcohol abusers. Their formation is catalysed by the enzyme FAEE synthase which is present in both animal and human brain. In the present study, we investigated the effects of acute and chronic EtOH exposure on FAEE synthase activity in crude cerebellar membrane preparation of mice, using oleic, linoleic and arachidonic acids as substrates. The results indicate that FAEE synthase activity exists in synaptosomal membranes and the activity of this enzyme varied with various fatty acid substrates. The synthase activity was optimal in the membranes from the animals exposed acutely to EtOH when oleic acid was used as a substrate. A 14% increase in the incorporation of oleic acid was observed in the membranes from animals exposed to acute dose of EtOH. However, there was a 10% reduction in the synthase activity when arachidonic acid was used as a substrate in the membrane preparations from mice exposed chronically to EtOH. The results suggest that substrate specificity for FAEE synthase varied with the duration of exposure to EtOH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1080/13556219872380
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  • 4
    Electronic Resource
    Electronic Resource
    Methylphenidate oral dose plasma concentrations and behavioral response in children (1982)
    Springer
    Psychopharmacology 76 (1982), S. 329-332 
    Details
    ISSN: 1432-2072
    Keywords: Methylphenidate dosage ; Attention deficit disorder with hyperactivity ; Methylphenidate plasma concentration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between methylphenidate (MP) oral dose and plasma concentration to social and cognitive behaviors was studied in 25 boys diagnosed as having “attention deficit disorder with hyperactivity”. Children were administered successive 1-week treatment conditions under the following schedule of fixed oral doses given twice daily: placebo; 0.25 mg/kg; 0.50 mg/kg; 1.0 mg/kg; placebo. Teacher and parent ratings showed increased improvement in social behavior as a function of MP dose. No drug effects were obtained on cognitive performance. MP plasma concentrations were significantly associated with oral dose and with measures of social behavior. No relationship was found with cognitive behavior. Side effects at the largest dose were severe enough to require discontinuation of treatment for five children, but were relatively mild for the remaining children.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00449120
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  • 5
    Electronic Resource
    Electronic Resource
    A chemical ionization selected ion monitoring assay for methylphenidate and ritalinic acidAbbreviations: MePPA = methyl-2-phenyl-2-(2′-piperidyl) acetate; HPPA = 2-phenyl-2-(2′-piperidyl) acetic acid; EtPPA = ethyl-2-phenyl-2-(2′-piperidyl) acetate, TFAA = trifluoroacetic anhydride. (1979)
    Chichester : Wiley-Blackwell
    Biological Mass Spectrometry 6 (1979), S. 422-426 
    Details
    ISSN: 0306-042X
    Keywords: Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: A methane chemical ionization quantitative assay for methylphenidate and its major metabolite, ritalinic acid, is described. Methylphenidate and the internal standard, ethylphenidate, were extracted from plasma samples and derivatized to prevent thermal decomposition in the gas chromatograph. Ritalinic acid was esterified with diazomethane and extracted as methylphenidate. The intensity of the protonated molecular ion of the derivatized drug and internal standard was measured by selected ion monitoring. Calibration curves were prepared from drug standards dissolved in drug-free plasma, and the lower limit of the curves extended to 0.5 ng methylphenidate per ml plasma. The method was used to generate plasma decay curves for pediatric patients undergoing methylphenidate therapy.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bms.1200061003
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