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ABSTRACT: Zebra finches have been widely used to study neurobiology underlying vocal development. Because only male zebra finches learn song, efficient developmental use of these animals requires early determination of sex at ages that precede maturation of secondary sex characteristics. We have developed a sex determination method that combines a forensics method of genomic DNA isolation (from very small blood samples) with PCR amplification from Z and W sex chromosomes (males are ZZ, females ZW). This combination results in a minimally invasive yet highly reliable and convenient genotyping method.
Journal of Neuroscience Methods 09/2007; 164(1):116-9. · 1.98 Impact Factor
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ABSTRACT: Periadolescent nicotine exposure is associated with increased consumption and rewarding properties of abused drugs. In the case of peri- but not post-adolescent animals, these effects are persistent and last to adulthood, suggesting that early nicotine treatment may alter postnatal CNS development in ways that contribute to long-term problems with drug abuse.
To begin to identify brain regions that may be altered by developmental nicotine exposure, we have measured expression of a transcription factor, FosB, within a series of reward- and memory-related brain regions of Sprague-Dawley rats.
FosB expression is known to acutely and cumulatively increase within a subset of brain regions, particularly nucleus accumbens, after exposure to many classes of abused drugs. Our results demonstrate that FosB is increased within nucleus accumbens and also the granule cell layer of hippocampal dentate gyrus after both peri- and post-adolescent nicotine exposure (0.4 mg kg(-1) day(-1) from days 34 to 43 and 60 to 69, respectively). In periadolescents, expression increases were detected 2 days after nicotine exposure, and persisted for weeks, through at least early adulthood at 80 days of age. In post-adolescents, expression increases persisted for at least 11 days to postnatal day 80.
These findings demonstrate that nicotine treatment during both peri- and post-adolescence persistently alters activity of brain regions involved in reward and memory.
Because this altered gene expression occurs after both peri- and post-adolescent treatment, it cannot be directly responsible for increased consumption and rewarding properties of abused drugs previously established to be distinctly associated with periadolescent nicotine exposure.
Psychopharmacologia 06/2007; 191(4):891-7. · 4.08 Impact Factor
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ABSTRACT: The purpose of this study was to explore the involvement of adenosine receptor(s) in porcine coronary artery (PCA) relaxation and to define the role of MAPK signaling pathways. Isometric tensions were recorded in denuded PCA rings. 5'-(N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine receptor agonist, induced a concentration-dependent relaxation (EC(50) = 16.8 nM) of PGF(2alpha) (10 microM)-preconstricted arterial rings. NECA-induced relaxation was completely blocked by 0.1 microM SCH-58261 (A(2A) antagonist) at lower doses (1-40 nM) but not at higher doses (80-1,000 nM). MRS-1706 (1 microM, A(2B) antagonist) was able to shift the NECA concentration-response curve to the right. CGS-21680 (selective A(2A) agonist) induced responses similarly to NECA, whereas N(6)-cyclopentyladenosine (A(1) agonist) and Cl-IB-MECA (A(3) agonist) did not. Furthermore, the effect of NECA was attenuated by the addition of SB-203580 (10 microM, p38 MAPK inhibitor) but not by PD-98059 (10 microM, MEK inhibitor). Interestingly, SB-203580 had no effect on CGS-21680-induced relaxation. Western blot analysis demonstrated that PGF(2alpha) and adenosine agonists stimulated p38 MAPK at a concentration of 40 nM in PCA smooth muscle cells. MRS-1706 (1 microM) significantly reduced NECA-induced p38 MAPK phosphorylation. Addition of NECA and SB-203580 alone or in combination inhibited PGF(2alpha)-induced p38 MAPK. Western blot data were further confirmed by p38 MAPK activity measurement using activating transcription factor-2 assay. Our results suggest that the adenosine receptor subtype involved in causing relaxation of porcine coronary smooth muscle is mainly A(2A) subtype, although A(2B) also may play a role, possibly through p38 MAPK pathway.
AJP Heart and Circulatory Physiology 07/2005; 288(6):H2574-80. · 3.71 Impact Factor
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ABSTRACT: We recently reported that adenosine caused bronchoconstriction and enhanced airway inflammation in an allergic mouse model. In this study, we further report the characterization of the subtype of adenosine receptor(s) involved in bronchoconstriction. 5'-(N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist, elicited bronchoconstriction in a dose-dependent manner. Little effects of N(6)-cyclopentyladenosine (A(1)-selective agonist) and 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (A(2A)-selective agonist) compared with NECA were observed in this model. 2-Chloro-N(6)-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-beta-d-ribofuranosyl]adenosine, an A(3)-selective receptor agonist, produced a dose-dependent bronchoconstrictor response, which was blocked by selective A(3) antagonist 2,3-diethyl-4,5-dipropyl-6-phenylpyridine-3-thiocarboxylate-5-carboxylate (MRS1523). However, MRS1523 only partially inhibited NECA-induced bronchoconstriction. Neither selective A(1) nor A(2A) antagonists affected NECA-induced bronchoconstriction. Enprofylline, a relatively selective A(2B) receptor antagonist, blocked partly NECA-induced bronchoconstriction. Furthermore, a combination of enprofylline and MRS1523 completely abolished NECA-induced bronchoconstrictor response. Using RT-PCR, we found that all four adenosine receptor subtypes are expressed in control lungs. Allergen sensitization and challenge significantly increased transcript levels of the A(2B) and A(3) receptors, whereas the A(1) receptor message decreased. No change in transcript levels of A(2A) receptors was observed after allergen sensitization and challenge. These findings suggest that A(2B) and A(3) adenosine receptors play an important role in adenosine-induced bronchoconstriction in our allergic mouse model. Finally, whether the airway effects of the receptor agonists/antagonists are direct or indirect needs further investigations.
AJP Lung Cellular and Molecular Physiology 07/2003; 284(6):L1012-9. · 3.66 Impact Factor
