Literature DB >> 9174074

Chemical sensory deafferentation abolishes hypothalamic pituitary activation induced by noxious stimulation or electroacupuncture but only decreases that caused by immobilization stress. A c-fos study.

B Pan1, J M Castro-Lopes, A Coimbra.   

Abstract

We have shown in previous c-fos studies that noxious stimulation or electroacupuncture in deeply anaesthetized rats activate the hypothalamic pituitary corticotrope axis in a specific way. C-fos expression was more pronounced in the arcuate than the paraventricular hypothalamic nuclei, and none occurred in the pituitary intermediate lobe. The absence of the usual autonomic responses to psychological stress, such as tachycardia or blood pressure elevation, suggested a specific action of the somatosensory input on the hypothalamic pituitary axis. To prove this hypothesis, c-fos expression was examined in the paraventricular, arcuate and other hypothalamic nuclei, the pituitary gland, and the A1 and A2 medullary catecholaminergic cell groups of animals deprived of nociceptive primary afferent input by neonatal capsaicin. After noxious stimulation or electroacupuncture, no c-fos enhancement occurred in any of those sites in capsaicin-treated animals, and there was no increased plasma release of adrenocorticotropic hormone. In contrast, the hypothalamic pituitary c-fos activation provoked by immobilization stress though markedly decreased, was not abolished by capsaicin, whereas plasma release of adrenocorticotropic hormone remained undiminished. These findings suggest that noxious stimulation or electroacupuncture act on the hypothalamic pituitary corticotrope axis through an exclusively physical effect depending on the noxious signal elicited in the somatosensory pathway. They also demonstrate the occurrence of a minor somatosensory physical component after forced immobilization, acting on the hypothalamic pituitary axis probably together with the prevalent component of emotional arousal elicited by this form of stress.

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Year:  1997        PMID: 9174074     DOI: 10.1016/s0306-4522(96)00661-6

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


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