Recently, the controversial role of cannabinoid receptors was reported in the pathophysiology of PD. In the present study we have investigated the role of CB1 receptors in motor behaviour. Repeated intranigral (day 1, 7, 14) infusion of MPTP was done to produce stable motor deficits in rats. CB1 receptor agonist, Noladin ether and antagonist AM 251, was administered alone or in combination in MPTP-infused rats. Grip strength, spontaneous locomotor activity and narrow beam walk tests were used to access motor behaviours. Oxidative stress and pro-inflammatory cytokine levels were determined in striatal brain homogenates. MPTP-infused rats showed stable motor deficit and elevation in oxidative stress and cytokine levels. AM 251 attenuated MPYP-induced motor dysfunction, oxidative stress and neuroinflammation in rats. Conversely, noladin ether synergized MPTP- mediated neurotoxicity, which was significantly attenuated by AM 251 pre-treatment. The above results suggests that sustained activation of CB1 receptors may play a crucial role in the development motor dysfunction and thus CB1 receptor blockade would be therapeutic in PD.
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Dr. Rahul Deshmukh, is serving as Associate Professor & HOD Pharmacology at ISFCP, Moga, Punjab; India. His major research area include cognitive and motor disorders. Dr. Deshmukh has clinched several research grants and awarded as a Young Scientist by DST, India. He gave invited talks & presented papers in national and international conferences.
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Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Recently, the controversial role of cannabinoid receptors was reported in the pathophysiology of PD. In the present study we have investigated the role of CB1 receptors in motor behaviour. Repeated intranigral (day 1, 7, 14) infusion of MPTP was done to produce stable motor deficits in rats. CB1 receptor agonist, Noladin ether and antagonist AM 251, was administered alone or in combination in MPTP-infused rats. Grip strength, spontaneous locomotor activity and narrow beam walk tests were used to access motor behaviours. Oxidative stress and pro-inflammatory cytokine levels were determined in striatal brain homogenates. MPTP-infused rats showed stable motor deficit and elevation in oxidative stress and cytokine levels. AM 251 attenuated MPYP-induced motor dysfunction, oxidative stress and neuroinflammation in rats. Conversely, noladin ether synergized MPTP- mediated neurotoxicity, which was significantly attenuated by AM 251 pre-treatment. The above results suggests that sustained activation of CB1 receptors may play a crucial role in the development motor dysfunction and thus CB1 receptor blockade would be therapeutic in PD. 108 pp. Englisch. Seller Inventory # 9783659645860
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Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Deshmukh RahulDr. Rahul Deshmukh, is serving as Associate Professor & HOD Pharmacology at ISFCP, Moga, Punjab India. His major research area include cognitive and motor disorders. Dr. Deshmukh has clinched several research grants an. Seller Inventory # 5170735
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Taschenbuch. Condition: Neu. This item is printed on demand - Print on Demand Titel. Neuware -Recently, the controversial role of cannabinoid receptors was reported in the pathophysiology of PD. In the present study we have investigated the role of CB1 receptors in motor behaviour. Repeated intranigral (day 1, 7, 14) infusion of MPTP was done to produce stable motor deficits in rats. CB1 receptor agonist, Noladin ether and antagonist AM 251, was administered alone or in combination in MPTP-infused rats. Grip strength, spontaneous locomotor activity and narrow beam walk tests were used to access motor behaviours. Oxidative stress and pro-inflammatory cytokine levels were determined in striatal brain homogenates. MPTP-infused rats showed stable motor deficit and elevation in oxidative stress and cytokine levels. AM 251 attenuated MPYP-induced motor dysfunction, oxidative stress and neuroinflammation in rats. Conversely, noladin ether synergized MPTP- mediated neurotoxicity, which was significantly attenuated by AM 251 pre-treatment. The above results suggests that sustained activation of CB1 receptors may play a crucial role in the development motor dysfunction and thus CB1 receptor blockade would be therapeutic in PD.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 108 pp. Englisch. Seller Inventory # 9783659645860
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Taschenbuch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Recently, the controversial role of cannabinoid receptors was reported in the pathophysiology of PD. In the present study we have investigated the role of CB1 receptors in motor behaviour. Repeated intranigral (day 1, 7, 14) infusion of MPTP was done to produce stable motor deficits in rats. CB1 receptor agonist, Noladin ether and antagonist AM 251, was administered alone or in combination in MPTP-infused rats. Grip strength, spontaneous locomotor activity and narrow beam walk tests were used to access motor behaviours. Oxidative stress and pro-inflammatory cytokine levels were determined in striatal brain homogenates. MPTP-infused rats showed stable motor deficit and elevation in oxidative stress and cytokine levels. AM 251 attenuated MPYP-induced motor dysfunction, oxidative stress and neuroinflammation in rats. Conversely, noladin ether synergized MPTP- mediated neurotoxicity, which was significantly attenuated by AM 251 pre-treatment. The above results suggests that sustained activation of CB1 receptors may play a crucial role in the development motor dysfunction and thus CB1 receptor blockade would be therapeutic in PD. Seller Inventory # 9783659645860
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Taschenbuch. Condition: Neu. CB1 Receptor Modulation Against Parkinson's disease in Rats | Rahul Deshmukh (u. a.) | Taschenbuch | 108 S. | Englisch | 2014 | LAP LAMBERT Academic Publishing | EAN 9783659645860 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu. Seller Inventory # 104948991
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