Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162473 (Frey)
 2,599 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was done to determine if the Fos and neurotensin immunoreactivities elicited in the rat striatal complex by the selective dopamine D2 receptor antagonist, S(-)-eticlopride hydrochloride are co-localized in the same neurons. Following injections of eticlopride, Fos and neurotensin immunoreactivity were both non-uniformly distributed among the striatal compartments and subterritories. Fos was co-localized in a significant number of small, lightly neurotensin-immunoreactive neurons, but not in a larger subset of neurons with significantly greater median diameter that exhibited intense neurotensin immunoreactivity extending well into the dendritic arbor. It is proposed that neurotensin-immunoreactive neurons lacking Fos immunoreactivity are prominent following selective blockade of the dopamine D2 receptor and represent a subset of striatal neurotensin-immunoreactive neurons. Neurotensin-immunoreactive cells containing Fos nuclei represent a distinct subset, possibly the one that is dominant following administration of reserpine [Zahm (1992) Neuroscience 46, 335-350]. Insofar as Fos expression has been reported to accompany activation of striatonigral and striatopallidal neurons, the absence of Fos in the subset of neurotensin neurons displayed following D2 receptor blockade may be at odds with activation and perhaps is more consistent with inactivation and accompanying decreased release of neurotensin [see Frey et al. (1988) Neurochem. Int. 12, 33-38, and Bean et al. (1989) J. Neurosci. 9, 4430-4438] as a mechanism underlying the accumulation of neurotensin in that subset of striatal neurons.
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PMID:Subsets of neurotensin-immunoreactive neurons in the rat striatal complex following antagonism of the dopamine D2 receptor: an immunohistochemical double-labeling study using antibodies against Fos. 830 28

The main purpose of this study was to evaluate the effects of early dexamethasone treatment on pain-related peptides at an early stage in the development of neuropathic pain induced by implantation of a sciatic nerve cuff in Sprague Dawley rats (body weight 250 to 350 g). The rats were tested for touch sensitivity with the use of von Frey filaments before and 3 d after cuff implantation (n = 12) or sham surgery (n = 6). Half of the cuff-implanted rats received dexamethasone, 1 mg/kg intraperitoneally, 1 h after surgery. Spinal cords were collected on the 3rd day after surgery, and the lumbar enlargement was processed for the detection of selected peptides (neurotensin, substance P, cholecystokinin [CCK], vasoactive intestinal peptide, and calcitonin gene-related peptide) by means of liquid chromatography and tandem mass spectrometry. The right sciatic nerve of each rat was collected, fixed, and stained for histopathological evaluation. Except for neurotensin, all the peptides showed an increased concentration with neuropathic pain; however, the differences were significant (P < 0.05) only for substance P and CCK. In the animals treated with dexamethasone, mechanical allodynia was less pronounced (P < 0.01), and only the concentration of substance P was decreased significantly (P < 0.05). Sciatic nerve sections showed a decrease in C (P < 0.01) and Adelta (P < 0.03) fibres with neuropathic pain and a nearly normal percentage of C fibres after dexamethasone treatment. The dexamethasone-treated animals also had less inflammation detectable microscopically at the nerve constriction site compared with cuff-implanted animals that were not treated with dexamethasone. Our results suggest that in the early stages of neuropathic pain induced by an inflammatory process, dexamethasone may be a useful treatment and that substance P plays an important role in pain perception.
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PMID:Early dexamethasone treatment after implantation of a sciatic-nerve cuff decreases the concentration of substance P in the lumbar spinal cord of rats with neuropathic pain. 1747 71