Immunohistochemical localization of the high‐affinity NGF receptor (gp 140‐<i>trk</i>A) in the adult human dorsal root and sympathetic ganglia and in the nerves and sensory corpuscles supplying digital skin

Vega, J.A.; Vázquez, Esther; Naves, F.J.; Soto, Miguel; Calzada, Begoña Calvo; Represa, Juan

doi:10.1002/ar.1092400415

Cited by 58 publications

(32 citation statements)

References 57 publications

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“…TrkA-like IR was also reported in human cuatenous Meissner and Pacinian corpuscles (Vega et al, 1994b). Furthermore, both p75 (Chesa et al, 1988;Wyatt et al, 1990;Narisawa et al, 1992;Vega et al, 1992Vega et al, , 1993English et al, 1994) and TrkA (Vega et al, 1994b;Shibayama and Koizumi, 1996) are expressed too in different cutaneous nonnervous tissues.…”

Section: Nerves and Sensory Corpusclesmentioning

confidence: 85%

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

et al. 1998

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Human skin, including nerves and sensory corpuscles, displays immunoreactivity (IR) for low-(p75) and high-affinity (TrkA-like) receptors for nerve growth factor (NGF), the best characterized member of the family of neurotrophins. This study was designed to analyze the changes induced by spinal cord and peripheral nerve injuries in the expression of neurotrophin receptors in digital skin, with special reference to nerves and sensory corpuscles.Skin biopsy samples were obtained from 1) the hand and toes of normal subjects, 2) below the level of the lesion of patients with spinal cord injury affecting dorsal and lateral funiculi, 3) the cutaneous territory of entrapped peripheral nerves (median and ulnar nerves), and 4) the cutaneous territory of sectioned and grafted nerves (median nerve). The pieces were formalinfixed and paraffin-embedded, cut in serial sections, and processed for immunohistochemistry using antibodies against human p75 and TrkA proteins. The percentage of sensory corpuscles displaying IR for p75 and TrkA-like, as well as the intensity of IR developed within them, was assessed using quantitative image analysis.Spinal cord severance causes a decrease in p75 IR in Meissner and Pacinian corpuscles, whereas TrkA-like IR did not vary. In other nonnervous tissues (i.e., epidermis, sweat glands), both p75 and TrkA-like IR was diminished or even absent. Similar but more severe changes were encountered in the skin from the territory of entrapped nerves. Finally, in subjects with sectioned-grafted nerves, p75 IR was found close to controls in nerves, reduced in Meissner corpuscles, and absent in the inner core of the Pacinian ones; TrkA-like IR was in the perineurium, a small percentage of Meissner corpuscles (about 7%), and the outer core and capsule of the Pacinan corpuscles. In the nonnervous tissues, p75 IR was practically absent, whereas TrkA-like IR did not change. No changes in the expression of neurotrophin receptors were observed in Merkel cells of the different groups.Present results show the following: 1) expression of nerve p75 IR in human cutaneous sensory corpuscles is sensitive to central deafferentation, to blockade or difficulty in axonal transport, and to disruption of axonal

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Section: Nerves and Sensory Corpusclesmentioning

confidence: 85%

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

et al. 1998

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“…Vega et al [37] previously reported the occurrence of TrkA immunoreactivity in perineurial cells, endoneurial fibroblasts, Schwann cells and large axons of the nerve truncus supplying human digital skin. In the present study, using the same commercial antibody as that used by the previous authors, we have demonstrated the presence of TrkA immunoreactivity in perineurial cells and axons of the carotid body.…”

Section: Discussionmentioning

confidence: 98%

“…They were then incubated with a rabbit anti-TrkA antibody (Santa Cruz Biotechnology, Inc., Santa Cruz, CA) at 1 mg/ml overnight at room temperature. The specificity of this antibody was characterized in a previous study [37]. After washing with PBS, the immunoreaction sites were made visible by incubating the sections successively at room temperature with a biotinylated anti-rabbit IgG antibody (Vector Laboratories, Inc., Burlingame, CA) diluted at 1:200 in PBS for 1 hr, streptavidin-conjugated horseradish peroxidase (Dakopatts) diluted at 1:500 in PBS for 1 hr, and finally with a mixture of 0.01% 3'-diaminobenzidine tetrahydrochloride and 0.02% hydrogen peroxide in 50 mM Tris-HCl buffer, pH 7.6 [2].…”

Section: Immunohistochemistrymentioning

confidence: 99%

Co-expression of NGF and Its High-affinity Receptor TakA in the Rat Carotid Body Chief Cells

Yamamoto

Iseki

2003

Acta Histochem. Cytochem

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The expression and localization of NGF and its high-affinity receptor, TrkA, in the rat carotid body was investigated by use of in situ hybridization and immunohistochemistry, respectively. The immunoreactivity for TrkA was detected in most of chief cells and sustentacular cells, as well as in some nerve axons and perineurial cells, but not in Schwann cells. In electron microscopy, the immunoreactivity was localized to the cytoplasm. The mRNA for NGF was localized to most of chief cells and possibly also to sustentacular cells. These results demonstrated that carotid body chief cells, having the neural crest origin, produce both NGF and TrkA, implying a paracrine-autocrine role of NGF in the carotid body.

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“…In the skin, NTRK1 is expressed in specialized sensory cells (Meissner corpuscles, Pacinian corpuscles, and Merkel-neurite mechanoreceptors). 9 Innervation and development of Merkel cells has been shown to be dependent on NTRK1. 10 Thus, NTRK1 is apparently responsible for normal development of several aspects of peripheral pain sensation.…”

Section: Discussionmentioning

confidence: 99%

An Infant With Primary Tooth Loss and Palmar Hyperkeratosis: A Novel Mutation in the NTRK1 Gene Causing Congenital Insensitivity to Pain With Anhidrosis

Bonkowsky¹,

Johnson

Carey³

et al. 2003

Pediatrics

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ABSTRACT. Patients with congenital insensitivity to pain and anhidrosis (CIPA), caused by mutations in the NTRK1 gene, can be difficult to diagnose because of their variable presentation, the lack of simple diagnostic tests, and the paucity of cases reported in North America. We describe a 1-year-old infant who had tooth loss and palmar hyperkeratosis as the primary manifestations of CIPA. He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered, but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture. Nerve conduction studies were normal, as was his response to subdermal histamine injection. Sequence analysis of his NTRK1 gene revealed 2 mutations: 1 mutation is novel, while the other has been described previously in a patient of northern European descent. An antibody directed against NTRK1 revealed persistent expression in keratinocytes, consistent with the mutations in this patient. Skin biopsy specimens revealed a lack of epidermal and sweat gland innervation. Immunohistochemistry of skin biopsy specimens, together with routine nerve conduction studies, can provide quick and reliable confirmation if CIPA is clinically suspected. Pediatrics 2003;112:e237-e241. URL: http://www.pediatrics.org/cgi/content/full/112/3/e237; CIPA, NTRK1, tooth loss, hyperkeratosis, insensitivity to pain.

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Immunohistochemical localization of the high‐affinity NGF receptor (gp 140‐trkA) in the adult human dorsal root and sympathetic ganglia and in the nerves and sensory corpuscles supplying digital skin

Cited by 58 publications

References 57 publications

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

Co-expression of NGF and Its High-affinity Receptor TakA in the Rat Carotid Body Chief Cells

An Infant With Primary Tooth Loss and Palmar Hyperkeratosis: A Novel Mutation in the NTRK1 Gene Causing Congenital Insensitivity to Pain With Anhidrosis

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