Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injuries to the cauda equina and conus medullaris of the spinal cord commonly result in paraplegia, sensory deficits, neuropathic pain, as well as bladder, bowel, and reproductive dysfunctions. In a recently developed lower motoneuron model for cauda equina injury and repair, we have demonstrated that an acute surgical implantation of avulsed lumbosacral ventral roots into the conus medullaris is neuroprotective, promotes regeneration of efferent spinal cord axons into the implanted roots, and may result in functional reinnervation of the lower urinary tract. Here, we investigated the effects of a bilateral lumbosacral ventral root avulsion (VRA) injury and re-implantation on the morphology of the rat bladder at twelve weeks post-operatively. We demonstrated a VRA-induced overall thinning of the bladder wall, which exhibited reduced thickness of both the lamina propria and smooth muscle. In contrast, the bladder epithelium markedly increased its thickness in the injured series. Quantitative immunohistochemical studies showed a selective increase in CGRP immunoreactivity in the lamina propria after the VRA injury. Interestingly, the injury-induced changes in bladder wall morphology were ameliorated by an acute implantation of the lesioned roots into the conus medullaris. Specifically, bladders of the implanted group showed a partial restoration of the thickness of the lamina propria and epithelium as well as a return of CGRP immunoreactivity to baseline levels in the lamina propria. Our results support the notion that surgical implantation of severed ventral roots into the spinal cord may promote the recovery of a normal morphological phenotype in peripheral end organs.
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PMID:Surgical implantation of avulsed lumbosacral ventral roots promotes restoration of bladder morphology in rats. 1876 Feb 75

Innervation is required to preserve several aspects of skin homeostasis. Previous studies in rodents have shown that sciatic nerve transection leads to epidermal thinning and reduced keratinocyte proliferation. As the sciatic nerve is composed of sensory and motor axons, it is not clear whether skin alterations reflect motor or sensory disturbances. In this study, we used neonatal capsaicin treatment to evaluate whether sensory chemical denervation affects keratinocyte proliferation at 1, 3, and 6 months of age. Using design-based stereological methods, we estimated the total length of intraepidermal nerve fibers (IENF) that were of peptidergic type and the number of bromodeoxyuridine-labeled (BrdU(+) ) nuclei in the hind paw glabrous epidermis of control and capsaicin-treated rats. We found that the treatment decreased the total fiber length of IENF immunoreactive for both protein gene product 9.5 (PGP(+) ) and of IENF immunoreactive for calcitonin gene-related peptide (CGRP(+) ). The length of PGP(+) fibers decreased by 83%, 81%, and 77% and that of CGRP(+) fibers decreased by 48%, 58%, and 58% at 1, 3, and 6 months, respectively. Double-immunofluorescence staining for neural beta III tubulin and CGRP revealed that the majority of the remaining fibers in the epidermis after capsaicin treatment were of peptidergic type. The number of BrdU(+) nuclei was similar in both groups. Our findings suggest that IENF present after capsaicin treatment are sufficient to maintain epidermal replacement.
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PMID:Long-term effects of neonatal capsaicin treatment on intraepidermal nerve fibers and keratinocyte proliferation in rat glabrous skin. 2115 28

Besides their deleterious action on cardiac muscle, anthracycline-type cytostatic agents exert significant neurotoxic effects on primary sensory neurons. Since cardiac sensory nerves confer protective effects on heart muscle and share common traits with cutaneous chemosensitive nerves, this study examined the effects of cardiotoxic doses of adriamycin on the function and morphology of epidermal nerves. Sensory neurogenic vasodilatation, plasma extravasation, and the neural CGRP release evoked by TRPV1 and TRPA1 agonists in vitro were examined by using laser Doppler flowmetry, the Evans blue technique, and ELISA, respectively. Carrageenan-induced hyperalgesia was assessed with the Hargreaves method. Immunohistochemistry was utilized to study cutaneous innervation. Adriamycin treatment resulted in profound reductions in the cutaneous neurogenic sensory vasodilatation and plasma extravasation evoked by the TRPV1 and TRPA1 agonists capsaicin and mustard oil, respectively. The in vitro capsaicin-, but not high potassium-evoked neural release of the major sensory neuropeptide, CGRP, was markedly attenuated after adriamycin treatment. Carrageenan-induced inflammatory hyperalgesia was largely abolished following the administration of adriamycin. Immunohistochemistry revealed a substantial loss of epidermal TRPV1-expressing nociceptive nerves and a marked thinning of the epidermis. These findings indicate impairments in the functions of TRPV1 and TRPA1 receptors expressed on cutaneous chemosensitive nociceptive nerves and the loss of epidermal axons following the administration of cardiotoxic doses of adriamycin. Monitoring of the cutaneous nociceptor function in the course of adriamycin therapy may well be of predictive value for early detection of the deterioration of cardiac nerves which confer protection against the deleterious effects of the drug.
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PMID:Multiple impairments of cutaneous nociceptor function induced by cardiotoxic doses of Adriamycin in the rat. 2734 18