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Mohammad-reza Zarrindast - One of the best experts on this subject based on the ideXlab platform.
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Involvement of NMDA receptors in morphine State-Dependent Learning in mice.
International Journal of Neuroscience, 2020Co-Authors: Mohammad-reza Zarrindast, M. Rezayat, Majid Jafari-sabet, Bijan Djahanguiri, Ameneh RezayofAbstract:In the present study, the effects of intracerebroventricular (i.c.v.) injection of NMDA receptor agonist and antagonist on impairment of memory formation and the State-Dependent Learning by morphine have been investigated in mice. Pretraining administration of morphine (5 mg/kg; s.c.) decreased the Learning of one-trial passive avoidance task. Pretest administration of morphine (5 mg/kg) induced State-Dependent Learning acquired under pretraining morphine influence. Pretest administration of NMDA receptor agonist, L-glutamate (0.00001 and 0.0001 and 0.001 μg/mouse, i.c.v.) following pretraining saline treatment did not affect retention. Amnesia induced by pretraining morphine was significantly reversed by pretest administration of L-glutamate (0.0001 and 0.001 μg/mouse, i.c.v.). Pretest administration of noncompetitive NMDA receptor antagonist, MK-801 (0.5, 1, and 2 μg/mouse, i.c.v.) significantly impaired memory formation. Amnesia induced by pretraining morphine was increased by pretest administration of...
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P02-168 Intra-dorsal hippocampal microinjection of lithium and scopolamine induce a cross State-Dependent Learning in mice
European Psychiatry, 2020Co-Authors: Batool Ghorbanalizadeh-khalifeh-mahaleh, Ameneh Rezayof, Ali Haeri-rohani, Saba Taheri, M. Sahengharani, Mohammad-reza ZarrindastAbstract:Background Lithium a mood stabilizer may exert adverse effects on memory. We have previously shown that lithium induces State-Dependent Learning. Cholinergic systems of the brain may play an important role in memory function and mood regulation. In the present study, effects of intra-dorsal hippocampal (intra-CA1) injections of lithium and scopolamine on memory and cross State-Dependent Learning between two drugs were investigated. Methods For memory assessment, a one-trial step-down inhibitory avoidance task was used in adult male NMRI mice. Results Intra-CA1 administration of lithium (0.5 and 1 μg/mouse) after training or injection of the drug (0.5μg/mouse) before testing impaired memory when retrieval was tested 24 h later. The memory impairment by post-training lithium was reversed by pre-test administration of the drug (0.5μg/mouse, intra-CA1) suggesting lithium State-Dependent Learning. On the other hand, intra-CA1 administration of scopolamine (0.5, 1 and 2 μg/mouse) after training or injection of the drug (2μg/mouse) before testing impaired memory when retrieval was tested 24 h later. The impairment of memory by post-training injection of scopolamine (2μg/mouse) was restored by the pre-test injection of the drug (1 and 2 μg/mouse). Furthermore, memory impairment induced by post-training injection of lithium (0.5 μg/mouse) and scopolamine (2 μg/mouse) were reversed by pre-test administration of scopolamine (0.5, 1 and 2 μg/mouse) and lithium (0.5 and 1 μg/mouse) respectively. The impairment by lithium was also reversed by physostigmine. Conclusion The results suggest that microinjection of both lithium and scopolamine induce State-Dependent memory and there may be a cross state-dependency between two drugs.
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THE INHIBITION OF NUCLEUS ACCUMBENS CHOLINERGIC RECEPTORS DECREASED MEMORY RETENTION IN RAT
Arak Medical University Journal, 2014Co-Authors: Ameneh Rezayof, Mohammad-reza Zarrindast, Niloufar DarbandiAbstract:Background: It is well known that morphine influence Learning and memory processes. The Nucleus accumbens (N.ac) which has an important role in reward participates in morphine-induced impairment of memory retention. Considering the cholinergic system is involved in the effects of morphine on Learning and memory, in the present study, the effects of intra-N.ac injections of acetylcholine receptor antagonists alone or with morphine on memory retention and morphine-induced memory has been investigated in rats. Materials and Methods: In this original research animals were bilaterally cannulated in the N.ac and a step-through passive avoidance task was used for the assessment of memory retention . Results: Post-training subcutaneous administration of morphine dose dependently decreased the Learning and induced amnesia. The administration of the same dose of morphine as pre-test treatment induced State-Dependent Learning. Pre-test intra- N.ac administration of atropine, scopolamine and mecamylamine in different doses alone cannot affect on memory retention. While, pretest intra- N.ac injection of these drugs before the administration of morphine dose dependently inhibited morphine State-Dependent Learning. The level of statistical significance was set at p
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The involvement of dorsal hippocampus in dextromethorphan-induced State-Dependent Learning in mice.
Pharmacology Biochemistry and Behavior, 2013Co-Authors: Mohammad-reza Zarrindast, Ameneh Rezayof, Vahid Ownegh, Farid OwneghAbstract:Abstract In an effort to understand the effect of dextromethorphan (DM; 3-methoxy-17-methylmorphinan), a noncompetitive antagonist of the N-methyl- d -aspartate (NMDA) receptors on memory retrieval, male NMRI mice received intraperitoneal (i.p.) or intra-CA1 injection of this drug before or after training and before testing in passive avoidance task. Pre-training i.p. (20 mg/kg) or intra-CA1 (0.5 and 1 μg/mouse) administration of DM induced amnesia in a dose-dependent manner. Post-training i.p. (10 and 20 mg/kg) or intra-CA administration of DM (0.5 and 1 μg/mouse) however, did not affect the memory retrieval. Moreover, memory retrieval was impaired in animals receiving either i.p. (20 mg/kg) or intra-CA1 administration of DM (0.5 and 1 μg/mouse) prior to testing, suggesting the DM-induced amnesia. Interestingly, the amnestic effect of pre-training i.p. (20 mg/kg) or intra-CA1 administration of DM (1 μg/mouse) was restored in mice receiving pre-test i.p. (5 and 10 mg/kg) or intra-CA1 (0.25 and 0.5 μg/mouse) administration of the drug, indicating DM-induced State-Dependent Learning. Taken together, it can be concluded that DM administration impairs memory retrieval in a dose- and time-dependent manner. Moreover, DM can induce State-Dependent Learning. Dorsal hippocampus appears to play an important role upon DM influence of Learning and memory processes.
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Blockade of dorsal hippocampal dopamine receptors inhibits State-Dependent Learning induced by cannabinoid receptor agonist in mice.
Neuroscience Research, 2010Co-Authors: Mohammad-reza Zarrindast, Mania Dorrani, Razieh Lachinani, Ameneh RezayofAbstract:Abstract To clarify the interaction between cannabinnoid CB1 receptors and the dopaminergic system in memory processes, the effects of dopamine receptor agents on the State-Dependent Learning induced by the non-selective CB1/CB2 receptor agonist, WIN55,212-2 have been investigated in mice. Animals implanted with unilateral cannula at the CA1 region of the dorsal hippocampus and microinjected with WIN55,212-2 and/or dopaminergic agents, were tested using a single-trial step-down passive avoidance task. Intra-CA1 microinjections of WIN55,212-2 (0.1–1 μg/mouse) immediately after training, decreased the step-down latency, indicating an amnesic effect of the drug. The amnesia was reversed by pre-test administration of the drug, suggesting State-Dependent Learning by the cannabinoid. Pre-test microinjection of apomorphine, a D1/D2 dopamine receptor agonist (0.1–0.3 μg/mouse) into the CA1 region reversed the amnesia induced by post-training WIN55,212-2 (1 μg/mouse). Moreover, pre-test co-administration of apomorphine with an ineffective dose of WIN55,212-2 (0.01 μg/mouse), showed a reversion of the impairment on retention performance. Pre-test administration of the same doses of apomorphine did not show any response by itself. Pre-test intra-CA1 administration of a D1 dopamine receptor antagonist, SCH23390 (0.05–0.3 μg/mouse) or D2 dopamine receptor antagonist, sulpiride (0.125–0.5 μg/mouse) inhibited the expression of WIN55,212-2-induced State-Dependent Learning. Pre-test microinjection of the same doses of SCH23390 or sulpiride had no effect on WIN55,212-2-induced amnesia. Moreover, single injection of SCH23390 (0.2 and 0.3 μg/mouse) or sulpiride (0.125 μg/mouse) decreased memory retrieval. The results suggest that the dorsal hippocampal dopaminergic system participates in the modulation of WIN55,212-2-induced State-Dependent Learning.
Ameneh Rezayof - One of the best experts on this subject based on the ideXlab platform.
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Involvement of NMDA receptors in morphine State-Dependent Learning in mice.
International Journal of Neuroscience, 2020Co-Authors: Mohammad-reza Zarrindast, M. Rezayat, Majid Jafari-sabet, Bijan Djahanguiri, Ameneh RezayofAbstract:In the present study, the effects of intracerebroventricular (i.c.v.) injection of NMDA receptor agonist and antagonist on impairment of memory formation and the State-Dependent Learning by morphine have been investigated in mice. Pretraining administration of morphine (5 mg/kg; s.c.) decreased the Learning of one-trial passive avoidance task. Pretest administration of morphine (5 mg/kg) induced State-Dependent Learning acquired under pretraining morphine influence. Pretest administration of NMDA receptor agonist, L-glutamate (0.00001 and 0.0001 and 0.001 μg/mouse, i.c.v.) following pretraining saline treatment did not affect retention. Amnesia induced by pretraining morphine was significantly reversed by pretest administration of L-glutamate (0.0001 and 0.001 μg/mouse, i.c.v.). Pretest administration of noncompetitive NMDA receptor antagonist, MK-801 (0.5, 1, and 2 μg/mouse, i.c.v.) significantly impaired memory formation. Amnesia induced by pretraining morphine was increased by pretest administration of...
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P02-168 Intra-dorsal hippocampal microinjection of lithium and scopolamine induce a cross State-Dependent Learning in mice
European Psychiatry, 2020Co-Authors: Batool Ghorbanalizadeh-khalifeh-mahaleh, Ameneh Rezayof, Ali Haeri-rohani, Saba Taheri, M. Sahengharani, Mohammad-reza ZarrindastAbstract:Background Lithium a mood stabilizer may exert adverse effects on memory. We have previously shown that lithium induces State-Dependent Learning. Cholinergic systems of the brain may play an important role in memory function and mood regulation. In the present study, effects of intra-dorsal hippocampal (intra-CA1) injections of lithium and scopolamine on memory and cross State-Dependent Learning between two drugs were investigated. Methods For memory assessment, a one-trial step-down inhibitory avoidance task was used in adult male NMRI mice. Results Intra-CA1 administration of lithium (0.5 and 1 μg/mouse) after training or injection of the drug (0.5μg/mouse) before testing impaired memory when retrieval was tested 24 h later. The memory impairment by post-training lithium was reversed by pre-test administration of the drug (0.5μg/mouse, intra-CA1) suggesting lithium State-Dependent Learning. On the other hand, intra-CA1 administration of scopolamine (0.5, 1 and 2 μg/mouse) after training or injection of the drug (2μg/mouse) before testing impaired memory when retrieval was tested 24 h later. The impairment of memory by post-training injection of scopolamine (2μg/mouse) was restored by the pre-test injection of the drug (1 and 2 μg/mouse). Furthermore, memory impairment induced by post-training injection of lithium (0.5 μg/mouse) and scopolamine (2 μg/mouse) were reversed by pre-test administration of scopolamine (0.5, 1 and 2 μg/mouse) and lithium (0.5 and 1 μg/mouse) respectively. The impairment by lithium was also reversed by physostigmine. Conclusion The results suggest that microinjection of both lithium and scopolamine induce State-Dependent memory and there may be a cross state-dependency between two drugs.
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Hippocampal nicotinic receptors have a modulatory role for ethanol and MDMA interaction in memory retrieval
Brain Research, 2017Co-Authors: Maryam Rostami, Ameneh Rezayof, Sakineh Alijanpour, Khadijeh Alsadat SharifiAbstract:Abstract The aim of the current study was to examine the effect of dorsal hippocampal nicotinic acetylcholine receptors (nAChRs) activation on the functional interaction between ethanol and 3,4-methylenedioxy-N-methylamphetamine (MDMA or ecstasy) in memory retrieval. The dorsal hippocampal CA1 regions of adult male NMRI mice were bilaterally cannulated and memory retrieval was measured in a step-down type passive avoidance apparatus. Post-training or pre-test systemic administration of ethanol (1 g/kg, i.p.) induced amnesia. Pre-test administration of ethanol reversed pre-training ethanol-induced amnesia, suggesting ethanol State-Dependent Learning. Pre-test intra-CA1 microinjection of different doses of MDMA (0.25–1 µg/mouse) with an ineffective dose of ethanol (0.25 g/kg, i.p.) also induced amnesia. Interestingly, pre-test intra-CA1 microinjection of MDMA (0.25–1 µg/mouse) potentiated ethanol State-Dependent Learning. On the other hand, the activation of the dorsal hippocampal nAChRs by pre-test microinjection of nicotine (0.1–1 µg/mouse, intra-CA1) improved amnesia induced by the co-administration of MDMD and ethanol. It is important to note that intra-CA1 microinjection of the same doses of MDMA or nicotine could not affect memory formation by itself. Pre-test intra-CA1 microinjection of nicotine (0.3–0.9 µg/mouse) could not reverse amnesia induced by pre-training administration of ethanol while this treatment enhanced MDMA response on ethanol State-Dependent Learning. Thus, it can be concluded that there may be functional interactions among ethanol, MDMA and nicotine via the dorsal hippocampal nicotinic acetylcholine receptor mechanism in memory retrieval and drug State-Dependent Learning.
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Alterations in the hippocampal phosphorylated CREB expression in drug State-Dependent Learning.
Behavioural Brain Research, 2015Co-Authors: Sakineh Alijanpour, Ameneh Rezayof, Houri Sepehri, Ladan DelphiAbstract:Abstract The present study investigated the possible alterations of hippocampal CREB phosphorylation in drug State-Dependent memory retrieval. One-trial step-down passive avoidance task was used to assess memory retrieval in adult male NMRI mice. Pre-training administration of ethanol (1 g/kg, i.p.) induced amnesia. Pre-test administration of ethanol (1 g/kg, i.p) or nicotine (0.7 mg/kg, s.c.) reversed ethanol-induced amnesia, indicating ethanol- or ethanol–nicotine induced State-Dependent Learning (STD). Using Western blot analysis, it was found that the p -CREB/CREB ratio in the hippocampus increased in the mice that showed successful memory retrieval as compared with untrained mice. In contrast, pre-training administration of ethanol (1 g/kg, i.p.) decreased the hippocampal p -CREB/CREB ratio in comparison with the control group. The hippocampal p -CREB/CREB ratio enhanced in ethanol- and ethanol–nicotine induced STD. Moreover, memory impairment induced by pre-training administration of WIN (1 mg/kg, i.p.) improved in the animals that received pre-test administration of WIN (1 mg/kg, i.p.), ethanol (0.5 g/kg, i.p.) or nicotine (0.7 mg/kg, s.c.), suggesting a cross STD between the drugs. The p -CREB/CREB ratio in the hippocampus decreased in the of WIN-induced amnesia and STD groups in comparison with the control group. In addition, cross State-Dependent Learning between WIN and ethanol or nicotine was associated with the increase of the hippocampal p -CREB/CREB ratio. It can be concluded that phosphorylation of CREB in the hippocampus is a critical event underlying the interaction of co-administration of drugs on memory retrieval in passive avoidance Learning.
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Proteome Analysis of Rat Hippocampus Following Morphine-induced Amnesia and State-Dependent Learning.
Iranian Journal of Pharmaceutical Research, 2015Co-Authors: Saeideh Jafarinejad-farsangi, Ameneh Rezayof, Ali Farazmand, Niloufar DarbandiAbstract:Morphine’s effects on Learning and memory processes are well known to depend on synaptic plasticity in the hippocampus. Whereas the role of the hippocampus in morphine-induced amnesia and State-Dependent Learning is established, the biochemical and molecular mechanisms underlying these processes are poorly understood. The present study intended to investigate whether administration of morphine can change the expression level of rat hippocampal proteins during Learning of a passive avoidance task. A step-through type passive avoidance task was used for the assessment of memory retention. To identify the complex pattern of protein expression induced by morphine, we compared rat hippocampal proteome either in morphine-induced amnesia or in State-Dependent Learning by two-dimensional gel electerophoresis and combined mass spectrometry (MS and MS/MS). Post-training administration of morphine decreased step-through latency. Pre-test administration of morphine induced State-Dependent retrieval of the memory acquired under post-training morphine influence. In the hippocampus, a total of 18 proteins were identified whose MASCOT (Modular Approach to Software Construction Operation and Test) scores were inside 95% confidence level. Of these, five hippocampal proteins altered in morphine-induced amnesia and ten proteins were found to change in the hippocampus of animals that had received post-training and pre-test morphine. These proteins show known functions in cytoskeletal architecture, cell metabolism, neurotransmitter secretion and neuroprotection. The findings indicate that the effect of morphine on memory formation in passive avoidance Learning has a morphological correlate on the hippocampal proteome level. In addition, our proteomic screen suggests that morphine induces memory impairment and State-Dependent Learning through modulating neuronal plasticity.
Yutaka Nakagawa - One of the best experts on this subject based on the ideXlab platform.
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Muscimol Induces State-Dependent Learning Whereas Baclofen Impairs Place Learning in Morris Water Maze Task in Rats
GABA: Receptors Transporters and Metabolism, 1996Co-Authors: Yutaka Nakagawa, Yoshinori Ishibashi, Toshio Yoshii, Eijiro Tagashira, Tsuneo IwasakiAbstract:Effects of muscimol and baclofen on place Learning in the Morris water maze task were examined. Rats were given 4 training trials per day for 4 days. Performance was impaired on day 4 in the rats treated with muscimol on day 1 to 3 and saline on day 4, suggesting that muscimol induces State-Dependent Learning (SDL). Baclofen injected on day 1 to 4 dose-dependently increased latency, indicating that baclofen induces the deficit of place Learning. Thus it is concluded that GABA-A and GABA-B receptors play different roles in Learning and memory: activation of GABA-A receptors may induce SDL, whereas GABA-B receptor stimulation may impair Learning and memory.
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Ethanol-induced State-Dependent Learning is mediated by 5-hydroxytryptamine3 receptors but not byN-methyl-d-aspartate receptor complex
Brain Research, 1996Co-Authors: Yutaka Nakagawa, Tsuneo IwasakiAbstract:Abstract Involvement of N -methyl- d -aspartate (NMDA) receptor complex and 5-hydroxytryptamine 3 (5-HT 3 ) receptors in State-Dependent Learning (SDL) induced by ethanol (EtOH) was investigated in the step-through passive avoidance task in rats. Pre-training injections of EtOH or MK-801 reduced step-through latency in the test session conducted 24 h after the training session. Pre-test as well as pre-training injections of EtOH failed to reduce the latency, while pre-training and pre-test injections of MK-801 reduced the latency. These results show that EtOH but not MK-801 produces SDL. SDL induced by EtOH was blocked by ICS205-930 injected before either the training or test session. However, ICS205-930 failed to block SDL induced by diazepam and muscimol. These results suggest that NMDA receptor complex may not be involved in SDL, and that 5-HT 3 receptors may contribute to SDL induced by EtOH but not by diazepam and muscimol.
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Involvement of benzodiazepine/GABA-A receptor complex in ethanol-induced State-Dependent Learning in rats
Brain Research, 1995Co-Authors: Yutaka Nakagawa, Tsuneo IwasakiAbstract:Abstract State-Dependent Learning (SDL) induced by ethanol (EtOH) was investigated on the step-through passive avoidance task in rats. Pretraining injection of EtOH dose-dependently reduced step-through latency in the test session 24 h after the training. Injection of EtOH (1.0 g/kg) before both the training and test sessions, however, failed to reduce the latency. These results show that EtOH produces SDL. The failure of Learning performance in SDL (dissociation in SDL) induced by EtOH was blocked by bicuculline, Ro15–4513 and picrotoxin injected before the training session. The success of Learning performance in SDL (non-dissociation in SDL) induced by EtOH was also blocked by bicuculline, Ro15–4513 and picrotoxin injected before the test session. The antagonism of Ro15–4513 against EtOH was blocked by flumazenil. In the substitution test, pretest injection of EtOH produced non-dissociation in SDL in the both of pretraining diazepam-and muscimol-treated rats. On the other hand, neither pretest injection of diazepam nor muscimol produced non-dissociation in the pretraining EtOH-treated rats: asymmetrical cross-substitution between EtOH and diazepam and between EtOH and muscimol was observed. These results suggest that the EtOH-induced SDL is partially mediated by the benzodiazepine (BDZ)/GABA-A receptor complex.
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Muscimol induces State-Dependent Learning in Morris water maze task in rats.
Brain Research, 1995Co-Authors: Yutaka Nakagawa, Yoshinori Ishibashi, Toshio Yoshii, Eijiro TagashiraAbstract:Effects of muscimol on the place Learning in Morris water maze task were investigated in rats. Rats were given 4 training trials per day with the submerged platform at a fixed location in the maze for 4 days. On day 4, rats were required to swim in the pool without the platform after 4 training trials (probe test). Compared to the saline-treated rats, the rats treated with muscimol on day 1–4 showed no modifications of place Learning in the training trials and the probe test. However, in the rats treated with muscimol on day 1–3 and treated with saline on day 4, there was increased latency to reach the platform and reduced duration in the quadrant where the platform had been located on day 4. The increased latency in the training trials and reduced duration in the probe test on day 4 was blocked by bicuculline, when bicuculline and muscimol were co-administrated on day 1–3, and saline was injected on day 4. Moreover, in the rats treated with muscimol on day 1–3, co-administration of bicuculline and muscimol on day 4 blocked place Learning: increased latency in the training trials and reduced duration in the probe test was observed. These results suggest that muscimol induces State-Dependent Learning (SDL) in Morris water maze task, and that muscimol-induced SDL is mediated by GABAA receptors.
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Muscimol induces State-Dependent Learning in Morris water maze task in rats.
Brain research, 1995Co-Authors: Yutaka Nakagawa, Yoshinori Ishibashi, Toshio Yoshii, Eijiro TagashiraAbstract:Effects of muscimol on the place Learning in Morris water maze task were investigated in rats. Rats were given 4 training trials per day with the submerged platform at a fixed location in the maze for 4 days. On day 4, rats were required to swim in the pool without the platform after 4 training trials (probe test). Compared to the saline-treated rats, the rats treated with muscimol on day 1-4 showed no modifications of place Learning in the training trials and the probe test. However, in the rats treated with muscimol on day 1-3 and treated with saline on day 4, there was increased latency to reach the platform and reduced duration in the quadrant where the platform had been located on day 4. The increased latency in the training trials and reduced duration in the probe test on day 4 was blocked by bicuculline, when bicuculline and muscimol were co-administered on day 1-3, and saline was injected on day 4. Moreover, in the rats treated with muscimol on day 1-3, co-administration of bicuculline and muscimol on day 4 blocked place Learning: increased latency in the training trials and reduced duration in the probe test was observed. These results suggest that muscimol induces State-Dependent Learning (SDL) in Morris water maze task, and that muscimol-induced SDL is mediated by GABAA receptors.
Niloufar Darbandi - One of the best experts on this subject based on the ideXlab platform.
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Proteome Analysis of Rat Hippocampus Following Morphine-induced Amnesia and State-Dependent Learning.
Iranian Journal of Pharmaceutical Research, 2015Co-Authors: Saeideh Jafarinejad-farsangi, Ameneh Rezayof, Ali Farazmand, Niloufar DarbandiAbstract:Morphine’s effects on Learning and memory processes are well known to depend on synaptic plasticity in the hippocampus. Whereas the role of the hippocampus in morphine-induced amnesia and State-Dependent Learning is established, the biochemical and molecular mechanisms underlying these processes are poorly understood. The present study intended to investigate whether administration of morphine can change the expression level of rat hippocampal proteins during Learning of a passive avoidance task. A step-through type passive avoidance task was used for the assessment of memory retention. To identify the complex pattern of protein expression induced by morphine, we compared rat hippocampal proteome either in morphine-induced amnesia or in State-Dependent Learning by two-dimensional gel electerophoresis and combined mass spectrometry (MS and MS/MS). Post-training administration of morphine decreased step-through latency. Pre-test administration of morphine induced State-Dependent retrieval of the memory acquired under post-training morphine influence. In the hippocampus, a total of 18 proteins were identified whose MASCOT (Modular Approach to Software Construction Operation and Test) scores were inside 95% confidence level. Of these, five hippocampal proteins altered in morphine-induced amnesia and ten proteins were found to change in the hippocampus of animals that had received post-training and pre-test morphine. These proteins show known functions in cytoskeletal architecture, cell metabolism, neurotransmitter secretion and neuroprotection. The findings indicate that the effect of morphine on memory formation in passive avoidance Learning has a morphological correlate on the hippocampal proteome level. In addition, our proteomic screen suggests that morphine induces memory impairment and State-Dependent Learning through modulating neuronal plasticity.
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THE INHIBITION OF NUCLEUS ACCUMBENS CHOLINERGIC RECEPTORS DECREASED MEMORY RETENTION IN RAT
Arak Medical University Journal, 2014Co-Authors: Ameneh Rezayof, Mohammad-reza Zarrindast, Niloufar DarbandiAbstract:Background: It is well known that morphine influence Learning and memory processes. The Nucleus accumbens (N.ac) which has an important role in reward participates in morphine-induced impairment of memory retention. Considering the cholinergic system is involved in the effects of morphine on Learning and memory, in the present study, the effects of intra-N.ac injections of acetylcholine receptor antagonists alone or with morphine on memory retention and morphine-induced memory has been investigated in rats. Materials and Methods: In this original research animals were bilaterally cannulated in the N.ac and a step-through passive avoidance task was used for the assessment of memory retention . Results: Post-training subcutaneous administration of morphine dose dependently decreased the Learning and induced amnesia. The administration of the same dose of morphine as pre-test treatment induced State-Dependent Learning. Pre-test intra- N.ac administration of atropine, scopolamine and mecamylamine in different doses alone cannot affect on memory retention. While, pretest intra- N.ac injection of these drugs before the administration of morphine dose dependently inhibited morphine State-Dependent Learning. The level of statistical significance was set at p
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Nicotinic acetylcholine receptors of the ventral tegmental area are involved in mediating morphine-State-Dependent Learning.
Neurobiology of Learning and Memory, 2008Co-Authors: Ameneh Rezayof, Niloufar Darbandi, Mohammad-reza ZarrindastAbstract:Abstract In the present study, the possible role of nicotinic acetylcholine (nACh) receptors of the ventral tegmental area (VTA) on morphine-State-Dependent Learning was studied in adult male Wistar rats. As a model of memory, a step-through type passive avoidance task was used. All animals were bilaterally implanted with chronic cannulae in the VTA, trained using a 1 mA foot shock, and tested 24 h after training to measure step-through latency. Post-training subcutaneous (s.c.) injection of morphine (0.5–5 mg/kg) dose-dependently reduced the step-through latency, showing morphine-induced amnesia. Amnesia induced by post-training morphine was significantly reversed by pre-test administration of morphine (2.5–5 mg/kg, s.c.) and induced morphine-State-Dependent Learning. Pre-test injection of nicotine (0.25–1 μg/rat) into the VTA plus an ineffective dose of morphine (0.5 mg/kg) significantly restored the memory retrieval. It should be noted that pre-test intra-VTA injection of the same doses of nicotine (0.25–1 μg/rat) alone cannot affect memory retention. Furthermore, pre-test intra-VTA injection of the nicotinic acetylcholine receptor antagonist, mecamylamine (1–3 μg/rat) 5 min before the administration of morphine (5 mg/kg, s.c.) dose-dependently inhibited morphine-State-Dependent Learning. Pre-test injection of the higher dose of mecamylamine (3 μg/rat) into the VTA by itself decreased the step-through latency and induced amnesia. On the other hand, mecamylamine (0.5 and 1 μg/rat, intra-VTA) reversed the effect of nicotine on morphine response. The results indicate that nACh receptors in the VTA participate in the modulation of morphine-induced recovery of memory, on the test day.
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Potentiation of acetylcholine action in the ventral tegmental area facilitates morphine-state dependent Learning
Annals of General Psychiatry, 2008Co-Authors: Niloufar Darbandi, Ameneh Rezayof, Mohammad-reza ZarrindastAbstract:Meeting abstracts - A single PDF containing all abstracts in this Supplement is available here .
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Modulation of morphine State-Dependent Learning by muscarinic cholinergic receptors of the ventral tegmental area
Physiology & Behavior, 2008Co-Authors: Niloufar Darbandi, Ameneh Rezayof, Mohammad-reza ZarrindastAbstract:Abstract In the present study, the effects of bilateral intra-ventral tegmental area (intra-VTA) injections of an anticholinesterase, physostigmine and/or muscarinic acetylcholine receptor antagonist, atropine on memory retention and morphine State-Dependent Learning were examined in adult male Wistar rats. As a model of Learning, a step-through passive avoidance task was used. Post-training subcutaneous administration of morphine (0.5, 2.5 and 5 mg/kg) dose-dependently impaired memory retrieval on the test day. Pre-test administration of morphine (2.5 and 5 mg/kg) induced State-Dependent retrieval of the memory acquired under post-training morphine influence. Pre-test intra-VTA microinjection of physostigmine (0.5, 1 and 2 μg/rat) or atropine (1, 2 and 3 μg/rat) alone cannot affect memory retention. Interestingly, pre-test intra-VTA administration of physostigmine (1 and 2 μg/rat) reversed post-training morphine (5 mg/kg, s.c.)-induced retrieval impairment. Furthermore, pre-test intra-VTA microinjection of physostigmine (1 and 2 μg/rat) with an ineffective dose of morphine (0.5 mg/kg), synergistically improved memory performance impaired by post-training morphine. On the other hand, pre-test intra-VTA microinjection of atropine (2 and 3 μg/rat) 5 min before the administration of morphine (5 mg/kg, s.c.) dose-dependently inhibited morphine State-Dependent memory. Pre-test atropine microinjection also reversed the influence of physostigmine on morphine response. It may be concluded that the muscarinic acetylcholine receptors of the VTA play an important role in morphine-induced recovery of memory, on the test day.
Tsuneo Iwasaki - One of the best experts on this subject based on the ideXlab platform.
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Muscimol Induces State-Dependent Learning Whereas Baclofen Impairs Place Learning in Morris Water Maze Task in Rats
GABA: Receptors Transporters and Metabolism, 1996Co-Authors: Yutaka Nakagawa, Yoshinori Ishibashi, Toshio Yoshii, Eijiro Tagashira, Tsuneo IwasakiAbstract:Effects of muscimol and baclofen on place Learning in the Morris water maze task were examined. Rats were given 4 training trials per day for 4 days. Performance was impaired on day 4 in the rats treated with muscimol on day 1 to 3 and saline on day 4, suggesting that muscimol induces State-Dependent Learning (SDL). Baclofen injected on day 1 to 4 dose-dependently increased latency, indicating that baclofen induces the deficit of place Learning. Thus it is concluded that GABA-A and GABA-B receptors play different roles in Learning and memory: activation of GABA-A receptors may induce SDL, whereas GABA-B receptor stimulation may impair Learning and memory.
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Ethanol-induced State-Dependent Learning is mediated by 5-hydroxytryptamine3 receptors but not byN-methyl-d-aspartate receptor complex
Brain Research, 1996Co-Authors: Yutaka Nakagawa, Tsuneo IwasakiAbstract:Abstract Involvement of N -methyl- d -aspartate (NMDA) receptor complex and 5-hydroxytryptamine 3 (5-HT 3 ) receptors in State-Dependent Learning (SDL) induced by ethanol (EtOH) was investigated in the step-through passive avoidance task in rats. Pre-training injections of EtOH or MK-801 reduced step-through latency in the test session conducted 24 h after the training session. Pre-test as well as pre-training injections of EtOH failed to reduce the latency, while pre-training and pre-test injections of MK-801 reduced the latency. These results show that EtOH but not MK-801 produces SDL. SDL induced by EtOH was blocked by ICS205-930 injected before either the training or test session. However, ICS205-930 failed to block SDL induced by diazepam and muscimol. These results suggest that NMDA receptor complex may not be involved in SDL, and that 5-HT 3 receptors may contribute to SDL induced by EtOH but not by diazepam and muscimol.
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Involvement of benzodiazepine/GABA-A receptor complex in ethanol-induced State-Dependent Learning in rats
Brain Research, 1995Co-Authors: Yutaka Nakagawa, Tsuneo IwasakiAbstract:Abstract State-Dependent Learning (SDL) induced by ethanol (EtOH) was investigated on the step-through passive avoidance task in rats. Pretraining injection of EtOH dose-dependently reduced step-through latency in the test session 24 h after the training. Injection of EtOH (1.0 g/kg) before both the training and test sessions, however, failed to reduce the latency. These results show that EtOH produces SDL. The failure of Learning performance in SDL (dissociation in SDL) induced by EtOH was blocked by bicuculline, Ro15–4513 and picrotoxin injected before the training session. The success of Learning performance in SDL (non-dissociation in SDL) induced by EtOH was also blocked by bicuculline, Ro15–4513 and picrotoxin injected before the test session. The antagonism of Ro15–4513 against EtOH was blocked by flumazenil. In the substitution test, pretest injection of EtOH produced non-dissociation in SDL in the both of pretraining diazepam-and muscimol-treated rats. On the other hand, neither pretest injection of diazepam nor muscimol produced non-dissociation in the pretraining EtOH-treated rats: asymmetrical cross-substitution between EtOH and diazepam and between EtOH and muscimol was observed. These results suggest that the EtOH-induced SDL is partially mediated by the benzodiazepine (BDZ)/GABA-A receptor complex.
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Interaction between benzodiazepine and GABA-A receptors in State-Dependent Learning
Life Sciences, 1993Co-Authors: Yutaka Nakagawa, Tsuneo Iwasaki, Tsuyoshi Ishima, Kiyoshi KimuraAbstract:Abstract State-Dependent Learning (SDL) induced by benzodiazepine (BDZ) and GABA-A agonists was investigated in the step-through passive avoidance task in rats. Pre-training injection of diazepam or muscimol dose-dependently reduced step-through latency in the test session conducted 24 hr after the training. Injection of either drug before both the training and test sessions, however, failed to reduce the latency. The results show that passive avoidance failures induced by pre-training injections of diazepam and muscimol are due to SDL. In contrast to diazepam and muscimol, baclofen induced no SDL. Diazepam and muscimol were found to substitute for each other in producing SDL. The failure of Learning performance in SDL (dissociation in SDL) induced by diazepam was blocked by flumazenil and picrotoxin but not by bicuculline injected before the training session, whereas dissociation in SDL induced by muscimol was blocked by flumazenil, bicuculline and picrotoxin. On the other hand, the success of Learning performance in SDL (non-dissociation in SDL) induced by diazepam was blocked by flumazenil, bicuculline and picrotoxin injected before the test session, whereas non-dissociation in SDL induced by muscimol was blocked by bicuculline and picrotoxin but not by flumazenil. These results demonstrate that 1) BDZ and GABA-A agonists produce a common drug state, but, 2) roles of each receptor in SDL might be different, i.e., BDZ receptors for dissociation in SDL and GABA-A receptors for non-dissociation in SDL, and 3) chloride ion channels are essential for the induction of SDL by BDZ and GABA-A agonists.