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Maracamall9

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Than do healthy rats [23], it is possible that although EA does not produce stress in naive rats it may induce stress in inflamed rats. However, our previous study demonstrated that the same stimulation intensity at acupoint GB30 as that used in this study did not significantly change heart rate or blood pressure, both of which are indicators of stress response, in CFA-inflamed animals [2]. This s
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Than do healthy rats [23], it is possible that although EA does not produce stress in naive rats it may induce stress in inflamed rats. However, our previous study demonstrated that the same stimulation intensity at acupoint GB30 as that used in this study did not significantly change heart rate or blood pressure, both of which are indicators of stress response, in CFA-inflamed animals [2]. This s
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Ncluding beta-endorphin. Logically, less involvement of CRH and no involvement of ACTH in EA antihyperalgesia suggest that EA may produce anti-hyperalgesia by affecting the nervous system. Our recent studies [26] demonstrate that EA activates brainstem nuclei, which are involved in descending inhibitory modulation of spinal transmission of noxious messages, to inhibit the transmission of noxious m
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Ncluding beta-endorphin. Logically, less involvement of CRH and no involvement of ACTH in EA antihyperalgesia suggest that EA may produce anti-hyperalgesia by affecting the nervous system. Our recent studies [26] demonstrate that EA activates brainstem nuclei, which are involved in descending inhibitory modulation of spinal transmission of noxious messages, to inhibit the transmission of noxious m
1
Studies and no data were given about the hippocampal subregions. Our analysis revealed a prominent expression in granule cells of the dentate gyrus as well as an expression in the cornu ammonis pyramidal cell layer. Only single cells were labelled in the hilus of the hippocampus. In comparison to rat and macaque tissue labelling was less pronounced in human tissue. This might be related to the pro
1
Studies and no data were given about the hippocampal subregions. Our analysis revealed a prominent expression in granule cells of the dentate gyrus as well as an expression in the cornu ammonis pyramidal cell layer. Only single cells were labelled in the hilus of the hippocampus. In comparison to rat and macaque tissue labelling was less pronounced in human tissue. This might be related to the pro
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Atment with a CRH antagonists, astressin and an ACTH antagonist, ACTH(11?4), prevented EA anti-edema. Taken together, these results suggest that in pathological conditions EA activates the HPA axis to increase CRH, ACTH, and glucocorticoid secretion and suppress inflammatory responses. It should be mentioned that EA significantly increased plasma ACTH levels in inflamed rats but not in naive rats,
1
Atment with a CRH antagonists, astressin and an ACTH antagonist, ACTH(11?4), prevented EA anti-edema. Taken together, these results suggest that in pathological conditions EA activates the HPA axis to increase CRH, ACTH, and glucocorticoid secretion and suppress inflammatory responses. It should be mentioned that EA significantly increased plasma ACTH levels in inflamed rats but not in naive rats,