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      Hyperinnervation during Adrenal Regeneration Influences the Rate of Functional Recovery

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          The rat adrenal cortex has the uncommon ability to demonstrate morphological and functional regeneration after injury-induced loss of cortical tissue. Peripheral nerves are involved in tissue regeneration and healing after injury, implying that nerves may also be involved in modulating the regeneration of the adrenal cortex. Studies were initiated to assess changes in adrenal innervation during cortical tissue regeneration subsequent to adrenal enucleation. Innervation of regenerating adrenals was assessed from 3 to 62 days postenucleation by immunohistofluorescent detection of neuronal markers for primary afferent, preganglionic sympathetic, and postganglionic sympathetic fibers. The regenerating adrenal contained few nerves at 3 days postenucleation, but became differentially innervated, with extensive innervation by nerve fibers positive for calcitonin gene-related peptide (CGRP), tyrosine hydroxylase (TH), neuropeptide Y (NPY), and neuronal nitric oxide synthase (nNOS). In contrast, there was only minimal innervation by nerve fibers positive for vasoactive intestinal peptide. By 14 days postenucleation, the CGRP-, TH-, and NPY-positive innervation included areas of hyperinnervation in the capsule, cortex, and central inflammatory site of the regenerating gland. In addition, many chromaffin cells were present at all time points postenucleation. Quantification of the regenerating gland content of CGRP, norepinephrine, epinephrine, and nNOS verified the immunohistofluorescent observations. The period of extensive innervation correlated temporally with the time (3–30 days) during which the regenerating glands recovered steroidogenic function. Moreover, splanchnic nerve transection at the time of adrenal enucleation decreased the innervation by CGRP-positive and vesicular acetylcholine transporter-positive fibers and delayed regeneration. These results support the hypothesis that adrenal innervation modulates tissue regeneration and functional recovery of the enucleated adrenal gland.

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          Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity.

          Experimental inflammation produced by an intraplantar injection of complete Freund's adjuvant results in local sensory hypersensitivity and up-regulates the neuropeptides substance P and calcitonin gene related peptide in the primary sensory neurons innervating the inflamed tissue. The inflammation also elevates nerve growth factor levels in the skin. Systemic administration of anti-NGF neutralizing antibodies prevent the behavioral sensitivity, the up-regulation of neuropeptides and the inflammation-induced expression of the immediate early gene c-fos in dorsal horn neurons, without modifying swelling and erythema. Elevation of the neurotrophin NGF in the periphery is a major contributor, therefore, of inflammatory pain.
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            Sprouting of CGRP nerve fibers in response to dentin injury in rat molars.

            Light and electron microscopic immunocytochemistry showed extensive increases in the number of calcitonin gene-related peptide immunoreactive (CGRP-IR) nerve fibers subjacent to injured root dentin of rat molars. Sprouting was greatest at 4 days and returned to normal 10-21 days post injury. Non-CGRP-IR fibers were also increased at 4 days. The results suggest that rapid reversible sprouting of sensory nerve fibers may be an integral part of tissue reactions to injury.
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              Substance P-containing sensory neurons in the rat dorsal root ganglia innervate the adrenal medulla


                Author and article information

                S. Karger AG
                February 2000
                18 February 2000
                : 71
                : 2
                : 107-123
                Departments of Neuroscience and Surgery, University of Minnesota, Minneapolis, Minn., USA
                54527 Neuroendocrinology 2000;71:107–123
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 12, Tables: 2, References: 70, Pages: 17
                Stress and the Pituitary-Adrenal Axis


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