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Kinga Salat - One of the best experts on this subject based on the ideXlab platform.

  • phencyclidine and scopolamine for modeling amnesia in rodents direct comparison with the use of barnes Maze Test and contextual fear conditioning Test in mice
    Neurotoxicity Research, 2018
    Co-Authors: Natalia Malikowskaracia, Adrian Podkowa, Kinga Salat
    Abstract:

    Nowadays cognitive impairments are a growing unresolved medical issue which may accompany many diseases and therapies, furthermore, numerous researchers investigate various neurobiological aspects of human memory to find possible ways to improve it. Until any other method is discovered, in vivo studies remain the only available tool for memory evaluation. At first, researchers need to choose a model of amnesia which may strongly influence observed results. Thereby a deeper insight into a model itself may increase the quality and reliability of results. The most common method to impair memory in rodents is the pretreatment with drugs that disrupt learning and memory. Taking this into consideration, we compared the activity of agents commonly used for this purpose. We investigated effects of phencyclidine (PCP), a non-competitive NMDA receptor antagonist, and scopolamine (SCOP), an antagonist of muscarinic receptors, on short-term spatial memory and classical fear conditioning in mice. PCP (3 mg/kg) and SCOP (1 mg/kg) were administrated intraperitoneally 30 min before behavioral paradigms. To assess the influence of PCP and SCOP on short-term spatial memory, the Barnes Maze Test in C57BL/J6 mice was used. Effects on classical conditioning were evaluated using contextual fear conditioning Test. Additionally, spontaneous locomotor activity of mice was measured. These two Tests were performed in CD-1 mice. Our study reports that both Tested agents disturbed short-term spatial memory in the Barnes Maze Test, however, SCOP revealed a higher activity. Surprisingly, learning in contextual fear conditioning Test was impaired only by SCOP.

  • phencyclidine and scopolamine for modeling amnesia in rodents direct comparison with the use of barnes Maze Test and contextual fear conditioning Test in mice
    Neurotoxicity Research, 2018
    Co-Authors: Natalia Malikowskaracia, Adrian Podkowa, Kinga Salat
    Abstract:

    Nowadays cognitive impairments are a growing unresolved medical issue which may accompany many diseases and therapies, furthermore, numerous researchers investigate various neurobiological aspects of human memory to find possible ways to improve it. Until any other method is discovered, in vivo studies remain the only available tool for memory evaluation. At first, researchers need to choose a model of amnesia which may strongly influence observed results. Thereby a deeper insight into a model itself may increase the quality and reliability of results. The most common method to impair memory in rodents is the pretreatment with drugs that disrupt learning and memory. Taking this into consideration, we compared the activity of agents commonly used for this purpose. We investigated effects of phencyclidine (PCP), a non-competitive NMDA receptor antagonist, and scopolamine (SCOP), an antagonist of muscarinic receptors, on short-term spatial memory and classical fear conditioning in mice. PCP (3 mg/kg) and SCOP (1 mg/kg) were administrated intraperitoneally 30 min before behavioral paradigms. To assess the influence of PCP and SCOP on short-term spatial memory, the Barnes Maze Test in C57BL/J6 mice was used. Effects on classical conditioning were evaluated using contextual fear conditioning Test. Additionally, spontaneous locomotor activity of mice was measured. These two Tests were performed in CD-1 mice. Our study reports that both Tested agents disturbed short-term spatial memory in the Barnes Maze Test, however, SCOP revealed a higher activity. Surprisingly, learning in contextual fear conditioning Test was impaired only by SCOP.

Natalia Malikowskaracia - One of the best experts on this subject based on the ideXlab platform.

  • phencyclidine and scopolamine for modeling amnesia in rodents direct comparison with the use of barnes Maze Test and contextual fear conditioning Test in mice
    Neurotoxicity Research, 2018
    Co-Authors: Natalia Malikowskaracia, Adrian Podkowa, Kinga Salat
    Abstract:

    Nowadays cognitive impairments are a growing unresolved medical issue which may accompany many diseases and therapies, furthermore, numerous researchers investigate various neurobiological aspects of human memory to find possible ways to improve it. Until any other method is discovered, in vivo studies remain the only available tool for memory evaluation. At first, researchers need to choose a model of amnesia which may strongly influence observed results. Thereby a deeper insight into a model itself may increase the quality and reliability of results. The most common method to impair memory in rodents is the pretreatment with drugs that disrupt learning and memory. Taking this into consideration, we compared the activity of agents commonly used for this purpose. We investigated effects of phencyclidine (PCP), a non-competitive NMDA receptor antagonist, and scopolamine (SCOP), an antagonist of muscarinic receptors, on short-term spatial memory and classical fear conditioning in mice. PCP (3 mg/kg) and SCOP (1 mg/kg) were administrated intraperitoneally 30 min before behavioral paradigms. To assess the influence of PCP and SCOP on short-term spatial memory, the Barnes Maze Test in C57BL/J6 mice was used. Effects on classical conditioning were evaluated using contextual fear conditioning Test. Additionally, spontaneous locomotor activity of mice was measured. These two Tests were performed in CD-1 mice. Our study reports that both Tested agents disturbed short-term spatial memory in the Barnes Maze Test, however, SCOP revealed a higher activity. Surprisingly, learning in contextual fear conditioning Test was impaired only by SCOP.

  • phencyclidine and scopolamine for modeling amnesia in rodents direct comparison with the use of barnes Maze Test and contextual fear conditioning Test in mice
    Neurotoxicity Research, 2018
    Co-Authors: Natalia Malikowskaracia, Adrian Podkowa, Kinga Salat
    Abstract:

    Nowadays cognitive impairments are a growing unresolved medical issue which may accompany many diseases and therapies, furthermore, numerous researchers investigate various neurobiological aspects of human memory to find possible ways to improve it. Until any other method is discovered, in vivo studies remain the only available tool for memory evaluation. At first, researchers need to choose a model of amnesia which may strongly influence observed results. Thereby a deeper insight into a model itself may increase the quality and reliability of results. The most common method to impair memory in rodents is the pretreatment with drugs that disrupt learning and memory. Taking this into consideration, we compared the activity of agents commonly used for this purpose. We investigated effects of phencyclidine (PCP), a non-competitive NMDA receptor antagonist, and scopolamine (SCOP), an antagonist of muscarinic receptors, on short-term spatial memory and classical fear conditioning in mice. PCP (3 mg/kg) and SCOP (1 mg/kg) were administrated intraperitoneally 30 min before behavioral paradigms. To assess the influence of PCP and SCOP on short-term spatial memory, the Barnes Maze Test in C57BL/J6 mice was used. Effects on classical conditioning were evaluated using contextual fear conditioning Test. Additionally, spontaneous locomotor activity of mice was measured. These two Tests were performed in CD-1 mice. Our study reports that both Tested agents disturbed short-term spatial memory in the Barnes Maze Test, however, SCOP revealed a higher activity. Surprisingly, learning in contextual fear conditioning Test was impaired only by SCOP.

Roberto Frussafilho - One of the best experts on this subject based on the ideXlab platform.

  • anxiogenic effect of sleep deprivation in the elevated plus Maze Test in mice
    Psychopharmacology, 2004
    Co-Authors: Regina H Silva, Sonia R Kameda, Rita C Carvalho, Andre L Takatsucoleman, Suzy Tamie Niigaki, Vanessa C Abilio, Sergio Tufik, Roberto Frussafilho
    Abstract:

    Several clinical studies demonstrate that the absence of periods of sleep is closely related to occurrence of anxiety symptoms. However, the basis of these interactions is poorly understood. Studies performed with animal models of sleep deprivation and anxiety would be helpful in the understanding of the mechanisms underlying this relationship, but some animal studies have not corroborated clinical data, reporting anxiolytic effects of sleep deprivation. The aim of the present study was to verify the effects of different protocols of sleep deprivation in mice Tested in the elevated plus-Maze and to assess the effect of chlordiazepoxide and clonidine. Three-month-old male mice were sleep-deprived for 24 or 72 h using the methods of single or multiple platforms in water tanks. Mice kept in their home cages were used as controls. Plus-Maze behavior was observed immediately after the deprivation period. Mice that were sleep-deprived for 72 h spent a lower percent time in the open arms of the apparatus than control animals. This sleep deprivation-induced anxiety-like behavior was unaffected by treatment with chlordiazepoxide (5.0 and 7.5 mg/kg IP), but reversed by an administration of 5 or 10 μg/kg IP clonidine. The results indicate that under specific methodological conditions sleep deprivation causes an increase in anxiety-like behavior in mice exposed to the elevated plus-Maze.

  • anxiogenic effect of sleep deprivation in the elevated plus Maze Test in mice
    Psychopharmacology, 2004
    Co-Authors: Regina H Silva, Sonia R Kameda, Rita C Carvalho, Andre L Takatsucoleman, Suzy Tamie Niigaki, Vanessa C Abilio, Sergio Tufik, Roberto Frussafilho
    Abstract:

    Rationale Several clinical studies demonstrate that the absence of periods of sleep is closely related to occurrence of anxiety symptoms. However, the basis of these interactions is poorly understood. Studies performed with animal models of sleep deprivation and anxiety would be helpful in the understanding of the mechanisms underlying this relationship, but some animal studies have not corroborated clinical data, reporting anxiolytic effects of sleep deprivation.

Kenji Onodera - One of the best experts on this subject based on the ideXlab platform.

  • improvement by fub 181 a novel histamine h3 receptor antagonist of learning and memory in the elevated plus Maze Test in mice
    Naunyn-schmiedebergs Archives of Pharmacology, 1998
    Co-Authors: Kenji Onodera, Masahiro Imaizumi, S Miyazaki, Walter Schunack
    Abstract:

    Effects of FUB 181 [3-(4-chlorophenyl)propyl-3-(1H-imidazol-4-yl)propyl ether], a novel histamine H3-receptor antagonist, on a scopolamine-induced learning deficit in the elevated plus-Maze Test were studied in mice. FUB 181 alone (2.5 and 5 mg/kg, i.p.) ameliorated the scopolamine-induced learning deficit in mice. This effect was antagonized by BP 2.94 (10 mg/kg, i.p.), a prodrug of (R)-—methylhistamine (histamine H3-receptor agonist), and by ketotifen (4 mg/kg, i.p.), a histamine H1-receptor antagonist, both penetrating the blood-brain barrier. However, the ameliorating effect of FUB 181 (2.5 mg/kg) was not antagonized by either terfenadine (10 mg/kg, i.p.), a histamine H1-receptor antagonist with poor penetration of the blood-brain barrier, or zolantidine (20 mg/kg, i.p.), a centrally effective histamine H2-receptor antagonist. In a biochemical study, FUB 181 had no significant effect on either acetylcholine or choline level in mice brain at the doses Tested. These findings suggest that FUB 181 increases the release of histamine by blocking presynaptic histamine H3 autoreceptors, and that released histamine in turn activates postsynaptic H1 and H2 receptors, predominantly histamine H1 receptors, and in this fashion improves learning and memory in mice. Our findings also suggest that the histaminergic system may play an important role in learning and memory, and that FUB 181 may be a clinical candidate for the therapy of dementia.

  • effects of thioperamide a histamine h3 receptor antagonist on a scopolamine induced learning deficit using an elevated plus Maze Test in mice
    Life Sciences, 1995
    Co-Authors: S Miyazaki, Masahiro Imaizumi, Kenji Onodera
    Abstract:

    We examined the effects of thioperamide and (R)-α-methylhistamine, a histamine H3-receptor antagonist and an agonist, respectively, on a scopolamine-induced learning deficit using an elevated plus-Maze Test in mice. Thioperamide alone slightly improved the learning deficit induced by scopolamine, and pretreatment with zolantidine, a histamine H2-receptor antagonist, significantly enhanced the effect of thioperamide in this Test. (R)-α-Methylhistamine, pyrilamine, ketotifen, terfenadine, and zolantidine alone at the doses Tested had no effect. Moreover, the improvement by thioperamide plus zolantidine was antagonized by pretreatment with histamine H1-receptor antagonists such as pyrilamine or ketotifen, but not by terfenadine. Thus, thioperamide improved the scopolamine-induced learning deficit through central histamine H1 receptors in mice. The present results supported the hypothesis that histamine may play an important role in learning and memory.

Jong Hoon Ryu - One of the best experts on this subject based on the ideXlab platform.

  • nodakenin a coumarin compound ameliorates scopolamine induced memory disruption in mice
    Life Sciences, 2007
    Co-Authors: Donghyun Kim, Ji Wook Jung, Seungjoo Lee, Byung Hoon Yoon, Jae Hoon Cheong, Do Yoon Kim, Young Choong Kim, Yeong Shik Kim, Sam Sik Kang, Jong Hoon Ryu
    Abstract:

    Nodakenin is a coumarin compound initially isolated from the roots of Angelica gigas. In the present study, we investigated the effects of nodakenin on learning and memory impairments induced by scopolamine (1 mg/kg, i.p.) using the passive avoidance Test, the Y-Maze Test, and the Morris water Maze Test in mice. Nodakenin (10 mg/kg, p.o.) administration significantly reversed scopolamine-induced cognitive impairments in the passive avoidance Test and the Y-Maze Test (P<0.05), and also reduced escape latency during training in the Morris water Maze Test (P<0.05). Moreover, swimming times and distances within the target zone of the Morris water Maze were greater in the nodakenin-treated group than in the scopolamine-treated group (P<0.05). In an in vitro study, nodakenin was found to inhibit acetylcholinesterase activity in a dose-dependent manner (IC(50)=84.7 microM). In addition, nodakenin was also found to inhibit acetylcholinesterase activity for 6 h in an ex-vivo study. These results suggest that nodakenin may be a useful for the treatment of cognitive impairment, and that its beneficial effects are mediated, in part, via the enhancement of cholinergic signaling.

  • gomisin a improves scopolamine induced memory impairment in mice
    European Journal of Pharmacology, 2006
    Co-Authors: Donghyun Kim, Tran Manh Hung, Kihwan Bae, Ji Wook Jung, Seungjoo Lee, Byung Hoon Yoon, Jae Hoon Cheong, Jong Hoon Ryu
    Abstract:

    Gomisin A is a component of the fruits of Schizandra chinesis which are widely used as a tonic in traditional Chinese medicine. In the present study, we assessed the effect of gomisin A on the learning and memory impairments induced by scopolamine. The cognition-enhancing effect of gomisin A was investigated using a passive avoidance Test, the Y-Maze Test, and the Morris water Maze Test in mice. Drug-induced amnesia was induced by treating animals with scopolamine (1 mg/kg, i.p.). Gomisin A (5 mg/kg, p.o.) administration significantly reversed scopolamine-induced cognitive impairments in mice by the passive avoidance Test and the Y-Maze Test (P<0.05), and also improved escape latency in the Morris water Maze Test at 5 mg/kg (P<0.05). Moreover, in an in vitro study, gomisin A was found to inhibit acetylcholinesterase activity in a dose-dependent manner (IC50 value; 15.5 microM). These results suggest that gomisin A may be a useful cognitive impairment treatment, and its beneficial effects are mediated, in part, via enhancing the cholinergic nervous system.