INT8380
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Increased NPY expression was detected in both the Arcuate nucleus (ARN) and the Paraventricular nucleus (PVN) of the Hypothalamus in rats with in STZ-induced diabetes. | |||||||||||||||
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Increased NPY expression was detected in both the Arcuate nucleus (ARN) and the Paraventricular nucleus (PVN) of the Hypothalamus in rats with in STZ-induced diabetes. | |||||||||||||||
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Incubation of the hypothalamic explants with ghrelin significantly increased NPY and AGRP mRNA expression in the presence, but not absence, of dexamethasone. | |||||||||||||||
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Glucocorticoids were also necessary for ghrelin action in vivo because an intracerebroventricular injection of ghrelin significantly increased NPY and AGRP mRNA expression in the arcuate nucleus only in sham-operated, but not in adrenalectomized rats. | |||||||||||||||
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In conclusion, our observations suggest that NPY overexpression leads to reduced neuronal activity following nerve injury in a cell-specific manner. | |||||||||||||||
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Furthermore, NPY gene expression is induced within the population of medium- and large-diameter DRG neurons of the A beta-fiber class after experimental nerve injury. | |||||||||||||||
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Induction of NPY gene expression in injured DRG neurons is consistent with appearance of NPY-LI-positive end bulbs derived from regenerating sensory axons that are found in developing neuromas containing a relatively high density of transported prejunctional Y2 receptors. | |||||||||||||||
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In accord with previous studies, NAL infusion significantly increased plasma LH levels at 1400 h. concomitant with this activation of LH release, NPY gene expression was also augmented. | |||||||||||||||
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To examine further the relationship between the NAL-induced increase in LH release and increase in NPY gene expression, the effects of NPY mRNA antisense oligonucleotides (oligos) on NPY levels in the ME-ARC and on plasma LH levels were studied in NAL-infused rats. | |||||||||||||||
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In conclusion, 1) high levels of gene expression and secretion of NPY are found in a rat insulinoma cell line (INS-1). 2) Accumulation of cAMP induced by forskolin or a gluco-incretin (GLP-1) induces a further increase in NPY gene expression and release. 3) NPY secretion is not modulated by low or high glucose concentrations in the medium. 4) Induction of NPY, a known inhibitor of insulin secretion, may represent a novel counterregulatory mechanism of insulin secretion, limiting the stimulatory effect of GLP-1 on insulin secretion. | |||||||||||||||
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Increased NPY expression persisted in neurons resistant to seizure-induced cell death (6-48 h after i.p. | |||||||||||||||
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These results suggest that the increased NPY expression in laminae 3-4 of the spinal cord (the territory of the myelinated sensory input) may be crucial to the development of hyperalgesia in this model. | |||||||||||||||
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Based on experiments in the pithed guinea-pig, it is suggested that prejunctional facilitatory beta-adrenoceptors may also be involved in the regulation of the NPY release, since infusion of isoprenaline elicited a facilitation of the PNS-induced increase of plasma NPY-LI levels which could be antagonised by propranolol. | |||||||||||||||
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Because a subpopulation of neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (Arc) projects to the PVN, we measured NPY and POMC mRNA expression in the Arc using in situ hybridization histochemistry at several time points following daily administration of four different antidepressant drugs. | |||||||||||||||
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RT-PCR analyses showed that mRNA expression levels of both NPY and POMC were markedly reduced by fluoxetine treatment in all parts of the brain examined, including the hypothalamus. | |||||||||||||||
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Collectively, these results show that a decrease in opioid influence rapidly augments NPY gene expression in a subpopulation of neurons in the ARC, and support the hypothesis that a disinhibition from opioid influence acutely promotes NPY synthesis and release, which is necessary for phasic LH discharge in rats. | |||||||||||||||
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Furthermore, a marked upregulation of NPY (Y1) receptor mRNA expression was detected in the ipsilateral spinal dorsal horn 1 d and 3 d after inoculation. | |||||||||||||||
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Two weeks after footshock treatment NPY mRNA expression was increased in the basolateral amygdala and showed preshockxnoise interaction in the locus coeruleus (down after noise in controls, lower basal and unchanged after noise in preshocked). | |||||||||||||||
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However, in other brain regions, fluoxetine administration caused a differential effect on the induction of NPY-related genes in the two rat strains: in the CA region and dentate gyrus NPY mRNA expression was increased in the FSL, but decreased in the FRL. | |||||||||||||||
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In the FSL rats, NPY mRNA expression levels were significantly decreased in the nucleus accumbens and CA regions, but increased in the arcuate nucleus and anterior cingulate cortex. | |||||||||||||||
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