4,656 research outputs found
Obidoxime Antagonizes the Neuromuscular Failure Induced by Neostigmine and Diisopropylfluorophosphate via Different Mechanisms
No full textA Selective Inhibitor of C-AMP-Specific Phosphodiesterase, Ro 20-1724, has No Effect on the Quantal Release of Acetylcholine from the Mouse Phrenic Nerve
No full textImprovement by diazepam of Neuromuscular Transmission Blocked by Anticholinesterase Agents in Mouse Diaphragms
No full textAntagonisms Against Anticholinesterase Agents by β-Eudesmol, Benzodiazepines and Obidoxime in Neuromuscular Junction
No full textDifferential Antagonism by Naloxone Benzoylhydrazone of the Activation of Inward Rectifying K+ Channels by Nociceptin and a Mu-Opioid in Rat Periaqueductal Grey Slices
No full textA novel receptor, the opioid receptor-like orphan receptor ( ORL1), is homologous to, but distinct from, classical opioid receptors. Although initially developed as an opioid receptor ligand, naloxone benzoylhydrazone (NalBzOH) is one of the few antagonists at ORL1. The present electrophysiological study of the effects of NalBzOH on the activation of ORL1 and mu-opioid receptors was performed in brain slices of the ventrolateral periaqueductal grey (PAG), a crucial site for opioid- induced supraspinal analgesia. Both orphanin FQ/nociceptin (OFQ/N), an ORL 1 agonist, and [D -Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO), a mu-opioid receptor agonist, activated inwardly rectifying K+ (Kir) channels in the ventrolateral PAG. Of the neurons tested, 96 % responded to OFQ/N, but only 65% to DAMGO. NalBzOH (3-30 microM) antagonized the effect of OFQ/N competitively with a pA2 of 5.67. NalBzOH also antagonized, but more potently and non-competitively, the effect of DAMGO. In contrast, NalBzOH did not affect baclofen-induced activation of Kir channels. NalBzOH alone, at concentrations up to 30 microM, had little effect on this inwardly rectifying channel. It is concluded that NalBzOH antagonizes the activation of Kir channels mediated by both ORL1 and mu-opioid receptors in the ventrolateral PAG. It acts not only as a competitive antagonist at ORL1, but also as a more potent and non- competitive antagonist at mu- opioid receptors
β-Eudesmol Antagonizes Diisopropyl Fluorophosphate-Induced Lethal Toxicity and Electric Shock-Induced Convulsion
No full textQuantitative study of the antagonistic effect of (-)-cis-1-Methyl-7-[[4-(2,6-dichlorophenyl)piperidin-1-yl] methyl]-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol (SB-612111) on nociceptin/orphanin FQ-mediated potassium channel activation in rat periaqueductal gray slices
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Antiallodynic Effects of Intrathecal Orexins in a Rat Model of Postoperative Pain
No full textOrexin A and B (hypocretin 1 and 2) are the endogenous ligands of orexin receptors, a G-protein-coupled orphan receptor family containing orexin 1 (OX1) and orexin 2 (OX2) types. Orexin A induces analgesia in acute and inflammatory pain models. We further elucidated the possible antiallodynic effect of intrathecal orexins in a rat model of postoperative pain. Mechanical allodynia was induced by incising the rat hind paw and evaluated with the withdrawal threshold to von Frey filament stimulation. Intrathecal orexin A (0.03-1 nmol) and orexin B (0.1-3 nmol) dose dependently attenuated the incision-induced allodynia. Orexin A (ED50 = 0. 06 nmol) is more potent than orexin B. The effects of orexin A and B were abolished by their respective antibodies, but not by naloxone, and were attenuated by suramin and strychnine, the P-2X purinergic and glycine receptor antagonists, respectively. SB-334867, an OX1 receptor antagonist, at 30 nmol completely blocked the effect of orexin A but, even at 100 nmol, only partially antagonized the effect of orexin B. Orexin A antibody , SB- 334867, suramin, strychnine, or naloxone enhanced the incision- induced allodynic response. It is concluded that intrathecal orexins reduce incision-induced allodynia through OX1 receptors. Glycine and P-2X purinergic receptors , but not opioid receptors, might be involved in the antiallodynic effects of orexins. Endogenous orexin might be released after incision injury to activate the spinal OX1 receptors as an endogenous analgesic protector
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