Although extensively studied, the exact role of sleep in learning and memory is still not very clear. Sleep deprivation has been most frequently used to explore the effects of sleep on learning and memory, but the res...Although extensively studied, the exact role of sleep in learning and memory is still not very clear. Sleep deprivation has been most frequently used to explore the effects of sleep on learning and memory, but the results from such studies are inevitably complicated by concurrent stress and distress. Furthermore, it is not clear whether there is a strict time-window between sleep and memory consolidation. In the present study we were able to induce time-locked slow-wave sleep(SWS) in mice by optogenetically stimulating GABAergic neurons in the parafacial zone(PZ), providing a direct approach to analyze the influences of SWS on learning and memory with precise time-windows. We found that SWS induced by light for 30 min immediately or 15 min after the training phase of the object-in-place task significantly prolonged the memory from 30 min to 6 h. However, induction of SWS 30 min after the training phase did not improve memory, suggesting a critical time-window between the induction of a brief episode of SWS and learning for memory consolidation.Application of a gentle touch to the mice during light stimulation to prevent SWS induction also failed to improve memory, indicating the specific role of SWS,but not the activation of PZ GABAergic neurons itself, in memory consolidation. Similar influences of light-induced SWS on memory consolidation also occurred for Y-maze spatial memory and contextual fear memory, but not for cued fear memory. SWS induction immediately before the test phase had no effect on memory performance, indicating that SWS does not affect memory retrieval. Thus, by induction of a brief-episode SWS we have revealed a critical time window for the consolidation of hippocampusdependent memory.展开更多
OBJECTIVE To investigate the protective effect of Codonopsis Pilosula Polysaccharide(CPPS)on improving of the memory consolidation disorder induced by Cycloheximide and its possible mechanisms in mice.METHODS The mice...OBJECTIVE To investigate the protective effect of Codonopsis Pilosula Polysaccharide(CPPS)on improving of the memory consolidation disorder induced by Cycloheximide and its possible mechanisms in mice.METHODS The mice was divided into five groups,as normal control group,cycloheximid model group,piracetam positive control group,CPPS 300 mg·kg^(-1) group,and CPPS150 mg·kg^(-1) group.The mice respectively were given saline,piracetam,and CPPS for 15 d.The memory consolidation disorder model in mice was established by ip.Cyclohexylamine,and orally administered CPPS(300 mg·kg^(-1) or 150 mg·kg^(-1))every day.Then experimental groups were subjected Morris Water Maze test.Western blotting analysis were used to analysis the expression of Ca MKⅡ/CREB signaling pathways.RESULTS Morris water maze experiment showed that cyclohexylamine can cause memory consolidation disorder(P<0.01),and giving piracetam and CPPS(300 mg·kg-1)can improve spatial memory impairment in mice(P<0.05,P<0.01).Western blotting experiment results show that compared with normal control group,Ca MKⅡand CREB contents of brain in model group mice had significant decreased(P<0.001);Compared with model group,Ca MKⅡand CREB contents of brain tissue in piracetam and CPPS groups increased significantly(P<0.05,P<0.01,P<0.001).CONCLUSION Cycloheximide can induce the memory consolidation disorder,and its effect in mice related to Ca MK/CREB signaling pathways.CPPS can improved this memory disorder by influence Ca MKⅡ/CREB signaling pathways.展开更多
Insufficient sleep has been correlated to many physiological and psychoneurological disorders.Over the years,our understanding of the state of sleep has transcended from an inactive period of rest to a more active sta...Insufficient sleep has been correlated to many physiological and psychoneurological disorders.Over the years,our understanding of the state of sleep has transcended from an inactive period of rest to a more active state involving important cellular and molecular processes.In addition,during sleep,electrophysiological changes also occur in pathways in specific regions of the mammalian central nervous system(CNS).Activity mediated synaptic plasticity in the CNS can lead to long-term and sometimes permanent strengthening and/or weakening synaptic strength affecting neuronal network behaviour.Memory consolidation and learning that take place during sleep cycles,can be affected by changes in synaptic plasticity during sleep disturbances.G-protein coupled receptors(GPCRs),with their versatile structural and functional attributes,can regulate synaptic plasticity in CNS and hence,may be potentially affected in sleep deprived conditions.In this review,we aim to discuss important functional changes that can take place in the CNS during sleep and sleep deprivation and how changes in GPCRs can lead to potential problems with therapeutics with pharmacological interventions.展开更多
While a hippocampal–cortical dialogue is generally thought to mediate memory consolidation,which is crucial for engram function,how it works remains largely unknown.Here,we examined the interplay of neural signals fr...While a hippocampal–cortical dialogue is generally thought to mediate memory consolidation,which is crucial for engram function,how it works remains largely unknown.Here,we examined the interplay of neural signals from the retrosplenial cortex(RSC),a neocortical region,and from the hippocampus in memory consolidation by simultaneously recording sharp-wave ripples(SWRs)of dorsal hippocampal CA1 and neural signals of RSC in free-moving mice during the delayed spatial alternation task(DSAT)and subsequent sleep.Hippocampal–RSC coordination during SWRs was identified in nonrapid eye movement(NREM)sleep,reflecting neural reactivation of decision-making in the task,as shown by a peak reactivation strength within SWRs.Using modified generalized linear models(GLMs),we traced information flow through the RSC–CA1–RSC circuit around SWRs during sleep following DSAT.Our findings show that after spatial training,RSC excitatory neurons typically increase CA1 activity prior to hippocampal SWRs,potentially initiating hippocampal memory replay,while inhibitory neurons are activated by hippocampal outputs in post-SWRs.We further identified certain excitatory neurons in the RSC that encoded spatial information related to the DSAT.These neurons,classified as splitters and location-related cells,showed varied responses to hippocampal SWRs.Overall,our study highlights the complex dynamics between the RSC and hippocampal CA1 region during SWRs in NREM sleep,underscoring their critical interplay in spatial memory consolidation.展开更多
The purpose of this meta-analysis was to evaluate the effects of acute exercise on short-term memory improvement.The computerized literature searches using electronic databases and examinations of reference lists from...The purpose of this meta-analysis was to evaluate the effects of acute exercise on short-term memory improvement.The computerized literature searches using electronic databases and examinations of reference lists from relevant studies yielded six studies meeting our inclusionary criteria.In a total of six studies,16 standardized regression coefficient effect sizes(ESs)were calculated to be meta-analyzed.The meta-analyses showed a statistically significant increase in short-term memory improvement across both the exercise and non-exercise control groups in trials 1-5[ES=0.96,95%CI(0.95,0.97),P<0.001].However,there was no significant subgroup difference between exercise and control groups(Q_(b)=0.40,df=1,P=0.53).Our meta-analytic review provides suggestive evidence that an acute bout of exercise prior to learning does not result in short-term memory improvement to a greater extent than a non-exercise control.Additional research is needed to further evaluate whether acute exercise enhances long-term memory via enhanced learning and/or post-learning mechanisms.展开更多
基金supported by grants from the National Natural Science Foundation of China (31771167 and 31571090)the National Basic Research Development Program of China (2016YFC1306700)+1 种基金the Non-profit Central Research Institute Fund of the Chinese Academy of Medical Sciences (2018PT31041)the Fundamental Research Funds for the Central Universities of China (2017FZA7003)
文摘Although extensively studied, the exact role of sleep in learning and memory is still not very clear. Sleep deprivation has been most frequently used to explore the effects of sleep on learning and memory, but the results from such studies are inevitably complicated by concurrent stress and distress. Furthermore, it is not clear whether there is a strict time-window between sleep and memory consolidation. In the present study we were able to induce time-locked slow-wave sleep(SWS) in mice by optogenetically stimulating GABAergic neurons in the parafacial zone(PZ), providing a direct approach to analyze the influences of SWS on learning and memory with precise time-windows. We found that SWS induced by light for 30 min immediately or 15 min after the training phase of the object-in-place task significantly prolonged the memory from 30 min to 6 h. However, induction of SWS 30 min after the training phase did not improve memory, suggesting a critical time-window between the induction of a brief episode of SWS and learning for memory consolidation.Application of a gentle touch to the mice during light stimulation to prevent SWS induction also failed to improve memory, indicating the specific role of SWS,but not the activation of PZ GABAergic neurons itself, in memory consolidation. Similar influences of light-induced SWS on memory consolidation also occurred for Y-maze spatial memory and contextual fear memory, but not for cued fear memory. SWS induction immediately before the test phase had no effect on memory performance, indicating that SWS does not affect memory retrieval. Thus, by induction of a brief-episode SWS we have revealed a critical time window for the consolidation of hippocampusdependent memory.
基金supported by National Natural Science Foundation(81202192)Fund of Hebei Provincial Health Bureau(20130037)
文摘OBJECTIVE To investigate the protective effect of Codonopsis Pilosula Polysaccharide(CPPS)on improving of the memory consolidation disorder induced by Cycloheximide and its possible mechanisms in mice.METHODS The mice was divided into five groups,as normal control group,cycloheximid model group,piracetam positive control group,CPPS 300 mg·kg^(-1) group,and CPPS150 mg·kg^(-1) group.The mice respectively were given saline,piracetam,and CPPS for 15 d.The memory consolidation disorder model in mice was established by ip.Cyclohexylamine,and orally administered CPPS(300 mg·kg^(-1) or 150 mg·kg^(-1))every day.Then experimental groups were subjected Morris Water Maze test.Western blotting analysis were used to analysis the expression of Ca MKⅡ/CREB signaling pathways.RESULTS Morris water maze experiment showed that cyclohexylamine can cause memory consolidation disorder(P<0.01),and giving piracetam and CPPS(300 mg·kg-1)can improve spatial memory impairment in mice(P<0.05,P<0.01).Western blotting experiment results show that compared with normal control group,Ca MKⅡand CREB contents of brain in model group mice had significant decreased(P<0.001);Compared with model group,Ca MKⅡand CREB contents of brain tissue in piracetam and CPPS groups increased significantly(P<0.05,P<0.01,P<0.001).CONCLUSION Cycloheximide can induce the memory consolidation disorder,and its effect in mice related to Ca MK/CREB signaling pathways.CPPS can improved this memory disorder by influence Ca MKⅡ/CREB signaling pathways.
基金Supported by Canadian Institutes of Health Research Grant,No.TGS-1092194-Year Fellowship from the University of British Columbia.
文摘Insufficient sleep has been correlated to many physiological and psychoneurological disorders.Over the years,our understanding of the state of sleep has transcended from an inactive period of rest to a more active state involving important cellular and molecular processes.In addition,during sleep,electrophysiological changes also occur in pathways in specific regions of the mammalian central nervous system(CNS).Activity mediated synaptic plasticity in the CNS can lead to long-term and sometimes permanent strengthening and/or weakening synaptic strength affecting neuronal network behaviour.Memory consolidation and learning that take place during sleep cycles,can be affected by changes in synaptic plasticity during sleep disturbances.G-protein coupled receptors(GPCRs),with their versatile structural and functional attributes,can regulate synaptic plasticity in CNS and hence,may be potentially affected in sleep deprived conditions.In this review,we aim to discuss important functional changes that can take place in the CNS during sleep and sleep deprivation and how changes in GPCRs can lead to potential problems with therapeutics with pharmacological interventions.
基金supported by the National Key R&D Program of China(2019YFA0709504 and 2021ZD0202805)the National Natural Science Foundation of China(32471083,82271292,and 31900719)+2 种基金the Innovative Research Team of High-level Local Universities in Shanghai,111 Project(B18015)Shanghai Municipal Science and Technology Major Project(2018SHZDZX01)Shanghai Center for Brain Science and Brain-Inspired Technology.
文摘While a hippocampal–cortical dialogue is generally thought to mediate memory consolidation,which is crucial for engram function,how it works remains largely unknown.Here,we examined the interplay of neural signals from the retrosplenial cortex(RSC),a neocortical region,and from the hippocampus in memory consolidation by simultaneously recording sharp-wave ripples(SWRs)of dorsal hippocampal CA1 and neural signals of RSC in free-moving mice during the delayed spatial alternation task(DSAT)and subsequent sleep.Hippocampal–RSC coordination during SWRs was identified in nonrapid eye movement(NREM)sleep,reflecting neural reactivation of decision-making in the task,as shown by a peak reactivation strength within SWRs.Using modified generalized linear models(GLMs),we traced information flow through the RSC–CA1–RSC circuit around SWRs during sleep following DSAT.Our findings show that after spatial training,RSC excitatory neurons typically increase CA1 activity prior to hippocampal SWRs,potentially initiating hippocampal memory replay,while inhibitory neurons are activated by hippocampal outputs in post-SWRs.We further identified certain excitatory neurons in the RSC that encoded spatial information related to the DSAT.These neurons,classified as splitters and location-related cells,showed varied responses to hippocampal SWRs.Overall,our study highlights the complex dynamics between the RSC and hippocampal CA1 region during SWRs in NREM sleep,underscoring their critical interplay in spatial memory consolidation.
文摘The purpose of this meta-analysis was to evaluate the effects of acute exercise on short-term memory improvement.The computerized literature searches using electronic databases and examinations of reference lists from relevant studies yielded six studies meeting our inclusionary criteria.In a total of six studies,16 standardized regression coefficient effect sizes(ESs)were calculated to be meta-analyzed.The meta-analyses showed a statistically significant increase in short-term memory improvement across both the exercise and non-exercise control groups in trials 1-5[ES=0.96,95%CI(0.95,0.97),P<0.001].However,there was no significant subgroup difference between exercise and control groups(Q_(b)=0.40,df=1,P=0.53).Our meta-analytic review provides suggestive evidence that an acute bout of exercise prior to learning does not result in short-term memory improvement to a greater extent than a non-exercise control.Additional research is needed to further evaluate whether acute exercise enhances long-term memory via enhanced learning and/or post-learning mechanisms.
