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Anthony Robins - One of the best experts on this subject based on the ideXlab platform.
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Memory Retention the synaptic stability versus plasticity dilemma
Trends in Neurosciences, 2005Co-Authors: Wickliffe C. Abraham, Anthony RobinsAbstract:Memory maintenance is widely believed to involve long-term Retention of the synaptic weights that are set within relevant neural circuits during learning. However, despite recent exciting technical advances, it has not yet proved possible to confirm experimentally this intuitively appealing hypothesis. Artificial neural networks offer an alternative methodology as they permit continuous monitoring of individual connection weights during learning and Retention. In such models, ongoing alterations in connection weights are required if a network is to retain previously stored material while learning new information. Thus, the duration of synaptic change does not necessarily define the persistence of a Memory; rather, it is likely that a regulated balance of synaptic stability and synaptic plasticity is required for optimal Memory Retention in real neuronal circuits.
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Memory Retention – the synaptic stability versus plasticity dilemma
Trends in neurosciences, 2005Co-Authors: Wickliffe C. Abraham, Anthony RobinsAbstract:Memory maintenance is widely believed to involve long-term Retention of the synaptic weights that are set within relevant neural circuits during learning. However, despite recent exciting technical advances, it has not yet proved possible to confirm experimentally this intuitively appealing hypothesis. Artificial neural networks offer an alternative methodology as they permit continuous monitoring of individual connection weights during learning and Retention. In such models, ongoing alterations in connection weights are required if a network is to retain previously stored material while learning new information. Thus, the duration of synaptic change does not necessarily define the persistence of a Memory; rather, it is likely that a regulated balance of synaptic stability and synaptic plasticity is required for optimal Memory Retention in real neuronal circuits.
Wickliffe C. Abraham - One of the best experts on this subject based on the ideXlab platform.
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Memory Retention the synaptic stability versus plasticity dilemma
Trends in Neurosciences, 2005Co-Authors: Wickliffe C. Abraham, Anthony RobinsAbstract:Memory maintenance is widely believed to involve long-term Retention of the synaptic weights that are set within relevant neural circuits during learning. However, despite recent exciting technical advances, it has not yet proved possible to confirm experimentally this intuitively appealing hypothesis. Artificial neural networks offer an alternative methodology as they permit continuous monitoring of individual connection weights during learning and Retention. In such models, ongoing alterations in connection weights are required if a network is to retain previously stored material while learning new information. Thus, the duration of synaptic change does not necessarily define the persistence of a Memory; rather, it is likely that a regulated balance of synaptic stability and synaptic plasticity is required for optimal Memory Retention in real neuronal circuits.
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Memory Retention – the synaptic stability versus plasticity dilemma
Trends in neurosciences, 2005Co-Authors: Wickliffe C. Abraham, Anthony RobinsAbstract:Memory maintenance is widely believed to involve long-term Retention of the synaptic weights that are set within relevant neural circuits during learning. However, despite recent exciting technical advances, it has not yet proved possible to confirm experimentally this intuitively appealing hypothesis. Artificial neural networks offer an alternative methodology as they permit continuous monitoring of individual connection weights during learning and Retention. In such models, ongoing alterations in connection weights are required if a network is to retain previously stored material while learning new information. Thus, the duration of synaptic change does not necessarily define the persistence of a Memory; rather, it is likely that a regulated balance of synaptic stability and synaptic plasticity is required for optimal Memory Retention in real neuronal circuits.
Mohammad-reza Zarrindast - One of the best experts on this subject based on the ideXlab platform.
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The effect of CA1 α2 adrenergic receptors on Memory Retention deficit induced by total sleep deprivation and the reversal of circadian rhythm in a rat model
Neurobiology of learning and memory, 2016Co-Authors: Yaser Norozpour, Mohammad Nasehi, Vahid Sabouri-khanghah, Mohammad Torabi-nami, Mohammad-reza ZarrindastAbstract:Abstract The α2 adrenergic receptors which abundantly express in the CA1 region of the hippocampus play an important role in the regulation of sleep and Memory Retention processes. Based on the available evidence, the aim of our study was to investigate consequences of the activation and deactivation of CA1 α2 adrenergic receptors (by clonidine and yohimbine, respectively) on the impairment of Memory Retention induced by total sleep deprivation (TSD) and the reversal of circadian rhythm (RCR) in a rat model. To this end, the water box apparatus and passive avoidance task were in turn used to induce sleep deprivation and assess Memory Retention. Our findings suggested that TSD (for 24 and 36, but not 12 h) and RCR (12 h/day for 3 consecutive days) impair Memory function. The post-training intra-CA1 administration of yohimbine (α2 adrenergic receptor antagonist) on its own, at the dose of 0.1 μg/rat, decreased the step-through latency and locomotor activity in the TSD- sham treated but not undisturbed sleep rats. Unlike yohimbine, clonidine (α2 adrenergic receptor agonist), in all applied doses (0.001, 0.01 and 0.1 μg/rat), failed to induce such an effect. While the subthreshold dose of yohimbine (0.001 μg/rat) abrogated the impairment of Memory Retention induced by the 24-h TSD, it could potentiate the impairment of Memory Retention induced by 36-h TSD, suggesting the modulatory effect of yohimbine. Moreover, the subthreshold dose of clonidine (0.1 μg/rat) restored the Memory Retention deficit in TSD rats (24 and 36 h). On the other hand, the subthreshold dose of clonidine (0.1 μg/rat), but not yohimbine (0.001 μg/rat) restored the Memory Retention deficit in RCR rats. Such interventions however did not alter the locomotor activity. The above observations proposed that CA1 α2 adrenergic receptors play a potential role in Memory Retention deficits induced by TSD and RCR.
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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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post training intrahippocampal infusion of nicotine bucladesine combination causes a synergistic enhancement effect on spatial Memory Retention in rats
European Journal of Pharmacology, 2007Co-Authors: Mostafa Sharifzadeh, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Ali Roghani, Mohammad-reza ZarrindastAbstract:Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial Memory Retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial Memory Retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial Memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial Memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM bucladesine alone did not lead to an improvement in spatial Memory. However, such bilateral infusion of bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial Memory Retention. Taken together, our data suggest that intrahippocampal bucladesine infusions improve spatial Memory Retention in male rats and that bucladesine can interact synergistically with nicotine to improve spatial Memory.
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Post-training intrahippocampal infusion of nicotine–bucladesine combination causes a synergistic enhancement effect on spatial Memory Retention in rats
European Journal of Pharmacology, 2007Co-Authors: Mostafa Sharifzadeh, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Mohammad-reza Zarrindast, Ali RoghaniAbstract:Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial Memory Retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial Memory Retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial Memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial Memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM bucladesine alone did not lead to an improvement in spatial Memory. However, such bilateral infusion of bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial Memory Retention. Taken together, our data suggest that intrahippocampal bucladesine infusions improve spatial Memory Retention in male rats and that bucladesine can interact synergistically with nicotine to improve spatial Memory.
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Involvement of the ventral tegmental area (VTA) in morphine-induced Memory Retention in morphine-sensitized rats.
Behavioural brain research, 2005Co-Authors: Mohammad-reza Zarrindast, Ameneh Rezayof, Parvin Rostami, Zahra Farajzadeh, Parvaneh NourjahAbstract:Abstract In the present study, the effects of intra-ventral tegmental area (VTA) injections of morphine on Memory Retention of a one-trial passive avoidance task have been investigated in morphine-sensitized rats. Retrieval was examined 24 h after training and used as Memory Retention. Sensitization was obtained by subcutaneous (s.c.) injections of morphine, once daily for 3 and 5 days free of the opioid before training. Post-training administration of the both systemic (2.5, 5 and 7.5 mg/kg, s.c.) and intra-VTA (5 and 7.5 μg/rat) of morphine, dose-dependently decreased Memory Retention. The response induced by post-training administration of intra-VTA morphine (7.5 μg/rat) was significantly reversed in morphine-sensitized rats. The inhibition of morphine-induced amnesia in morphine-sensitized rats was decreased by once daily injections of naloxone (0.5, 1 and 2 mg/kg, s.c.), SCH 23390 (0.025, 0.05 and 0.1 mg/kg, s.c.) or sulpiride (25, 50 and 100 mg/kg, s.c.), during the sensitization. The results suggest that VTA has an important role in morphine-induced amnesia and morphine sensitization affects this process through opioid and dopamine receptors.
Ali Roghani - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of systemic administration of Boswellia papyrifera extracts on spatial Memory Retention in male rats
Journal of Natural Medicines, 2011Co-Authors: Ali Mahmoudi, Ali Hosseini-sharifabad, Ali R. Yazdinejad, Hamid Reza Monsef-esfahani, Ali Roghani, Mahnaz Khanavi, Cordian Beyer, Mostafa SharifzadehAbstract:Time-dependent effects of ethanolic extract of Boswellia papyrifera, administered systemically, on spatial Memory Retention in the Morris water maze were investigated in male rats. A total extract of Boswellia papyrifera (300 mg/kg) was administered every eight hours to three groups of rats by gavage for 1, 2 and 4 weeks. In a separate set of experiments, three doses of a fraction of the extract, called the boswellic acids (100, 200 and 300 mg/kg) were administered by gavage to three groups of rats three times a day for 2 weeks. Following these applications, animals were trained for 4 days. Behavioral testing for evaluation of spatial Memory Retention was performed 48 h after completion of training. Boswellia papyrifera extracts and boswellic acids caused a significant reduction in escape latency and distance traveled but had no influence on swimming speed. These findings provide evidence that Boswellia papyrifera extracts affect spatial Memory Retention irrespective of the treatment period. In addition our data show that systemic administration of the boswellic acids fraction enhanced spatial Memory Retention in a dose-dependent manner. These improving effects may be due to some extent to the interactions of these products with inflammatory mediators, neurotransmitter signaling cascades or protein kinase pathways in the brain.
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post training intrahippocampal infusion of nicotine bucladesine combination causes a synergistic enhancement effect on spatial Memory Retention in rats
European Journal of Pharmacology, 2007Co-Authors: Mostafa Sharifzadeh, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Ali Roghani, Mohammad-reza ZarrindastAbstract:Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial Memory Retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial Memory Retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial Memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial Memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM bucladesine alone did not lead to an improvement in spatial Memory. However, such bilateral infusion of bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial Memory Retention. Taken together, our data suggest that intrahippocampal bucladesine infusions improve spatial Memory Retention in male rats and that bucladesine can interact synergistically with nicotine to improve spatial Memory.
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Post-training intrahippocampal infusion of nicotine–bucladesine combination causes a synergistic enhancement effect on spatial Memory Retention in rats
European Journal of Pharmacology, 2007Co-Authors: Mostafa Sharifzadeh, Alireza Zamanian, Shervin Gholizadeh, Kaveh Tabrizian, Maryam Etminani, Siavash Khalaj, Mohammad-reza Zarrindast, Ali RoghaniAbstract:Abstract We previously had shown that bilateral intrahippocampal infusion of 1 μg nicotine (but not 0.5 μg dose) led to an improvement in spatial Memory Retention in the Morris water maze task in male rats. We also reported that a similar type of bilateral infusion of H89, a protein kinase AII (PKA II) inhibitor, caused a deficit in spatial Memory Retention. In the present study, we wished to test the hypothesis that intrahippocampal infusion of dibutyryl cyclic AMP (DB-cAMP also called bucladesine), a membrane permeable selective activator of PKA, into the CA1 region can cause an improvement in spatial Memory in this maze task. Indeed, bilateral infusion of 10 and 100 μM bucladesine (but not 1 and 5 μM doses) led to a significant reduction in escape latency and travel distance (showing an improvement in spatial Memory) compared to the control. Also, bilateral infusion of 0.5 μg nicotine or 1 μM bucladesine alone did not lead to an improvement in spatial Memory. However, such bilateral infusion of bucladesine at 1 and 5 μM concentrations infused within minutes after 0.5 μg nicotine infusion improved spatial Memory Retention. Taken together, our data suggest that intrahippocampal bucladesine infusions improve spatial Memory Retention in male rats and that bucladesine can interact synergistically with nicotine to improve spatial Memory.
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Post-training intrahippocampal infusion of nicotine prevents spatial Memory Retention deficits induced by the cyclo-oxygenase-2-specific inhibitor celecoxib in rats.
Journal of neurochemistry, 2005Co-Authors: Mostafa Sharifzadeh, Nasser Naghdi, Mahtab Tavasoli, Azam Ghanbari, Mohsen Amini, Ali RoghaniAbstract:Recently, we demonstrated that intrahippocampal infusion of the cyclo-oxygenase (COX)-2-specific inhibitor celecoxib impaired spatial Memory Retention in the Morris water maze. In the present work, we investigated the effects of nicotine, infused in the rat dorsal hippocampus several minutes after infusion of celecoxib, on Memory Retention in the Morris water maze. Rats were trained for 3 days; each day included two blocks, and each block contained four trials. Test trials were conducted 48 h after surgery. As expected, bilateral intrahippocampal infusion of celecoxib (19 µg/side; 0.1 m) increased escape latency and travel distance in rats, indicating significant impairment of spatial Memory Retention. We also examined the effects of bilateral infusion of nicotine (0.5, 1.0 and 2.0 µg/side) on Memory Retention. Infusion of 1 µg nicotine significantly decreased escape latency and travel distance but not swimming speed, compared with controls, suggesting Memory Retention enhancement by nicotine at this concentration. In separate experiments, bilateral infusion of nicotine, infused 5 min after 0.1 m (19 µg/side) celecoxib infusion, was associated with escape latency, travel distance and swimming speed profiles very similar to those in control animals. Brain tissue sections from several of these animals were subjected to immunohistochemical staining analysis with anti-COX-2 antibodies. Quantification analysis by optical density measurements showed that the celecoxib infusion reduced the immunoreactivity of COX-2-containing neurons in the CA1 area of the hippocampus compared with controls, although this reduction was not significant. However, infusion of a combination of celecoxib and nicotine significantly increased this immunoreactivity compared with levels in control and celecoxib-infused groups. These results suggest that nicotine prevented or reversed the adverse effects of celecoxib on spatial Memory Retention and protected or restored the immunostaining pattern of COX-2 neurons in the rat dorsal hippocampus.
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Post-training intrahippocampal infusion of the COX-2 inhibitor celecoxib impaired spatial Memory Retention in rats.
European journal of pharmacology, 2005Co-Authors: Mostafa Sharifzadeh, Nasser Naghdi, Sara Khosrovani, Seyed Nasser Ostad, Kurdistan Sharifzadeh, Ali RoghaniAbstract:In this study, we investigated the effects of intrahippocampal infusion of indomethacin as a non-selective cyclooxygenase inhibitor and celecoxib as a selective cyclooxygenase-2 inhibitor on spatial Memory in the Morris water maze. Rats were trained for 3 days; each day included two blocks, and each block contained 4 trials. Tests were performed 48 h after surgery. Bilateral intrahippocampal infusion of indomethacin (0.01, 0.1, or 1 M) did not show any significant effect on spatial Memory Retention at these concentrations in rats. We also examined effects of infusion of celecoxib (0.02, 0.06, or 0.1 M) on Memory Retention. Bilateral infusion of 0.1 M celecoxib significantly altered escape latency and traveled distance in rats. These results strongly suggest that cyclooxygenase-2 is involved in spatial Memory Retention.
Barry H. Kantowitz - One of the best experts on this subject based on the ideXlab platform.
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Driver Memory Retention of in-vehicle information system messages
Transportation Research Record, 1997Co-Authors: Richard J. Hanowski, Barry H. KantowitzAbstract:Memory Retention of drivers was tested for traffic- and traveler-related messages displayed on an in-vehicle information system (IVIS). Three research questions were asked: (a) How does in-vehicle visual message format affect comprehension? (b) How does message format affect Memory Retention? and (c) What impact does driver age have on recall of in-vehicle visual messages? Nine younger (less than 30 years old) and nine older (65 years old or older) drivers participated in the experiment. As subjects steered the Battelle Automobile Simulator, an IVIS presented traveler-related messages. Two types of messages, symbols and text, were presented. Message recognition was tested immediately or 50 sec after the message left the IVIS. Except for low comprehension symbols, driver recognition scores on both text and symbol messages were similar. Younger drivers scored higher than older drivers in identifying the meaning of messages, particularly in the 50-sec question delay condition. Latency to respond to the quest...
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Driver Memory Retention of In-Vehicle Information System Messages
Transportation Research Record: Journal of the Transportation Research Board, 1997Co-Authors: Richard J. Hanowski, Barry H. KantowitzAbstract:Memory Retention of drivers was tested for traffic- and traveler-related messages displayed on an in-vehicle information system (IVIS). Three research questions were asked: ( a) How does in-vehicle visual message format affect comprehension? ( b) How does message format affect Memory Retention? and ( c) What impact does driver age have on recall of in-vehicle visual messages? Nine younger (less than 30 years old) and nine older (65 years old or older) drivers participated in the experiment. As subjects steered the Battelle Automobile Simulator, an IVIS presented traveler-related messages. Two types of messages, symbols and text, were presented. Message recognition was tested immediately or 50 sec after the message left the IVIS. Except for low comprehension symbols, driver recognition scores on both text and symbol messages were similar. Younger drivers scored higher than older drivers in identifying the meaning of messages, particularly in the 50-sec question delay condition. Latency to respond to the questions and confidence in the responses were also affected by question delay, with longer response latencies and lower self-rated confidence scores for the longer delay conditions. Message presentation did not degrade vehicle control.