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Publication : Quantitative autoradiography of adenosine receptors and NBTI-sensitive adenosine transporters in the brains of mice deficient in the preproenkephalin gene.

First Author  Bailey A Year  2004
Journal  Brain Res Volume  1025
Issue  1-2 Pages  1-9
PubMed ID  15464738 Mgi Jnum  J:92981
Mgi Id  MGI:3055278 Doi  10.1016/j.brainres.2004.06.088
Citation  Bailey A, et al. (2004) Quantitative autoradiography of adenosine receptors and NBTI-sensitive adenosine transporters in the brains of mice deficient in the preproenkephalin gene. Brain Res 1025(1-2):1-9
abstractText  There is a large body of evidence indicating important interactions between the adenosine and the opioid systems in regulating pain, opioid dependence and withdrawal. Mice lacking the proenkephalin gene and therefore lacking the endogenous enkephalin peptides have been successfully developed and exhibit decreased locomotor activity, are hyperalgesic and show enhanced anxiety and aggression. In addition, an upregulation of ÎŒ and delta receptors was also observed in the brains of knockout mice. To investigate if there are any compensatory alterations in adenosine systems in the brains of mutant mice, we have carried out quantitative autoradiographic mapping of A(1) and A(2A) adenosine receptors and nitrobenzylthioinosine (NBTI)-sensitive adenosine transporters in the brains of wild-type and homozygous enkephalin knockout mice. Adjacent coronal brain sections were cut from brains of +/+ and -/- mice for the determination of binding of [(3)H]1,3-dipropyl-8-cyclopentylxanthine ([(3)H]DPCPX), [(3)H]2-[p-(2-carbonylethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenosi ne ([(3)H]CGS21680) or [(3)H]NBTI to A(1) and A(2A) adenosine receptors and NBTI-sensitive adenosine transporters, respectively. A small but significant increase in [(3)H]DPCPX and [(3)H]NBTI binding but no significant change in [(3)H]CGS21680 binding was detected in enkephalin knockout brains. The results provide further evidence of functional interactions in the brain between opioid receptors and A(1) adenosine receptors as well as NBTI-sensitive adenosine transporters but not A(2A) receptors.
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