Original contributionAutoradiographic distribution of tachykinin NK2 binding sites in the rat brain: comparison with NK1 and NK3 binding sites
Section snippets
Subjects
Male Sprague–Dawley rats (200–250 g; Charles River, Cléon, France) were housed in groups of five with food and water ad libitum in a room maintained at 22 °C with 12-h/12-h light/dark cycle. Animals were treated in accordance with the Guide for Care and Use of Laboratory Animals established by the National Institute of Health (NIH 80-23) and with the European Community Council Directive (86/609/EEC).
Ligands and drugs
[125I]NKA (2000 Ci/mmol) was from Amersham. [125I]Bolton and Hunter substance P ([125I]BHSP) and
Regional distribution of NK2-sensitive [125I]NKA binding sites
Brain sections were incubated with [125I]NKA (50 pM) in the presence of either senktide (1 μM, NK3 agonist) and SR 140333 (0.1 μM, NK1 antagonist; n=5) or senktide and [Pro9]SP (1 μM, NK1 agonist; n=3) to completely avoid labeling of NK3 and NK1 binding sites. For each area and in both conditions, the specific NK2 component of [125I]NKA total binding corresponds to the binding inhibited by 1 μM NKA or 0.1 μM SR 48968. Except in the cerebral cortex and the cerebellum, nonspecific binding was
Discussion
The autoradiographic distribution of tachykinin NK2 binding sites was determined in the brain of the adult rat using the agonist [125I]NKA, a ligand with a much higher specific radioactivity than tritiated ligands such as the antagonists [3H]SR 48968 or [3H]GR 100679. [125I]NKA labels two subtypes of NK1 binding sites (which present a high affinity not only for SP but also for NKA, NPK and NPγ) as well as NK3 binding sites in the rat brain (Beaujouan et al., 2000). Labeling of these NK1 and NK3
Acknowledgements
We would like to thank J. Prémont, A-M. Thierry and J-M. Deniau for fruitful discussions, A. M. Godeheu, J-P. Martin and P. Llegou for histological, photographic and photomontage assistance, respectively.
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2019, Journal of Chemical NeuroanatomyCitation Excerpt :The three endogenous tachykinins SP, NKA and NKB exhibit preferential (but not exclusive) binding for the tachykinin receptors NK1, NK2 and NK3 respectively (Saffroy et al., 2003; Page, 2005; Schable et al., 2012). The distribution patterns of the different NK receptors do not always match with that of their respective ligands: for example, it has been reported that a region rich in NKA such as the striatum is practically devoid of NK2 receptors (Saffroy et al., 2003). Comparing the distributions of the three receptors they display also marked differences, since structures rich in NK1 and NK3 binding sites are devoid of NK2 binding sites (Saffroy et al., 2003).
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2019, Behavioural Brain ResearchTachykinin NK1 receptor antagonist L-733,060 and substance P deletion exert neuroprotection through inhibiting oxidative stress and cell death after traumatic brain injury in mice
2019, International Journal of Biochemistry and Cell BiologyCitation Excerpt :NK receptors are 7-transmembrane domain, G-protein-coupled receptors, with three, known as the NK1, NK2, and NK3 receptor, having been identified to date (Maggi, 1995). SP normally has the highest affinity for the NK1 receptor, and the predominance of the NK1 receptor is in the adult brain (Saffroy et al., 2003). The present study showed that a significant increase of NK1R protein levels following TBI was observed both in the wild type and the SP knock out mice, but there was no significantly difference in the expression of NK1R at 24 h post-TBI between these two groups, indicating upregulation of NK1R is a consequence of TBI, independent of the levels of substance P.