The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Jianli Yang - One of the best experts on this subject based on the ideXlab platform.
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Enriched Environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress
Neurobiology of Learning and Memory, 2007Co-Authors: Jianli Yang, Yan Zhang, Cailan Hou, Jun Liu, Jiansong ZhouAbstract:Prenatal stress can cause long-term eVects on cognitive functions in oVspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether Enriched Environment treatment (EE) in early postnatal periods can cause a recovery from these deWcits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1 s, 2–3 min apart) in 30 min per day at gestational day 13–19. After weaning at postnatal day 22, experimental oVspring were given the Enriched Environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the eVects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deWcits induced by prenatal stress were recovered by Enriched Environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deWcit, prenatal stress and Enriched Environment treatment. Enriched Environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.
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Enriched Environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress
Neurobiology of Learning and Memory, 2007Co-Authors: Jianli Yang, Lin Xu, Yan Zhang, Jiansong Zhou, Lingjiang LiAbstract:Prenatal stress can cause long-term eVects on cognitive functions in oVspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether Enriched Environment treatment (EE) in early postnatal periods can cause a recovery from these deWcits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1 s, 2–3 min apart) in 30 min per day at gestational day 13–19. After weaning at postnatal day 22, experimental oVspring were given the Enriched Environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the eVects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deWcits induced by prenatal stress were recovered by Enriched Environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deWcit, prenatal stress and Enriched Environment treatment. Enriched Environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.
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Enriched Environment treatment counteracts enhanced addictive and depressive like behavior induced by prenatal chronic stress
Brain Research, 2006Co-Authors: Jianli Yang, Weihui Li, Zexuan Li, Hongying Li, Guifu Yang, Lin Xu, Lingjiang LiAbstract:Abstract Prenatal stress can cause many long-term behavior changes in offspring, but whether prenatal stress can alter addictive behavior in offspring and postnatal Enriched Environment treatment (EE) can restore these changes are unknown. We reported here that prenatal chronic stress (10 unpredictable, 1 s, 0.8 mA foot-shocks per day during gestational days 13–19) enhanced morphine-induced (10 mg/kg, s.c., per day, 6 consecutive days) place preference. Moreover, prenatal chronic stress caused higher depressive-like behavior in forced swimming test in adult offspring. However, Enriched Environment housing treatment on postnatal days 22–52 counteracted both the abnormal behaviors alterations. This work observed a phenomenon that might contribute to the understanding of clinically important interactions among addiction, prenatal stress and Enriched Environment treatment. Postnatal Enriched Environment treatment might be an important therapeutic intervention in preventing the prenatal stress-induced addictive disorders.
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Enriched Environment experience overcomes the memory deficits and depressive like behavior induced by early life stress
Neuroscience Letters, 2006Co-Authors: Minghu Cui, Jianli Yang, Ya Yang, Jichuan Zhang, Huili Han, Rongrong MaoAbstract:Stress in early life is believed to cause cognitive and affective disorders, and to disrupt hippocampal synaptic plasticity in adolescence into adult, but it is unclear whether exposure to Enriched Environment (EE) can overcome these effects. Here, we reported that housing rats in cages with limited nesting/bedding materials on postnatal days 2-21 reduced body weight gain, and this type of early life stress impaired spatial learning and memory of the Morris water maze and increased depressive-like behavior of the forced swim test in young adult rats (postnatal days 53-57). Early life stress also impaired long-term potentiation in hippocampal CA1 area of slices of young adult rats. Remarkably, EE experience on postnatal days 22-52 had no effect on spatial learning/memory and depressive-like behavior, but it significantly facilitated LTP in control rats, and completely overcame the effects of early life stress on young adult rats. These findings suggest that EE experience may be useful for clinical intervention in preventing cognitive and affective disorders during development.
Lingjiang Li - One of the best experts on this subject based on the ideXlab platform.
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Enriched Environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress
Neurobiology of Learning and Memory, 2007Co-Authors: Jianli Yang, Lin Xu, Yan Zhang, Jiansong Zhou, Lingjiang LiAbstract:Prenatal stress can cause long-term eVects on cognitive functions in oVspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether Enriched Environment treatment (EE) in early postnatal periods can cause a recovery from these deWcits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1 s, 2–3 min apart) in 30 min per day at gestational day 13–19. After weaning at postnatal day 22, experimental oVspring were given the Enriched Environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the eVects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deWcits induced by prenatal stress were recovered by Enriched Environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deWcit, prenatal stress and Enriched Environment treatment. Enriched Environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.
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Enriched Environment treatment counteracts enhanced addictive and depressive like behavior induced by prenatal chronic stress
Brain Research, 2006Co-Authors: Jianli Yang, Weihui Li, Zexuan Li, Hongying Li, Guifu Yang, Lin Xu, Lingjiang LiAbstract:Abstract Prenatal stress can cause many long-term behavior changes in offspring, but whether prenatal stress can alter addictive behavior in offspring and postnatal Enriched Environment treatment (EE) can restore these changes are unknown. We reported here that prenatal chronic stress (10 unpredictable, 1 s, 0.8 mA foot-shocks per day during gestational days 13–19) enhanced morphine-induced (10 mg/kg, s.c., per day, 6 consecutive days) place preference. Moreover, prenatal chronic stress caused higher depressive-like behavior in forced swimming test in adult offspring. However, Enriched Environment housing treatment on postnatal days 22–52 counteracted both the abnormal behaviors alterations. This work observed a phenomenon that might contribute to the understanding of clinically important interactions among addiction, prenatal stress and Enriched Environment treatment. Postnatal Enriched Environment treatment might be an important therapeutic intervention in preventing the prenatal stress-induced addictive disorders.
Lin Xu - One of the best experts on this subject based on the ideXlab platform.
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Enriched Environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress
Neurobiology of Learning and Memory, 2007Co-Authors: Jianli Yang, Lin Xu, Yan Zhang, Jiansong Zhou, Lingjiang LiAbstract:Prenatal stress can cause long-term eVects on cognitive functions in oVspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether Enriched Environment treatment (EE) in early postnatal periods can cause a recovery from these deWcits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1 s, 2–3 min apart) in 30 min per day at gestational day 13–19. After weaning at postnatal day 22, experimental oVspring were given the Enriched Environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the eVects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deWcits induced by prenatal stress were recovered by Enriched Environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deWcit, prenatal stress and Enriched Environment treatment. Enriched Environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.
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Enriched Environment treatment counteracts enhanced addictive and depressive like behavior induced by prenatal chronic stress
Brain Research, 2006Co-Authors: Jianli Yang, Weihui Li, Zexuan Li, Hongying Li, Guifu Yang, Lin Xu, Lingjiang LiAbstract:Abstract Prenatal stress can cause many long-term behavior changes in offspring, but whether prenatal stress can alter addictive behavior in offspring and postnatal Enriched Environment treatment (EE) can restore these changes are unknown. We reported here that prenatal chronic stress (10 unpredictable, 1 s, 0.8 mA foot-shocks per day during gestational days 13–19) enhanced morphine-induced (10 mg/kg, s.c., per day, 6 consecutive days) place preference. Moreover, prenatal chronic stress caused higher depressive-like behavior in forced swimming test in adult offspring. However, Enriched Environment housing treatment on postnatal days 22–52 counteracted both the abnormal behaviors alterations. This work observed a phenomenon that might contribute to the understanding of clinically important interactions among addiction, prenatal stress and Enriched Environment treatment. Postnatal Enriched Environment treatment might be an important therapeutic intervention in preventing the prenatal stress-induced addictive disorders.
V Bhagya - One of the best experts on this subject based on the ideXlab platform.
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short term exposure to Enriched Environment rescues chronic stress induced impaired hippocampal synaptic plasticity anxiety and memory deficits
Journal of Neuroscience Research, 2017Co-Authors: V Bhagya, J Veena, B N Srikumar, Byrathnahalli Shankaranarayana S RaoAbstract:Exposure to prolonged stress results in structural and functional alterations in the hippocampus including reduced long-term potentiation (LTP), neurogenesis, spatial learning and working memory impairments, and enhanced anxiety-like behavior. On the other hand, Enriched Environment (EE) has beneficial effects on hippocampal structure and function, such as improved memory, increased hippocampal neurogenesis, and progressive synaptic plasticity. It is unclear whether exposure to short-term EE for 10 days can overcome restraint stress–induced cognitive deficits and impaired hippocampal plasticity. Consequently, the present study explored the beneficial effects of short-term EE on chronic stress–induced impaired LTP, working memory, and anxiety-like behavior. Male Wistar rats were subjected to chronic restraint stress (6 hr/day) over a period of 21 days, and then they were exposed to EE (6 hr/day) for 10 days. Restraint stress reduced hippocampal CA1-LTP, increased anxiety-like symptoms in elevated plus maze, and impaired working memory in T-maze task. Remarkably, EE facilitated hippocampal LTP, improved working memory performance, and completely overcame the effect of chronic stress on anxiety behavior. In conclusion, exposure to EE can bring out positive effects on synaptic plasticity in the hippocampus and thereby elicit its beneficial effects on cognitive functions. © 2016 Wiley Periodicals, Inc.
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Enriched Environment ameliorates depression induced cognitive deficits and restores abnormal hippocampal synaptic plasticity
Neurobiology of Learning and Memory, 2016Co-Authors: K Mahati, V Bhagya, T Christofer, A Sneha, B Shankaranarayana S RaoAbstract:Severe depression compromises structural and functional integrity of the brain and results in impaired learning and memory, maladaptive synaptic plasticity as well as degenerative changes in the hippocampus and amygdala. The precise mechanisms underlying cognitive dysfunctions in depression remain largely unknown. On the other hand, Enriched Environment (EE) offers beneficial effects on cognitive functions, synaptic plasticity in the hippocampus. However, the effect of EE on endogenous depression associated cognitive dysfunction has not been explored. Accordingly, we have attempted to address this issue by investigating behavioural, structural and synaptic plasticity mechanisms in an animal model of endogenous depression after exposure to Enriched Environment. Our results demonstrate that depression is associated with impaired spatial learning and enhanced anxiety-like behaviour which is correlated with hypotrophy of the dentate gyrus and amygdalar hypertrophy. We also observed a gross reduction in the hippocampal long-term potentiation (LTP). We report a complete behavioural recovery with reduced indices of anhedonia and behavioural despair, reduced anxiety-like behaviour and improved spatial learning along with a complete restoration of dentate gyrus and amygdalar volumes in depressive rats subjected to EE. Enrichment also facilitated CA3-Schaffer collateral LTP. Our study convincingly proves that depression-induces learning deficits and impairs hippocampal synaptic plasticity. It also highlights the role of Environmental stimuli in restoring depression-induced cognitive deficits which might prove vital in outlining more effective strategies to treat major depressive disorders.
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Enriched Environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats
Journal of Neuroscience Research, 2009Co-Authors: J Veena, K Mahati, V Bhagya, B N Srikumar, T R Raju, B Shankaranarayana S RaoAbstract:Adult neurogenesis, particularly in the subgranular zone, is thought to be linked with learning and memory. Chronic stress inhibits adult hippocampal neurogenesis and also impairs learning and memory. On the other hand, exposure to Enriched Environment (EE) is reported to enhance the survival of new neurons and improve cognition. Accordingly, in the present study, we examined whether short-term EE after stress could ameliorate the stress-induced decrease in hippocampal cell proliferation and impairment in radial arm maze learning. After restraint stress (6 hr/day, 21 days) adult rats were exposed to EE (6 hr/day, 10 days). We observed that chronic restraint stress severely affected formation of new cells and learning. Stressed rats showed a significant decrease (70%) in the number of BrdU (5-bromo-2'-deoxyuridine)-immunoreactive cells and impairment in the performance of the partially baited radial arm maze task. Interestingly, EE after stress completely restored the hippocampal cell proliferation. On par with the restoration of hippocampal cytogenesis, short-term EE after stress resulted in a significant increase in percentage correct choices and a decrease in the number of reference memory errors compared with the stressed animals. Also, EE per se significantly increased the cell proliferation compared with controls. Furthermore, stress significantly reduced the hippocampal volume that was reversed after EE. Our observations demonstrate that short-term EE completely ameliorates the stress-induced decrease in cell proliferation and learning deficit, thus demonstrating the efficiency of rehabilitation in reversal of stress-induced deficits and suggesting a probable role of newly formed cells in the effects of EE.
B Shankaranarayana S Rao - One of the best experts on this subject based on the ideXlab platform.
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Enriched Environment ameliorates depression induced cognitive deficits and restores abnormal hippocampal synaptic plasticity
Neurobiology of Learning and Memory, 2016Co-Authors: K Mahati, V Bhagya, T Christofer, A Sneha, B Shankaranarayana S RaoAbstract:Severe depression compromises structural and functional integrity of the brain and results in impaired learning and memory, maladaptive synaptic plasticity as well as degenerative changes in the hippocampus and amygdala. The precise mechanisms underlying cognitive dysfunctions in depression remain largely unknown. On the other hand, Enriched Environment (EE) offers beneficial effects on cognitive functions, synaptic plasticity in the hippocampus. However, the effect of EE on endogenous depression associated cognitive dysfunction has not been explored. Accordingly, we have attempted to address this issue by investigating behavioural, structural and synaptic plasticity mechanisms in an animal model of endogenous depression after exposure to Enriched Environment. Our results demonstrate that depression is associated with impaired spatial learning and enhanced anxiety-like behaviour which is correlated with hypotrophy of the dentate gyrus and amygdalar hypertrophy. We also observed a gross reduction in the hippocampal long-term potentiation (LTP). We report a complete behavioural recovery with reduced indices of anhedonia and behavioural despair, reduced anxiety-like behaviour and improved spatial learning along with a complete restoration of dentate gyrus and amygdalar volumes in depressive rats subjected to EE. Enrichment also facilitated CA3-Schaffer collateral LTP. Our study convincingly proves that depression-induces learning deficits and impairs hippocampal synaptic plasticity. It also highlights the role of Environmental stimuli in restoring depression-induced cognitive deficits which might prove vital in outlining more effective strategies to treat major depressive disorders.
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Enriched Environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats
Journal of Neuroscience Research, 2009Co-Authors: J Veena, K Mahati, V Bhagya, B N Srikumar, T R Raju, B Shankaranarayana S RaoAbstract:Adult neurogenesis, particularly in the subgranular zone, is thought to be linked with learning and memory. Chronic stress inhibits adult hippocampal neurogenesis and also impairs learning and memory. On the other hand, exposure to Enriched Environment (EE) is reported to enhance the survival of new neurons and improve cognition. Accordingly, in the present study, we examined whether short-term EE after stress could ameliorate the stress-induced decrease in hippocampal cell proliferation and impairment in radial arm maze learning. After restraint stress (6 hr/day, 21 days) adult rats were exposed to EE (6 hr/day, 10 days). We observed that chronic restraint stress severely affected formation of new cells and learning. Stressed rats showed a significant decrease (70%) in the number of BrdU (5-bromo-2'-deoxyuridine)-immunoreactive cells and impairment in the performance of the partially baited radial arm maze task. Interestingly, EE after stress completely restored the hippocampal cell proliferation. On par with the restoration of hippocampal cytogenesis, short-term EE after stress resulted in a significant increase in percentage correct choices and a decrease in the number of reference memory errors compared with the stressed animals. Also, EE per se significantly increased the cell proliferation compared with controls. Furthermore, stress significantly reduced the hippocampal volume that was reversed after EE. Our observations demonstrate that short-term EE completely ameliorates the stress-induced decrease in cell proliferation and learning deficit, thus demonstrating the efficiency of rehabilitation in reversal of stress-induced deficits and suggesting a probable role of newly formed cells in the effects of EE.