Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sensitivity to the pungent vanilloid, capsaicin, defines a subpopulation of primary sensory neurons that are mainly polymodal nociceptors. The recently cloned vanilloid receptor subtype 1 (VR1) is activated by capsaicin and noxious heat. Using combined in situ hybridization and histochemical methods, we have characterized in sensory ganglia the expression of VR1 mRNA. We show that this receptor is almost exclusively expressed by neurofilament-negative small- and medium-sized dorsal root ganglion cells. Within this population, VR1 mRNA is detected at widely varying levels in both the NGF receptor (trkA)-positive, peptide-producing cells that elicit neurogenic inflammation and the functionally less characterized glial cell line-derived neurotrophic factor-responsive cells that bind lectin Griffonia simplicifolia isolectin B4 (IB4). Cells without detectable levels of VR1 mRNA are found in both classes. A subpopulation of the IB4-binding cells that produce somatostatin has relatively low levels of VR1 mRNA. A previously uncharacterized population of very small cells that express the receptor tyrosine kinase (RET) and that do not label for trkA or IB4-binding has the highest relative levels of VR1 mRNA. The majority of small visceral sensory neurons of the nodose ganglion also express VR1 mRNA, in conjunction with the BDNF receptor trkB but not trkA. Axotomy results in the downregulation of VR1 mRNA in dorsal root ganglion cells. Our data emphasize the heterogeneity of VR1 mRNA expression by subclasses of small sensory neurons, and this may result in their differential sensitivity to chemical and noxious heat stimuli. Our results also indicate that peripherally derived trophic factors may regulate levels of VR1 mRNA.
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PMID:Differential expression of the mRNA for the vanilloid receptor subtype 1 in cells of the adult rat dorsal root and nodose ganglia and its downregulation by axotomy. 1002 68

Immunohistochemistry for the somatostatin sst2A receptor was performed on the rat trigeminal ganglion to know its function in the trigeminal nervous system. The immunoreactivity was detected in 9.4% of primary sensory neurons in the ganglion. These neurons were small to medium-sized (range=106.5-1123.2 microm(2); mean+/-S.D.=506.3+/-213.2 microm(2)) and predominantly located in the rostromedial part of the ophthalmo-maxillary division. They were also immunoreactive for calcitonin gene-related peptide and the vanilloid receptor subtype 1. In addition, 13.7% of trigeminal neurons which were retrogradely traced with fluorogold from the nasal mucosa exhibited sst2A receptor-immmunoreactivity. Trigeminal neurons which innervated the facial skin and tooth pulp were devoid of the immunoreactivity. In the brainstem trigeminal sensory nuclear complex, both the neuronal cell body and the neuropil exhibited sst2A receptor-immunoreactivity in the superficial medullary dorsal horn.The present study indicates that sst2A receptor-immunoreactive trigeminal nociceptors innervate the nasal mucosa. They may project to the superficial laminae of the medullary dorsal horn.
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PMID:The somatostatin sst2A receptor in the rat trigeminal ganglion. 1289 20

Immunohistochemistry for substance P, somatostatin and vanilloid receptor subtype 1 as well as receptors for somatostatin and opioids was performed on the trigeminal ganglion in wild-type and Brn-3a knockout mice at postnatal day 0. In wild-type mice, the trigeminal ganglion contained abundant substance P-, vanilloid receptor subtype 1-, sst2A receptor- and delta-opioid receptor-immunoreactive neurons, while the ganglion had only a few mu-opioid receptor-immunoreactive neurons. The Brn-3a deficiency had an effect on the cell size but not the number of substance P-immunoreactive neurons. In knockout mice, the proportion of small immunoreactive neurons markedly increased and that of medium- to large-sized immunoreactive ones correspondingly decreased (mean +/- S.D. = 54.7 +/- 29.1 microm2, range = 10.9-220.8 microm2) compared to wild-type mice (mean +/- S.D. = 116.6 +/- 58.6 microm2, range = 27.3-400.7 microm2). As for vanilloid receptor subtype 1-immunoreactive neurons, the number and cell size was barely affected by the deficiency. On the other hand, the loss of Brn-3a caused a decrease in the number of sst2A receptor- or delta-opioid receptor-immunoreactive neurons (more than 95% reduction) and an increase in the number of mu-opioid receptor-immunoreactive neurons (9.3-fold increase). Somatostatin-immunoreactive neurons were not detected in the trigeminal ganglion of wild-type or mutant mice at postnatal day 0. The present study suggests that Brn-3a deficiency may have effects on the survival of trigeminal nociceptors and their expression of some neurochemical substances.
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PMID:Effect of Brn-3a deficiency on primary nociceptors in the trigeminal ganglion. 1574 Aug 7