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February 2007 NIDA - Director's Report - February 2007 NIDA Home > Publications > Director's Reports Director's Report to the National Advisory Council on Drug Abuse - February, 2007 Index Research Findings Basic Neurosciences Research Basic Behavioral Research Behavioral and Brain Development Research Clinical Neuroscience Research Epidemiology and Etiology Research Prevention Research Research on Behavioral and Combined Treatments for Drug Abuse Research on Pharmacotherapies for Drug Abuse Research on Medical Consequences of Drug Abuse and Co-Occurring Infections (HIV/AIDS, HCV) Services Research Clinical Trials Network Research International Research Intramural Research Program Activities Extramural Policy and Review Activities Congressional Affairs International Activities Meetings and Conferences Media and Education Activities Planned Meetings Publications Staff Highlights Grantee Honors https://archives.drugabuse.gov/DirReports/DirRep207/Default.html[11/17/16, 10:55:09 PM] NIDA - Director's Report - February 2007 Archive Home | Accessibility | Privacy | FOIA (NIH) | Current NIDA Home Page The National Institute on Drug Abuse (NIDA) is part of the National Institutes of Health (NIH) , a component of the U.S. Department of Health and Human Services. Questions? _ See our Contact Information. https://archives.drugabuse.gov/DirReports/DirRep207/Default.html[11/17/16, 10:55:09 PM] NIDA - Director's Report - February, 2007 NIDA Home > Publications > Director's Reports > February, 2007 Index Director's Report to the National Advisory Council on Drug Abuse - February, 2007 Index Research Findings - Basic Neuroscience Research Research Findings Paternal Cocaine Exposure & Its Consequences Basic Neurosciences Research In a recent study, NIDA supported researchers, Dr. Michael Lidow and his Basic Behavioral Research associates report that paternal cocaine abuse may have a significant negative impact on offspring development and that such paternal impact could be Behavioral and Brain brought about by long-term cocaine exposure of males prior to coitus. This Development Research study conducted using a novel drug inhalation model revealed that male mice Clinical Neuroscience were capable of learning self-administration of cocaine via inhalation route as Research well as achieving and maintaining blood levels of this drug during daily Epidemiology and Etiology inhalation sessions comparable to that reported for females. Authors also noted Research a reduction in biparietal head diameter in newborn pups sired by cocaine- inhaling males suggesting a decreased cerebral volume. Most importantly, they Prevention Research observed a greater negative impact in female offspring compared to males with Research on Behavioral and respect to working memory and light stimulus duration. This study also showed Combined Treatments for that chronic cocaine exposure in male mice did not result in substantial Drug Abuse breakage of spermatozoal DNA, but significantly altered expression of DNA Research on methyltransferase 1 and 3a in the germ cell-rich seminiferous tubules of the Pharmacotherapies for Drug testis. Since these enzymes are essential for generating and maintaining Abuse parental gene imprinting in germ cells, the authors' observations point to an intriguing possibility that cocaine may cause paternally induced Research on Medical neuroteratological effects by interfering with gene-imprinting patterns in male Consequences of Drug gametes. He, F., Lidow, I.A., and Lidow, M.S. Consequences of Paternal Abuse and Co-Occurring Cocaine Exposure in Mice, Neurotoxicology and Teratology, 28, pp. 198-209, Infections (HIV/AIDS, HCV) 2006. Services Research Clinical Trials Network Supraspinal Brain-derived Neurotrophic Factor Acts at the TrkB Research Receptor to Produce International Research Intramural Research Pain Sensitivity Brain-derived neurotrophic factor, or BDNF, plays a critical role Program Activities in learning and memory by actions at the TrkB receptor. NIDA grantees Drs. Ronald Dubner and Ke Ren (University of Maryland, Baltimore) and colleagues Extramural Policy and now report that BDNF-TrkB signaling also plays a critical role within the brain Review Activities to produce pain hypersensitivity. They found that after tissue injury, the BDNF- TrkB complex in the brain stem triggers pain facilitating signals to the spinal Congressional Affairs cord. This facilitating signal causes the amplification and spreads the pain. This discovery not only helps us understand the mechanisms of chronic pain, but International suggests the possibility of targeting the BDNF-TrkB complex in the Activities development of novel pain therapies. Guo, W., Robbins, M.T., Wei, F., Zou, S., Dubner, R., and Ren, K. Supraspinal Brain-Derived Neurotrophic Factor Meetings and Signaling: A Novel Mechanism for Descending Pain Facilitation, Journal of Conferences Neuroscience, 26(1), pp. 126-137, 2006. Media and Education Buprenorphine Pharmacokinetics https://archives.drugabuse.gov/DirReports/DirRep207/DirectorReport1.html[11/17/16, 10:55:14 PM] NIDA - Director's Report - February, 2007 Activities Buprenorphine, a partial mu agonist, was approved by the Food and Drug Planned Meetings Administration in 2001, in part for the treatment of dependence on opioids such as heroin, morphine, and oxycontin. It is formulated under the trade Publications name Suboxone, consisting of a sublingual tablet of 2 or 8 mg buprenorphine, together with 0.5 or 2 mg naloxone as a mu antagonist. In work supported by Staff Highlights NIDA awards to the University of Utah and the Virginia Commonwealth University, Dr. David Moody and Dr. Elinore McCance-Katz have recently Grantee Honors collaborated to determine the in-vivo pharmacokinetics of this formulation in human plasma and urine samples. Five opioid-dependent subjects were treated with sixteen mg daily doses of buprenorphine for twenty-one days, with collection of blood and urine (twenty-four hour) samples obtained. These clinical samples were treated with appropriate deuterated internal standards, centrifuged in the case of blood samples, and the supernatants applied to solid phase extraction cartridges for extraction, solvent removal, and reconstitution. Separation of four particular analytes, buprenorphine, norbuprenorphine, and the three position glucuronides of both buprenorphine and norbuprenorphine, was carried out. The pharmacokinetic data indicated that norbuprenorphine-3- glucuronide was the predominant metabolite found in both urine and plasma, and that buprenorphine was converted to its glucuronide and to norbuprenorphine in approximately the same time frame (i.e, one hour after administration). Huang, W., Moody D.E., and McCance-Katz, E.F. The In-vivo Glucuronidation of Buprenorphine and Norbuprenorphine Determined by Liquid Chromatography-Electrospray Ionization-Tandem Mass Spectrometry, Therapeutic Drug Monitoring, 28(2), pp. 245-251, 2006. Tritiation of the Cannabinoid Receptor Antagonist SR144528 Involving Lithium Aluminum Tritide Reduction; Assessment of the Kinetic Isotope by 3H-NMR The pyrazole caboxamide SR144528 is a selective antagonist at the peripheral cannabinoid CB2 receptor. The potential value of this compound to researchers for pharmacological studies of the CB2 receptor and its potential role in immune function prompted the synthesis of the tritiated compound. In this paper the authors reported the synthesis of this compound and used an approach that enabled the incorporation of highly specific activity tritium label while circumventing the liability of the target compound to catalytic hydrogenation. Lithium aluminum tritide of less than maximum specific activity was employed to introduce tritium, resulting in hydride/tritide incorporation indicative of non kinetic isotope effect for the hydride/tritide reduction of a methyl benzoate. Seltzman, H.H., Foster, M.C., Wyrick, C.D., Burgess, J.P. and Carroll, F.I. Tritiation of the Cannabinoid Receptor Antagonist SR144528 Involving Lithium Aluminum Tritide Reduction; Assessment of the Kinetic Isotope Effect by 3H-NMR, Journal of Labeled Compounds and Radiopharmaceuticals, 48, pp. 589-596, 2005. Marijuana Smoke and Rimonabant Precipitated Withdrawal The goals of the present study were to assess whether the CB1 antagonist SR 141716 (rimonabant) precipitates withdrawal in mice that had been repeatedly exposed to marijuana smoke, and to compare these precipitated withdrawal effects to those elicited following intravenous administration of its chief psychoactive component _9-tetrahydrocannabinol _9-THC. SR 141716 elicited a significant increase in paw tremors in mice that were repeatedly dosed with either marijuana or _9-THC. Unexpectedly, the blood and brain concentrations of _9-THC following marijuana exposure were considerably lower than those found following _9-THC injection when comparing an equivalent magnitude of paw tremors in both conditions. Finally, _9-THC dose-dependently alleviated SR 141716-induced paw tremors in marijuana-dependent mice, but marijuana https://archives.drugabuse.gov/DirReports/DirRep207/DirectorReport1.html[11/17/16, 10:55:14 PM] NIDA - Director's Report - February, 2007 itself failed to reverse the precipitated withdrawal effect. It is likely that marijuana exposure generated insufficient _9-THC brain levels to reverse the withdrawal signs compared with the brain levels following intravenous injection. These findings taken together indicate that mice exposed repeatedly to marijuana smoke exhibit similar precipitated withdrawal effects as _9-THC-
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