preprotachykinin

プレプロタキキニン

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/24 04:41:41」(JST)

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1. 気道の神経制御 neuronal control of the airways

English Journal

Mapping of alpha-neo-endorphin- and neurokinin B-immunoreactivity in the human brainstem.

Duque E, Mangas A, Salinas P, Díaz-Cabiale Z, Narváez JA, Coveñas R.SourceLaboratory of Neuroscience (Lab. 143), Pontificia Bolivariana-Montería University, Montería, Colombia.
Brain structure & function.Brain Struct Funct.2012 Feb 9. [Epub ahead of print]
We have studied the distribution of alpha-neo-endorphin- or neurokinin B-immunoreactive fibres and cell bodies in the adult human brainstem with no prior history of neurological or psychiatric disease. A low density of alpha-neo-endorphin-immunoreactive cell bodies was only observed in the medullary
PMID 22318412

Implication of substance P neuronal system in the amygdala as a possible mechanism for hypergravity-induced motion sickness.

Horii A, Nakagawa A, Uno A, Kitahara T, Imai T, Nishiike S, Takeda N, Inohara H.AbstractWe previously reported that motion sickness was prevented in rats with amygdala lesion and that provocative motion stimuli increased the number of Fos-positive neurons in the amygdala, suggesting that the amygdala is one of the neural substrates involved in the development of motion sickness. NK-1 receptors in the brain stem and amygdala are thought to play an important role in emesis and affective disorders, respectively. In the present study, to elucidate a role of substance P neuronal system and NK-1 receptors in the brain stem and amygdala in the development of motion sickness, we measured changes in gene expression of NK-1 receptors and preprotachykinin, a precursor of substance P, using quantitative real-time PCR methods in solitary tract nucleus and amygdala in rats after provocative motion stimuli induced by 2G hypergravity load. Effects of systemic administration of CP-99,994, an antagonist for NK-1 receptors, on hypergravity-induced motion sickness were also examined using pica behavior, eating non-nutritive substances such as kaolin, as an index of motion sickness in rats. Hypergravity-induced motion sickness was inhibited by CP-99,994 with a dose-dependent and enantioselective manner. Preprotachykinin mRNA expression was increased in basolateral nucleus of amygdala and solitary tract nucleus after hypergravity load for 3h, whereas NK-1 receptor mRNA expression was not changed by hypergravity in amygdala and solitary tract nucleus. Present results suggest that 2G hypergravity load activated the substance P neuronal system in amygdala as well as in the brain stem and this activation would be related to the development of motion sickness.
Brain research.Brain Res.2012 Jan 30;1435:91-8. Epub 2011 Dec 1.
We previously reported that motion sickness was prevented in rats with amygdala lesion and that provocative motion stimuli increased the number of Fos-positive neurons in the amygdala, suggesting that the amygdala is one of the neural substrates involved in the development of motion sickness. NK-1 r
PMID 22192410

Japanese Journal

Volume Transmission of Substance P in Striatum Induced by Intraplantar Formalin Injection Attenuates Nociceptive Responses via Activation of the Neurokinin 1 Receptor