The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
A.t. Mcknight - One of the best experts on this subject based on the ideXlab platform.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
Nick Andrews - One of the best experts on this subject based on the ideXlab platform.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
Leila Moezi - One of the best experts on this subject based on the ideXlab platform.
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a role for atp sensitive potassium channels in the anticonvulsant effects of triamterene in mice
Epilepsy Research, 2016Co-Authors: Hamed Shafaroodi, Saghar Barati, Ali Almasirad, Mehdi Ghasemi, Leila MoeziAbstract:Abstract There are reports indicating that diuretics including chlorothiazide, furosemide, ethacrynic acid, amiloride and bumetanide can have anticonvulsant properties. Intracellular acidification appears to be a mechanism for the anticonvulsant action of some diuretics. This study was conducted to investigate whether or not triamterene, a K + -sparing diuretic, can generate protection against Seizures induced by intravenous or intraperitoneal pentylenetetrazole (PTZ) models. And to see if, triamterene can withstand maximal electroshock Seizure (MES) in mice. We also investigated to see if there is any connection between triamterene's anti-Seizure effect and ATP-sensitive K + (K ATP ) channels. Five days triamterene oral administration (10, 20 and 40mg/kg), significantly increased clonic Seizure threshold which was induced by intravenous pentylenetetrazole. Triamterene (10, 20 and 40mg/kg) treatment also increased the latency of clonic Seizure and decreased its frequency in intraperitoneal PTZ model. Administration of triamterene (20mg/kg) also decreased the incidence of Tonic Seizure in MES-induced Seizure. Co-administration of a K ATP sensitive channel blocker, glibenclamide, in the 6th day, 60min before intravenous PTZ blocked triamterene's anticonvulsant effect. A K ATP sensitive channel opener, diazoxide, enhanced triamterene's anti-Seizure effect in both intravenous PTZ or MES Seizure models. At the end, triamterene exerts anticonvulsant effect in 3 Seizure models of mice including intravenous PTZ, intraperitoneal PTZ and MES. The anti-Seizure effect of triamterene probably is induced through K ATP channels.
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a role for atp sensitive potassium channels in the anticonvulsant effects of triamterene in mice
Epilepsy Research, 2016Co-Authors: Hamed Shafaroodi, Saghar Barati, Ali Almasirad, Mehdi Ghasemi, Leila MoeziAbstract:Abstract There are reports indicating that diuretics including chlorothiazide, furosemide, ethacrynic acid, amiloride and bumetanide can have anticonvulsant properties. Intracellular acidification appears to be a mechanism for the anticonvulsant action of some diuretics. This study was conducted to investigate whether or not triamterene, a K + -sparing diuretic, can generate protection against Seizures induced by intravenous or intraperitoneal pentylenetetrazole (PTZ) models. And to see if, triamterene can withstand maximal electroshock Seizure (MES) in mice. We also investigated to see if there is any connection between triamterene's anti-Seizure effect and ATP-sensitive K + (K ATP ) channels. Five days triamterene oral administration (10, 20 and 40mg/kg), significantly increased clonic Seizure threshold which was induced by intravenous pentylenetetrazole. Triamterene (10, 20 and 40mg/kg) treatment also increased the latency of clonic Seizure and decreased its frequency in intraperitoneal PTZ model. Administration of triamterene (20mg/kg) also decreased the incidence of Tonic Seizure in MES-induced Seizure. Co-administration of a K ATP sensitive channel blocker, glibenclamide, in the 6th day, 60min before intravenous PTZ blocked triamterene's anticonvulsant effect. A K ATP sensitive channel opener, diazoxide, enhanced triamterene's anti-Seizure effect in both intravenous PTZ or MES Seizure models. At the end, triamterene exerts anticonvulsant effect in 3 Seizure models of mice including intravenous PTZ, intraperitoneal PTZ and MES. The anti-Seizure effect of triamterene probably is induced through K ATP channels.
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chronic administration of atorvastatin induced anti convulsant effects in mice the role of nitric oxide
Epilepsy & Behavior, 2012Co-Authors: Leila Moezi, Hamed Shafaroodi, Mahsa Hassanipour, Ali Fakhrzad, S Hassanpour, Ahmad Reza DehpourAbstract:Atorvastatin has neuroprotective effects, and there is some evidence that nitric oxide is involved in atorvastatin effects. In this study, we evaluated whether the nitrergic system is involved in the anticonvulsant effects of chronic atorvastatin administration. Intravenous and intraperitoneal pentylenetetrazol were used to induce Seizures in mice. Chronic atorvastatin treatment significantly increased the Seizure threshold which is induced by both intravenous and intraperitoneal pentylenetetrazol. Intraperitoneal pentylenetetrazol also decreased the incidence of Tonic Seizure and death in atorvastatin-treated groups. Chronic co-administration of a non-selective nitric oxide synthase inhibitor, l-NAME, or a selective inducible nitric oxide synthase inhibitor, aminoguanidine, with atorvastatin inhibited atorvastatin-induced anticonvulsant effects in intravenous model of pentylenetetrazol. Acute injection of l-NAME or aminoguanidine inhibited the anticonvulsant effects of atorvastatin in both models of intravenous- and intraperitoneal-pentylenetetrazol-induced Seizures. In conclusion, we demonstrated that nitric oxide signaling probably through inducible nitric oxide synthase could be involved in the anticonvulsant effects of atorvastatin.
Mehdi Ghasemi - One of the best experts on this subject based on the ideXlab platform.
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a role for atp sensitive potassium channels in the anticonvulsant effects of triamterene in mice
Epilepsy Research, 2016Co-Authors: Hamed Shafaroodi, Saghar Barati, Ali Almasirad, Mehdi Ghasemi, Leila MoeziAbstract:Abstract There are reports indicating that diuretics including chlorothiazide, furosemide, ethacrynic acid, amiloride and bumetanide can have anticonvulsant properties. Intracellular acidification appears to be a mechanism for the anticonvulsant action of some diuretics. This study was conducted to investigate whether or not triamterene, a K + -sparing diuretic, can generate protection against Seizures induced by intravenous or intraperitoneal pentylenetetrazole (PTZ) models. And to see if, triamterene can withstand maximal electroshock Seizure (MES) in mice. We also investigated to see if there is any connection between triamterene's anti-Seizure effect and ATP-sensitive K + (K ATP ) channels. Five days triamterene oral administration (10, 20 and 40mg/kg), significantly increased clonic Seizure threshold which was induced by intravenous pentylenetetrazole. Triamterene (10, 20 and 40mg/kg) treatment also increased the latency of clonic Seizure and decreased its frequency in intraperitoneal PTZ model. Administration of triamterene (20mg/kg) also decreased the incidence of Tonic Seizure in MES-induced Seizure. Co-administration of a K ATP sensitive channel blocker, glibenclamide, in the 6th day, 60min before intravenous PTZ blocked triamterene's anticonvulsant effect. A K ATP sensitive channel opener, diazoxide, enhanced triamterene's anti-Seizure effect in both intravenous PTZ or MES Seizure models. At the end, triamterene exerts anticonvulsant effect in 3 Seizure models of mice including intravenous PTZ, intraperitoneal PTZ and MES. The anti-Seizure effect of triamterene probably is induced through K ATP channels.
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a role for atp sensitive potassium channels in the anticonvulsant effects of triamterene in mice
Epilepsy Research, 2016Co-Authors: Hamed Shafaroodi, Saghar Barati, Ali Almasirad, Mehdi Ghasemi, Leila MoeziAbstract:Abstract There are reports indicating that diuretics including chlorothiazide, furosemide, ethacrynic acid, amiloride and bumetanide can have anticonvulsant properties. Intracellular acidification appears to be a mechanism for the anticonvulsant action of some diuretics. This study was conducted to investigate whether or not triamterene, a K + -sparing diuretic, can generate protection against Seizures induced by intravenous or intraperitoneal pentylenetetrazole (PTZ) models. And to see if, triamterene can withstand maximal electroshock Seizure (MES) in mice. We also investigated to see if there is any connection between triamterene's anti-Seizure effect and ATP-sensitive K + (K ATP ) channels. Five days triamterene oral administration (10, 20 and 40mg/kg), significantly increased clonic Seizure threshold which was induced by intravenous pentylenetetrazole. Triamterene (10, 20 and 40mg/kg) treatment also increased the latency of clonic Seizure and decreased its frequency in intraperitoneal PTZ model. Administration of triamterene (20mg/kg) also decreased the incidence of Tonic Seizure in MES-induced Seizure. Co-administration of a K ATP sensitive channel blocker, glibenclamide, in the 6th day, 60min before intravenous PTZ blocked triamterene's anticonvulsant effect. A K ATP sensitive channel opener, diazoxide, enhanced triamterene's anti-Seizure effect in both intravenous PTZ or MES Seizure models. At the end, triamterene exerts anticonvulsant effect in 3 Seizure models of mice including intravenous PTZ, intraperitoneal PTZ and MES. The anti-Seizure effect of triamterene probably is induced through K ATP channels.
Isabel M Gonzalez - One of the best experts on this subject based on the ideXlab platform.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
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effect of gastrin releasing peptide on rat hippocampal extracellular gaba levels and Seizures in the audiogenic Seizure prone dba 2 mouse
Brain Research, 2000Co-Authors: Nick Andrews, Isabel M Gonzalez, R J Oles, Lakhbir Singh, Ben Davis, A.t. McknightAbstract:Gastrin-releasing peptide (GRP), a selective agonist for the BB2 subtype of bombesin receptor, is reported to depolarise GABAergic interneurons in the stratum oriens layer of the hippocampus. Such an action might lead to increased extracellular levels of GABA in the hippocampus, and result in an anti-convulsant effect with this peptide. We have tested this hypothesis by determining the effect of GRP on extracellular levels of GABA in the ventral hippocampus of the freely moving rat using in vivo microdialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic Seizure-prone DBA/2 mice prior to exposure to the noise of an electric bell. Following local perfusion in the ventral hippocampus by reverse dialysis GRP (10 μM) significantly raised levels of GABA in the recovered dialysates by approximately 40%. In the Seizure studies, GRP (30–300 ng) increased the latency to Tonic Seizure, the number of mice convulsing and reduced the incidence of lethality. In both dialysis and Seizure studies, the effects of GRP were blocked by the selective BB2 receptor antagonist, [d-Phe6, Leu-NHEt13]bombesin (6–13). These experiments provide further functional evidence that activation of the BB2 receptor may modulate neurotransmission in the hippocampus, and that this action may confer anti-convulsant properties on agonists acting at the BB2 receptor in the brain.
