Title of article :
Exploration of P2X3 in the rat stellate ganglia after myocardial ischemia
Author/Authors :
Shao، نويسنده , , Li-Jian and Liang، نويسنده , , Shang-Dong and Li، نويسنده , , Gui-Ling and Xu، نويسنده , , Chang-Shui and Zhang، نويسنده , , Chun-Ping، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
Pages :
8
From page :
330
To page :
337
Abstract :
Summary implicated in peripheral pain signaling by actions on P2X receptors, especially P2X3 receptor. Cardiac primary afferents running in the sympathetic nerves are considered to be essential pathways for transmission of cardiac nociception to the central nervous system. Because little is known about P2X3 involvement in cardiac nociception, this study observed the difference in P2X3 localization and expression in stellate ganglia (SG) from naive rats and in a pathological model of myocardial ischemic injury induced by repeated subcutaneous isoprenaline injections. Distribution of P2X3 and morphometry of neurons in SG were investigated by immunohistochemistry, Western blotting, in situ hybridization (ISH) and by sterological study. Diffuse cytoplasmic P2X3 immunolabelling was observed by light microsocopy. No nuclear labeling was detected. The intensity of P2X3 labeling in the experimental myocardial ischemic injury group was increased in relation to that of the control group. Numerical densities of stellate ganglion neurons in the experimental group were higher than those of the control group. By Western blotting and ISH, the signals of P2X3 protein and its mRNA in the myocardial ischemic group were higher than those of the control group. The P2X3 labeling intensity and the numerical density in SG of the experimental myocardial ischemic injury group were enhanced, suggesting the involvement of P2X3 receptor for the transmission of pain after myocardial ischemic injury.
Keywords :
stellate ganglia , P2X3 receptor , Myocardial Ischemia
Journal title :
Acta Histochemica
Serial Year :
2007
Journal title :
Acta Histochemica
Record number :
1759518
Link To Document :
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