The Experts below are selected from a list of 11934 Experts worldwide ranked by ideXlab platform
Pascal Roullet - One of the best experts on this subject based on the ideXlab platform.
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creb antisense oligodeoxynucleotide administration into the dorsal Hippocampal CA3 Region impairs long but not short term spatial memory in mice
Learning & Memory, 2006Co-Authors: Cédrick Florian, Nicole Mons, Pascal RoulletAbstract:The transcription factor cAMP response-element binding protein (CREB) has a pivotal role in Hippocampal synaptic plasticity and hippocampus-dependent long-term memory. We recently demonstrated that the dorsal Hippocampal CA3 Region is involved in memory consolidation of spatial information tested on a Morris water maze in mice. To test whether activation of CREB in the CA3 Region is required for memory consolidation of spatial information, bilaterally cannulated mice were infused 18 h before the beginning of the behavioral training with antisense or control sense CREB oligodeoxynucleotides (ODNs) or buffer. Mice were then subjected to massed training in a spatial version of the water maze and tested for retention 0 or 24 h after the last training session. We showed that CREB antisense ODN-infusion in the CA3 Region impaired long-term memory when tested 24 h later but had no effect on spatial acquisition or short-term memory tested immediately after behavioral training. These findings provide evidence that the Regionally restricted activation of CREB in the dorsal Hippocampal CA3 Region is critical for the long-term memory consolidation phase of spatial learning but not for short-term memory.
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Hippocampal CA3-Region is crucial for acquisition and memory consolidation in Morris water maze task in mice.
Behavioural Brain Research, 2004Co-Authors: Cédrick Florian, Pascal RoulletAbstract:This experiment investigated the involvement of the dorsal Hippocampal CA3-Region in the different phases of learning and memory in spatial and non-spatial tasks. To do so, we temporarily inactivated the CA3-subfield by a focal injection of diethyldithiocarbamate (DDC) which chelates most of the heavy metals present in this Region. The effects of temporary inactivation of the CA3-Region were examined in an associative task, the Morris water maze (MWM). To study the different phase of memory we used a new behavioural massed-procedure founded on four massed training sessions in the spatial and the non-spatial (cue) version of this task. In the spatial version, we showed that a bilateral injection of DDC into the CA3-Region impairs the acquisition but not the recall of spatial information. The main result of this study is that the same injection performed immediately after the training session also perturbed memory consolidation. In the cue version of the MWM, we found no difference between the DDC-injected mice and their controls in acquisition or memory consolidation of non-spatial information. These results suggest that the Hippocampal CA3-Region is essential for spatial memory processes and specifically in memory consolidation of spatial information.
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Involvement of the Hippocampal CA3-Region in acquisition and in memory consolidation of spatial but not in object information in mice.
Neurobiology of Learning and Memory, 2003Co-Authors: Grégory Stupien, Cédrick Florian, Pascal RoulletAbstract:This study investigates the implication of the Hippocampal CA3-Region in the different phases of learning and memory in spatial and non-spatial tasks. For that purpose, we performed focal injections of diethyldithiocarbamate (DDC) into the CA3-Region of the dorsal hippocampus. The DDC chelates most of the heavy metals in the brain which blocks selectively and reversibly the synapses containing heavy metals, i.e., the mossy fibres synaptic buttons and synapses of the dendrites of pyramidal cells. The effects of temporal inactivation of the CA3-Region was examined in a non-associative task, the spatial open-field, designed to estimate the ability of mice to react to spatial changes, and in the object recognition task, designed to estimate the ability of mice to identify a familiar object. The results show that DDC induced a specific impairment on learning and memory consolidation in the spatial open-field but had no effect on recall in this task. In the object recognition task, DDC did not induce any impairment in the different phases of learning and memory. These data demonstrate that the Hippocampal CA3-Region is specifically implicated in spatial information processing and seems to be involved not only in acquisition but also in consolidation of spatial information.
Cédrick Florian - One of the best experts on this subject based on the ideXlab platform.
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creb antisense oligodeoxynucleotide administration into the dorsal Hippocampal CA3 Region impairs long but not short term spatial memory in mice
Learning & Memory, 2006Co-Authors: Cédrick Florian, Nicole Mons, Pascal RoulletAbstract:The transcription factor cAMP response-element binding protein (CREB) has a pivotal role in Hippocampal synaptic plasticity and hippocampus-dependent long-term memory. We recently demonstrated that the dorsal Hippocampal CA3 Region is involved in memory consolidation of spatial information tested on a Morris water maze in mice. To test whether activation of CREB in the CA3 Region is required for memory consolidation of spatial information, bilaterally cannulated mice were infused 18 h before the beginning of the behavioral training with antisense or control sense CREB oligodeoxynucleotides (ODNs) or buffer. Mice were then subjected to massed training in a spatial version of the water maze and tested for retention 0 or 24 h after the last training session. We showed that CREB antisense ODN-infusion in the CA3 Region impaired long-term memory when tested 24 h later but had no effect on spatial acquisition or short-term memory tested immediately after behavioral training. These findings provide evidence that the Regionally restricted activation of CREB in the dorsal Hippocampal CA3 Region is critical for the long-term memory consolidation phase of spatial learning but not for short-term memory.
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Hippocampal CA3-Region is crucial for acquisition and memory consolidation in Morris water maze task in mice.
Behavioural Brain Research, 2004Co-Authors: Cédrick Florian, Pascal RoulletAbstract:This experiment investigated the involvement of the dorsal Hippocampal CA3-Region in the different phases of learning and memory in spatial and non-spatial tasks. To do so, we temporarily inactivated the CA3-subfield by a focal injection of diethyldithiocarbamate (DDC) which chelates most of the heavy metals present in this Region. The effects of temporary inactivation of the CA3-Region were examined in an associative task, the Morris water maze (MWM). To study the different phase of memory we used a new behavioural massed-procedure founded on four massed training sessions in the spatial and the non-spatial (cue) version of this task. In the spatial version, we showed that a bilateral injection of DDC into the CA3-Region impairs the acquisition but not the recall of spatial information. The main result of this study is that the same injection performed immediately after the training session also perturbed memory consolidation. In the cue version of the MWM, we found no difference between the DDC-injected mice and their controls in acquisition or memory consolidation of non-spatial information. These results suggest that the Hippocampal CA3-Region is essential for spatial memory processes and specifically in memory consolidation of spatial information.
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Involvement of the Hippocampal CA3-Region in acquisition and in memory consolidation of spatial but not in object information in mice.
Neurobiology of Learning and Memory, 2003Co-Authors: Grégory Stupien, Cédrick Florian, Pascal RoulletAbstract:This study investigates the implication of the Hippocampal CA3-Region in the different phases of learning and memory in spatial and non-spatial tasks. For that purpose, we performed focal injections of diethyldithiocarbamate (DDC) into the CA3-Region of the dorsal hippocampus. The DDC chelates most of the heavy metals in the brain which blocks selectively and reversibly the synapses containing heavy metals, i.e., the mossy fibres synaptic buttons and synapses of the dendrites of pyramidal cells. The effects of temporal inactivation of the CA3-Region was examined in a non-associative task, the spatial open-field, designed to estimate the ability of mice to react to spatial changes, and in the object recognition task, designed to estimate the ability of mice to identify a familiar object. The results show that DDC induced a specific impairment on learning and memory consolidation in the spatial open-field but had no effect on recall in this task. In the object recognition task, DDC did not induce any impairment in the different phases of learning and memory. These data demonstrate that the Hippocampal CA3-Region is specifically implicated in spatial information processing and seems to be involved not only in acquisition but also in consolidation of spatial information.
Brian E Derrick - One of the best experts on this subject based on the ideXlab platform.
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Endogenous opioid peptides contribute to associative LTP in the Hippocampal CA3 Region.
Neurobiology of learning and memory, 2011Co-Authors: Carlo O Martinez, Viet H., Brian E DerrickAbstract:The medial and lateral perforant path projections to the Hippocampal CA3 Region display distinct mechanisms of long-term potentiation (LTP) induction, N-methyl-d-aspartate (NMDA) and opioid receptor dependent, respectively. However, medial and lateral perforant path projections to the CA3 Region display associative LTP with coactivation, suggesting that while they differ in receptors involved in LTP induction they may share common downstream mechanisms of LTP induction. Here we address this interaction of LTP induction mechanisms by evaluating the contribution of opioid receptors to the induction of associative LTP among the medial and lateral perforant path projections to the CA3 Region in vivo. Local application of the opioid receptor antagonists naloxone or Cys2-Tyr3-Orn5-Pen7-amide (CTOP) normally block induction of lateral perforant path-CA3 LTP. However, these opioid receptor antagonists failed to block associative LTP in lateral perforant path-CA3 synapses when it was induced by strong coactivation of the medial perforant pathway which displays NMDAR-dependent LTP. Thus strong activation of non-opioidergic afferents can substitute for the opioid receptor activation required for lateral perforant path LTP induction. Conversely, medial perforant path-CA3 associative LTP was blocked by opioid receptor antagonists when induced by strong coactivation of the opioidergic lateral perforant path. These data indicate endogenous opioid peptides contribute to associative LTP at coactive synapses when induced by strong coactivation of an opioidergic afferent system. These data further suggest that associative LTP induction is regulated by the receptor mechanisms of the strongly stimulated pathway. Thus, while medial and lateral perforant path synapses differ in their mechanisms of LTP induction, associative LTP at these synapses share common downstream mechanisms of induction.
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Associative long-term potentiation (LTP) among extrinsic afferents of the Hippocampal CA3 Region in vivo.
Brain research, 2002Co-Authors: Carlo O Martinez, J L Martinez, Brian E DerrickAbstract:Monosynaptic perforant path projections to the CA3 Region of the hippocampus are anatomically and physiologically substantial pathways that relay cortical input directly to the hippocampus proper. Despite the suggested relevance of these direct pathways in models of information processing within the CA3 Region, surprisingly few studies have characterized synaptic plasticity in these direct cortical projections to the CA3 Region. We assessed the ability of perforant path projections, and commissural/associational projections to the Hippocampal CA3 Region to both induce or display associative LTP in vivo. In pentobarbital-anesthetized adult rats, trains delivered to either the medial or lateral perforant pathway at current intensities normally insufficient to induce LTP displayed associative LTP when these same trains were delivered in conjunction with high-intensity trains to the alternate perforant pathway. Similarly, associative LTP is induced at intrinsic commissural/associational-CA3 (C/A-CA3) synapses when weak C/A trains were delivered in conjunction with high-intensity trains to either the medial or lateral perforant pathway. Associative LTP also was observed at medial and lateral perforant path-CA3 synapses when weak perforant path trains were tetanized in conjunction with high-intensity trains delivered to C/A-CA3 synapses. Thus direct perforant path-CA3 synapses and commissural/associational-CA3 synapses can modify and be modified by other CA3 afferents in an associative manner, verifying a requirement for synaptic plasticity explicit in models of autoassociative information processing in the CA3 Region.
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Long-term potentiation in direct perforant path projections to the Hippocampal CA3 Region in vivo.
Journal of neurophysiology, 2002Co-Authors: Viet H., Carlo O Martinez, J L Martinez, Brian E DerrickAbstract:The perforant path constitutes the primary projection system relaying information from the neocortex to the Hippocampal formation. Long-term synaptic potentiation (LTP) in the perforant path projec...
M. Satoh - One of the best experts on this subject based on the ideXlab platform.
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Specific binding sites for bifemelane in the hippocampus of the guinea pig, relevant to its pharmacological actions
Neuropharmacology, 1991Co-Authors: Takeshi Fujii, Yasushi Kuraishi, Mutsuaki Ueda, M. SatohAbstract:Abstract Bifemelane has an anti-amnesic effect, produces the translocation of protein kinase C in the Hippocampal CA3 Region but not in CA1 and enhances long-term potentiation in the mossy fibre-CA3 system but not in the Schaffer collateral-CA1 system. The present study examined the specific binding of [ 3 H]bifemelane in membrane preparations of guinea pig hippocampus and Regional differences in such a binding. The binding of [ 3 H]bifemelane was reversible and greater when incubated at 4°C than at 25 or 37°C. The binding of [ 3 H]bifemelane appeared to be composed of at least 2 different affinity components. Imipramine significantly suppressed the binding of [ 3 H]bifemelane at 1 μM and, in the presence of 1 μM imipramine, the low-affinity component of the binding of [ 3 H]bifemelane was eliminated. The density of specific binding sites for 1 nM [ 3 H]bifemelane was significantly higher in the Hippocampal CA3 Region than in the CA1. The specific binding of 1 nM [ 3 H]bifemelane was not inhibited by other nootropic drugs, such as idebenone, calcium hopantenate, vinpocetine, indeloxazine and piracetam. The present results suggest that there are specific binding sites for bifemelane in hippocampus, which are different from those for other nootropic drugs tested and that the Regional differences in the pharmacological susceptibilities to bifemelane are at least, in part, attributed to those in the density of binding sites for bifemelane.
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Specific binding sites for bifemelane in the hippocampus of the guinea pig, relevant to its pharmacological actions.
Neuropharmacology, 1991Co-Authors: Takeshi Fujii, Yasushi Kuraishi, Mutsuaki Ueda, M. SatohAbstract:Bifemelane has an anti-amnesic effect, produces the translocation of protein kinase C in the Hippocampal CA3 Region but not in CA1 and enhances long-term potentiation in the mossy fibre-CA3 system but not in the Schaffer collateral-CA1 system. The present study examined the specific binding of [3H]bifemelane in membrane preparations of guinea pig hippocampus and Regional differences in such a binding. The binding of [3H]bifemelane was reversible and greater when incubated at 4 degrees C than at 25 or 37 degrees C. The binding of [3H]bifemelane appeared to be composed of at least 2 different affinity components. Imipramine significantly suppressed the binding of [3H]bifemelane at 1 microM and, in the presence of 1 microM imipramine, the low-affinity component of the binding of [3H]bifemelane was eliminated. The density of specific binding sites for 1 nM [3H]bifemelane was significantly higher in the Hippocampal CA3 Region than in the CA1. The specific binding of 1 nM [3H]bifemelane was not inhibited by other nootropic drugs, such as idebenone, calcium hopantenate, vinpocetine, indeloxazine and piracetam. The present results suggest that there are specific binding sites for bifemelane in hippocampus, which are different from those for other nootropic drugs tested and that the Regional differences in the pharmacological susceptibilities to bifemelane are at least, in part, attributed to those in the density of binding sites for bifemelane.
Hong Won Suh - One of the best experts on this subject based on the ideXlab platform.
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Effects of resveratrol and oxyresveratrol on Hippocampal cell death induced by kainic acid
Animal cells and systems, 2019Co-Authors: Hee-jung Lee, Jae-yong Lee, Jing-hui Feng, Su-min Sim, Soon Sung Lim, Hong Won SuhAbstract:In the present study, we have examined the possible neuroprotective effects of resveratrol and oxyresveratrol against kainic-acid (KA)-induced Hippocampal neuronal cell death. Either resveratrol or oxyresvertrol was orally administered 30 min prior to intracerebroventricular (i.c.v.) administration with KA (0.05 μg). Oral pretreatment with oxyresveratrol (50 mg/kg) significantly protected KA-induced Hippocampal CA3 neuronal cell death. However, the same dose (50 mg/kg) or a higher dose (100 mg/kg) pretreatment with resveratrol did not affect KA-induced Hippocampal neuronal cell death. Furthermore, the i.c.v. pretreatment with 30 μg of oxyresveratrol or resveratrol did not show the protective effect against KA-induced Hippocampal neuronal cell death. In the immunohistochemical analysis, FoxO3a and pFoxO3a expressions in the Hippocampal CA3 Region were significantly increased 30 min after KA administration. Oral pretreatment with oxyresveratrol (50 mg/kg) significantly reduced KA-induced Forkhead homeobox type O3a (FoxO3a) and pFoxO3a expression in CA3 Region of the hippocampus, suggesting that oxyresveratrol may exert a neuroprotective effect against KA-induced Hippocampal neuronal cell death by reducing the levels of FoxO3a and pFoxO3a protein expression in the Hippocampal CA3 Region. Furthermore, it is suggested that the neuroprotective effect of orally administered oxyresveratrol against KA-induced neurotoxicity might be possibly mediated by some metabolites rather than direct action of oxyresveratrol on the central nervous system.
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Characterization of temporal expressions of FOXO and pFOXO proteins in the hippocampus by kainic acid in mice: involvement of NMDA and non-NMDA receptors
Archives of pharmacal research, 2016Co-Authors: S.-h. Park, Jin-koo Lee, Yun-beom Sim, Jae-yong Lee, Hong Won SuhAbstract:In the present study, we characterized the expression and role of forkhead box O (FoxO3a) in kainic acid (KA)-induced Hippocampal neuronal cell death. FoxO3a and pFoxO3a expression in the CA1, CA2, and dentate gyrus Regions in the hippocampus increased 0.5 and 1 h after intracerebroventricular administration of KA. In addition, both FoxO3a and pFoxO3a expression in the Hippocampal CA3 Region increased significantly and equally for 1 h but decreased gradually for 24 h after KA administration. In particular, the KA-induced increases in FoxO3a and pFoxO3a expression in the Hippocampal CA3 Region were inhibited by pretreatment with the N-methyl-d-aspartate (NMDA) receptor antagonist (MK-801, dizocilpine, 1 µg/5 µl) or a non-NMDA receptor antagonist (CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione, 0.5 µg/5 µl). Furthermore, dizocilpine and CNQX produced a neuroprotective effect against KA-induced neuronal death in the CA3 Region of the hippocampus. Our results suggest that FoxO3a and pFoxO3 expression is upregulated by KA. Both FoxO3a and pFoxO3a expression appear to be responsible for KA-induced neuronal death in the CA3 Region of the hippocampus.
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Temporal expression of Hippocampal lysophosphatidic acid receptors and their roles in kainic acid-induced neurotoxicity
Genes & Genomics, 2013Co-Authors: Jin-koo Lee, M.-s. Kwon, S.-h. Park, Hak Rim Kim, Hyung-gun Kim, Yun-beom Sim, Hong Won SuhAbstract:In this investigation, the role of Hippocampal lysophosphatidic acid (LPA) receptors in the regulation of kainic acid (KA)-induced neurotoxicity was investigated. KA (0.07 μg) intracerebroventricular (i.c.v.) administration increased Hippocampal Lpar1, 2, 3, and 5 mRNA levels. In the immunohistochemical study, alteration of LPA1 or LPA3 immunoreactivity was different depending on the Hippocampal Regions, such as CA1, CA2, CA3, and dentate gyrus. In addition, the i.c.v. pretreatment with LPA1 and LPA3 antagonists, such as VPC12249 (0.05 μg) and VPC32183 (0.05 μg) attenuated KA-induced neuronal cell death in the Hippocampal CA3 Region. However, the i.c.v. 18:1 LPA (0.05 μg) pretreatment aggravated KA-induced neuronal cell death in the Hippocampal CA3 Region. Our results suggest that LPA receptors, such as LPA1 and LPA3 activation might play an important role in the regulation of KA-induced neuronal cell death in the Hippocampal CA3 Region.
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The time-dependent effect of lipopolysaccharide on kainic acid-induced neuronal death in Hippocampal CA3 Region: possible involvement of cytokines via glucocorticoid
Neuroscience, 2009Co-Authors: M.-s. Kwon, Y.-j. Seo, S.-m. Choi, Moo-ho Won, J.-k. Lee, S.-h. Park, J.-s. Jung, Y.-b. Sim, Hong Won SuhAbstract:Abstract It has been reported that glucocorticoid (Gc) can induce neuronal cell toxicity in the hippocampus. In addition, we examined that serum Gc increased by restraint stress aggravated kainic acid (KA)-induced neuronal death in Hippocampal CA3 Region. However, the effect of other stressful stimulus like lipopolysaccharide (LPS) increasing serum Gc on KA-induced neuronal death was not elucidated until now. Thus, we examined the time course effect of LPS on KA-induced neuronal death in the Hippocampal CA3 Region of mice, especially to address the role of Gc and inflammatory mediators. In the present study, we found that an aggravating effect of LPS on KA-induced neuronal death was correlated with an alteration of Hippocampal IL-1β mRNA level at all time points, and the serum Gc and Hippocampal IL-1β mRNA level was peak at 90 min after LPS treatment (LPS 90 min) when the aggravating effect of LPS on KA-induced neuronal death was maximum. In addition, RU38486 (glucocorticoid receptor antagonist) decreased the Hippocampal IL-1β mRNA level and abolished the aggravating effect of LPS on KA-induced neuronal death at LPS 90 min and 24 h. In the immunohistochemical study, we found activated and ramified microglia (OX-42) and astrocyte (GFAP) at 24 h after LPS treatment (LPS 24 h) in the hippocampus. These results suggest that Gc itself, cytokines triggered by Gc, or both appears to be involved in the LPS effect depending on LPS pretreatment time.
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The differential effects of single or repeated restraint stress on kainic acid-induced neuronal death in the Hippocampal CA3 Region: the role of glucocorticoid and various signal molecules.
Journal of neurochemistry, 2007Co-Authors: M.-s. Kwon, Y.-j. Seo, S.-m. Choi, S.-h. Park, J.-s. Jung, Hee-woo Choi, Hong Won SuhAbstract:The effect of stress mediators following the stress period and addition time is a controversial issue until now. Thus, we aim to clarify the differential effects of single restraint stress (SS) or repeated restraint stress (RS) on kainic acid (KA)-induced neuronal death especially as addressing not only the role of glucocorticoid (Gc) and its receptor but also the signal pathway leading to cAMP response element binding protein phosphorylation (pCREB) and its functional role during stress. In the present study, we found that although RS did not show any difference on serum Gc level and Hippocampal Gc receptor level compared to SS, SS exacerbated KA-induced neuronal death in Hippocampal CA3 Region, but RS did not. Moreover, pre-treatment with RU 38486 (Gc receptor antagonist) abolished the effect of SS on KA-induced neuronal death without an effect on KA toxicity itself. Furthermore, RS aggravates KA-induced neuronal death when CREB phosphorylation was deprived by KN-93 (calcium/calmodulin-dependent protein kinase II inhibitor). However, other signal molecules inhibitors such as PD98059 (MEK1/2 inhibitor) and SP600125 (p-p38 inhibitor) have no effect on KA-induced neuronal death after RS although these signal molecule were increased during SS or RS. These findings suggest that pCREB expression via calcium/calmodulin-dependent protein kinase II phosphorylation during RS comprise one of the balancers against Gc induced by stress.