Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent in vivo and in vitro studies have shown the involvement of gamma-aminobutyric acid (GABA) in analgesia. We investigated if the analgesia induced by an acute valproic acid (VPA) administration might be related to the activation of the enkephalinergic system. VPA administration (i.p.) induces 30 min after treatment a significant and dose-dependent increase of Leu-enkephalin and Met-enkephalin in the striatum, hypothalamus, cortex and brainstem. In the hypophysis no modification was observed for these two neuropeptides. The Met-enkephalin-Arg-Gly-Leu levels are affected by VPA administration in a more complex pattern. Such results suggest the implication of an enkephalinergic system in GABAergic analgesia.
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PMID:Analgesic properties of valproic acid might be related to activation of pro-enkephalin system in rat brain. 310 87

Previous studies in this laboratory have shown that electroacupuncture (EA) accelerated the release of enkephalin in the spinal cord. The present study was undertaken to investigate the effect of EA stimulation on the expression of preproenkephalin (PPE) mRNA in the rat spinal cord and medulla by in situ hybridization histochemical technique. Animals were administrated with 2 Hz EA stimulation (1-2-3 mA, 30 min) applied at acupoints sanyingjiao and zusanli of one hind leg. The rats were perfused 24 h after EA, and quantitative changes of PPE-mRNA expression were determined by emulsion autoradiography. EA stimulation was found to increase the number of neurons expressing PPE-mRNA in spinal cord and medulla. Increased expression of PPE-mRNA was more marked in ipsilateral dorsal horn of spinal cord (especially in laminae III-IV and contralateral ventromedial medulla (especially in the lateral paragigantocellular reticular nucleus). The results provide evidence in support of the enkephalinergic hypothesis of acupuncture analgesia. It is suggested that increased biosynthesis of enkephalin precursor would help to compensate for the loss of tissue storage of enkephalin during the period of EA stimulation.
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PMID:[Electroacupuncture enhances enkephalin mRNA expression in the spinal cord and medulla, an in situ hybridization study]. 829 16

FLFQPQRF-NH2 (F8Famide; morphine-modulating peptide), isolated from bovine brain, is an FMRFamide-like peptide with opioid analgesia modulating effects. In the rat brain, F8Famide is immunohistochemically localized in neurons of the medial hypothalamus and medulla oblongata. Neuropeptide Y (NPY) is structurally related to F8Famide and the mammalian FMRFamide-like immunoreactivity (LI) was once thought to be due to an NPY-like peptide. We compared the anatomical distribution of F8Famide-LI with the localization of enkephalin- and NPY-LI-containing structures in the rat brain to find out if NPY or enkephalins coexist with F8Famide-LI. Cryostat sections of colchicine-treated Wistar rat brains were incubated with specific antisera against F8Famide, NPY, YGGFMRGL (Met-enkephalin-Arg-Gly-Leu), or YGGFMRF (Met-enkephalin-Arg-Phe) raised in rabbits. The immunoreactivity was visualized by the peroxidase - antiperoxidase or immunofluorescence method. The light microscopic mirror method was applied to study the colocalization of F8Famide and NPY. The F8Famide-immunoreactivity was concentrated in smaller areas of medial hypothalamus and nucleus of the solitary tract than that of enkephalins and NPY. In all brain areas, the distributions of F8Famide-, enkephalin- and NPY-immunoreactive neurons were distinct. F8Famide-, NPY- and enkephalin-LI-containing nerve terminals were seen in the nucleus of the solitary tract and in the lateral parabrachial nucleus. These results show that the neuronal systems containing F8Famide-, enkephalin- or NPY-LI are anatomically separate in all brain regions. However, there are terminal areas in which more than one type of these immunoreactivities are detected. These results have anatomical correlation with pharmacological reports, suggesting modulatory functions for these peptides on regulation of blood pressure, feeding behaviour and endocrine functions.
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PMID:Comparative Distribution of Neurons Containing FLFQPQRFamide-like (morphine-modulating) Peptide and Related Neuropeptides in the Rat Brain. 1210 16

Loss-of-function mutations in the SCN9A gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain in humans and mice. Surprisingly, many potent selective antagonists of Nav1.7 are weak analgesics. We investigated whether Nav1.7, as well as contributing to electrical signalling, may have additional functions. Here we report that Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons. In contrast, Nav1.8-null mutant sensory neurons show no upregulated Penk mRNA expression. Application of the opioid antagonist naloxone potentiates noxious peripheral input into the spinal cord and dramatically reduces analgesia in both female and male Nav1.7-null mutant mice, as well as in a human Nav1.7-null mutant. These data suggest that Nav1.7 channel blockers alone may not replicate the analgesic phenotype of null mutant humans and mice, but may be potentiated with exogenous opioids.
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PMID:Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7. 2663 8