The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
James M Fujimoto - One of the best experts on this subject based on the ideXlab platform.
-
antianalgesic action of nociceptin originating in the brain is mediated by spinal prostaglandin e 2 in mice
Journal of Pharmacology and Experimental Therapeutics, 2001Co-Authors: Jodie J. Rady, William B Campbell, James M FujimotoAbstract:An antianalgesic action of Intracerebroventricularly administered nociceptin was elicited against intrathecal morphine-induced antinociception in the tail-flick test in mice and investigated as a descending neuronal system for the spinal mediator involved. The nociceptin-induced antianalgesia originating in the brain was inhibited by intrathecally administered indomethacin and suggested the mediation of spinal prostaglandin. The antianalgesic action of Intracerebroventricular nociceptin was closely matched by intrathecal prostaglandin (PG) E 2 . Both shifted the dose-response curve of morphine to the right and these actions were eliminated by intrathecal PGD 2. Desensitization of the antianalgesic action of PGE 2 by intrathecal PGE 2 pretreatment also produced cross-desensitization to the antianalgesic action of Intracerebroventricular nociceptin. Neither Intracerebroventricular nociceptin nor intrathecal PGE 2 produced antianalgesia against the δ-receptor agonists given intrathecally. Thus, the antianalgesic action of nociceptin originating in the brain is coupled to a descending neuronal pathway mediated by spinal PGE 2 .
-
supraspinal flumazenil inhibits the antianalgesic action of spinal dynorphin a 1 17
Pharmacology Biochemistry and Behavior, 1998Co-Authors: Jodie J. Rady, Blythe B Holmes, James M FujimotoAbstract:Abstract DynorphinA (Dyn) administered intrathecally or released spinally in mice produces antianalgesia, that is, antagonizes morphine analgesia (tail-flick test). Spinal transection eliminates this Dyn antianalgesia. Present results in mice show that Intracerebroventricular administration of flumazenil, a benzodiazepine receptor antagonist, also eliminated the antianalgesic action of Dyn; flumazenil in the brain eliminated the suppressant effect of intrathecal Dyn on intrathecal and Intracerebroventricular morphine-induced antinociception. Intracerebroventricular clonidine, naloxone, and norbinaltorphimine release spinal Dyn. The latent antinociceptive actions of these compounds were uncovered by Intracerebroventricular flumazenil. Thus, Dyn, given intrathecally or released spinally, activates a pathway that is inhibited by Intracerebroventricular flumazenil. Dyn antianalgesia is not significantly altered by Intracerebroventricular administration of bicuculline and picrotoxin, suggesting that activation of the gamma-aminobutyric acid receptor has little if any involvement in the antianalgesic action of Dyn. The antagonistic effect of Dyn seems to be mimicked by benzodiazepine agonists. Furthermore, administration of a benzodiazepine receptor inverse agonist (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate) inhibited Dyn antianalgesia as did flumazenil. Thus, flumazenil, through a benzodiazepine antagonist or inverse agonist action, interrupts, as does spinal transection, the neuronal circuit (cord/brain/cord) necessary for the antianalgesic action of spinal Dyn. Because Dyn antianalgesia is an indirect action, activation of the neuronal circuit must lead to the release of a direct-acting antianalgesic mediator in the spinal cord.
-
Supraspinal Flumazenil Inhibits the Antianalgesic Action of Spinal Dynorphin A [1–17]
Pharmacology Biochemistry and Behavior, 1998Co-Authors: Jodie J. Rady, Blythe B Holmes, James M FujimotoAbstract:Abstract DynorphinA (Dyn) administered intrathecally or released spinally in mice produces antianalgesia, that is, antagonizes morphine analgesia (tail-flick test). Spinal transection eliminates this Dyn antianalgesia. Present results in mice show that Intracerebroventricular administration of flumazenil, a benzodiazepine receptor antagonist, also eliminated the antianalgesic action of Dyn; flumazenil in the brain eliminated the suppressant effect of intrathecal Dyn on intrathecal and Intracerebroventricular morphine-induced antinociception. Intracerebroventricular clonidine, naloxone, and norbinaltorphimine release spinal Dyn. The latent antinociceptive actions of these compounds were uncovered by Intracerebroventricular flumazenil. Thus, Dyn, given intrathecally or released spinally, activates a pathway that is inhibited by Intracerebroventricular flumazenil. Dyn antianalgesia is not significantly altered by Intracerebroventricular administration of bicuculline and picrotoxin, suggesting that activation of the gamma-aminobutyric acid receptor has little if any involvement in the antianalgesic action of Dyn. The antagonistic effect of Dyn seems to be mimicked by benzodiazepine agonists. Furthermore, administration of a benzodiazepine receptor inverse agonist (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate) inhibited Dyn antianalgesia as did flumazenil. Thus, flumazenil, through a benzodiazepine antagonist or inverse agonist action, interrupts, as does spinal transection, the neuronal circuit (cord/brain/cord) necessary for the antianalgesic action of spinal Dyn. Because Dyn antianalgesia is an indirect action, activation of the neuronal circuit must lead to the release of a direct-acting antianalgesic mediator in the spinal cord.
Frans H H Leenen - One of the best experts on this subject based on the ideXlab platform.
-
role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt induced hypertension in dahl salt sensitive rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: Bing S Huang, Roselyn White, Arco Y Jeng, Frans H H LeenenAbstract:In Dahl salt-sensitive (S) rats, high salt intake increases cerebrospinal fluid (CSF) Na+ concentration ([Na+]) and blood pressure (BP). Intracerebroventricular (ICV) infusion of a mineralocorticoi...
Jodie J. Rady - One of the best experts on this subject based on the ideXlab platform.
-
antianalgesic action of nociceptin originating in the brain is mediated by spinal prostaglandin e 2 in mice
Journal of Pharmacology and Experimental Therapeutics, 2001Co-Authors: Jodie J. Rady, William B Campbell, James M FujimotoAbstract:An antianalgesic action of Intracerebroventricularly administered nociceptin was elicited against intrathecal morphine-induced antinociception in the tail-flick test in mice and investigated as a descending neuronal system for the spinal mediator involved. The nociceptin-induced antianalgesia originating in the brain was inhibited by intrathecally administered indomethacin and suggested the mediation of spinal prostaglandin. The antianalgesic action of Intracerebroventricular nociceptin was closely matched by intrathecal prostaglandin (PG) E 2 . Both shifted the dose-response curve of morphine to the right and these actions were eliminated by intrathecal PGD 2. Desensitization of the antianalgesic action of PGE 2 by intrathecal PGE 2 pretreatment also produced cross-desensitization to the antianalgesic action of Intracerebroventricular nociceptin. Neither Intracerebroventricular nociceptin nor intrathecal PGE 2 produced antianalgesia against the δ-receptor agonists given intrathecally. Thus, the antianalgesic action of nociceptin originating in the brain is coupled to a descending neuronal pathway mediated by spinal PGE 2 .
-
supraspinal flumazenil inhibits the antianalgesic action of spinal dynorphin a 1 17
Pharmacology Biochemistry and Behavior, 1998Co-Authors: Jodie J. Rady, Blythe B Holmes, James M FujimotoAbstract:Abstract DynorphinA (Dyn) administered intrathecally or released spinally in mice produces antianalgesia, that is, antagonizes morphine analgesia (tail-flick test). Spinal transection eliminates this Dyn antianalgesia. Present results in mice show that Intracerebroventricular administration of flumazenil, a benzodiazepine receptor antagonist, also eliminated the antianalgesic action of Dyn; flumazenil in the brain eliminated the suppressant effect of intrathecal Dyn on intrathecal and Intracerebroventricular morphine-induced antinociception. Intracerebroventricular clonidine, naloxone, and norbinaltorphimine release spinal Dyn. The latent antinociceptive actions of these compounds were uncovered by Intracerebroventricular flumazenil. Thus, Dyn, given intrathecally or released spinally, activates a pathway that is inhibited by Intracerebroventricular flumazenil. Dyn antianalgesia is not significantly altered by Intracerebroventricular administration of bicuculline and picrotoxin, suggesting that activation of the gamma-aminobutyric acid receptor has little if any involvement in the antianalgesic action of Dyn. The antagonistic effect of Dyn seems to be mimicked by benzodiazepine agonists. Furthermore, administration of a benzodiazepine receptor inverse agonist (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate) inhibited Dyn antianalgesia as did flumazenil. Thus, flumazenil, through a benzodiazepine antagonist or inverse agonist action, interrupts, as does spinal transection, the neuronal circuit (cord/brain/cord) necessary for the antianalgesic action of spinal Dyn. Because Dyn antianalgesia is an indirect action, activation of the neuronal circuit must lead to the release of a direct-acting antianalgesic mediator in the spinal cord.
-
Supraspinal Flumazenil Inhibits the Antianalgesic Action of Spinal Dynorphin A [1–17]
Pharmacology Biochemistry and Behavior, 1998Co-Authors: Jodie J. Rady, Blythe B Holmes, James M FujimotoAbstract:Abstract DynorphinA (Dyn) administered intrathecally or released spinally in mice produces antianalgesia, that is, antagonizes morphine analgesia (tail-flick test). Spinal transection eliminates this Dyn antianalgesia. Present results in mice show that Intracerebroventricular administration of flumazenil, a benzodiazepine receptor antagonist, also eliminated the antianalgesic action of Dyn; flumazenil in the brain eliminated the suppressant effect of intrathecal Dyn on intrathecal and Intracerebroventricular morphine-induced antinociception. Intracerebroventricular clonidine, naloxone, and norbinaltorphimine release spinal Dyn. The latent antinociceptive actions of these compounds were uncovered by Intracerebroventricular flumazenil. Thus, Dyn, given intrathecally or released spinally, activates a pathway that is inhibited by Intracerebroventricular flumazenil. Dyn antianalgesia is not significantly altered by Intracerebroventricular administration of bicuculline and picrotoxin, suggesting that activation of the gamma-aminobutyric acid receptor has little if any involvement in the antianalgesic action of Dyn. The antagonistic effect of Dyn seems to be mimicked by benzodiazepine agonists. Furthermore, administration of a benzodiazepine receptor inverse agonist (methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate) inhibited Dyn antianalgesia as did flumazenil. Thus, flumazenil, through a benzodiazepine antagonist or inverse agonist action, interrupts, as does spinal transection, the neuronal circuit (cord/brain/cord) necessary for the antianalgesic action of spinal Dyn. Because Dyn antianalgesia is an indirect action, activation of the neuronal circuit must lead to the release of a direct-acting antianalgesic mediator in the spinal cord.
Bing S Huang - One of the best experts on this subject based on the ideXlab platform.
-
role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt induced hypertension in dahl salt sensitive rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: Bing S Huang, Roselyn White, Arco Y Jeng, Frans H H LeenenAbstract:In Dahl salt-sensitive (S) rats, high salt intake increases cerebrospinal fluid (CSF) Na+ concentration ([Na+]) and blood pressure (BP). Intracerebroventricular (ICV) infusion of a mineralocorticoi...
Arco Y Jeng - One of the best experts on this subject based on the ideXlab platform.
-
role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt induced hypertension in dahl salt sensitive rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: Bing S Huang, Roselyn White, Arco Y Jeng, Frans H H LeenenAbstract:In Dahl salt-sensitive (S) rats, high salt intake increases cerebrospinal fluid (CSF) Na+ concentration ([Na+]) and blood pressure (BP). Intracerebroventricular (ICV) infusion of a mineralocorticoi...
