Evaluation of the long-term memory for thermosensation regulated by neuronal calcium sensor-1 in Caenorhabditis elegans

Objective To evaluate whether the thermotaxis tracking model is suitable for assessing long-term memory （LTM） in the nematode Caenorhabditis elegans. Methods Animals were trained at 20℃ overnight in presence of food. The percentage of animals performing isothermal tracking （IT） behavior was measured at different time intervals after the training. Results The percentage of animals performing IT behavior, the numbers of body bends inside and outside the training temperature, and the expression patterns of AFD and AIY neurons were similar to those in control animals at 36 and 48 h after training; whereas when extending to 60, 72, and 84 h, locomotory behavior defects were observed in the assayed animals, suggesting that this thermal tracking model is feasible for analyzing LTM at 36 and 48 h after training. Moreover, the percent-age of animals performing IT behavior was reduced at 18, 36, and 48 h after training in neuronal calcium sensor-1 gene （nsc-1） mutant animals compared with that in wild-type N2 animals. In addition, exposure to plumbum （Pb） significantly repressed the LTM at 18, 36, and 48 h after training in both wild-type N2 and ncs-1 mutant animals. Conclusion The thermotaxis tracking model is suitable for evaluating the LTM regulated by NCS-1, and can be employed for elucidating regulatory functions of specific genes or effects of stimuli on memory in C. elegans.

Understanding long-term memory in global mean temperature:An attribution study based on model simulations

Long-term memory(LTM)in the climate system has been well recognized and applied in different research fields,but the origins of this property are still not clear.In this work,the authors contribute to this issue by studying model simulations under different scenarios.The global mean temperatures from pre-industrial control runs(pi Control),historical(all forcings)simulations,natural forcing only simulations(Historical Nat),greenhouse gas forcing only simulations(Historical GHG),etc.,are analyzed using the detrended fluctuation analysis.The authors find that the LTM already exists in the pi Control simulations,indicating the important roles of internal natural variability in producing the LTM.By comparing the results among different scenarios,the LTM from the piControl runs is further found to be strengthened by adding natural forcings such as the volcanic forcing and the solar forcing.Accordingly,the observed LTM in the climate system is suggested to be mainly controlled by both the‘internal’natural variability and the‘external’natural forcings.The anthropogenic forcings,however,may weaken the LTM.In the projections from RCP2.6 to RCP8.5,a weakening trend of the LTM strength is found.In view of the close relations between the climate memory and the climate predictability,a reduced predictability may be expected in a warming climate.

Ro 20-1724 Ameliorates Learning Deficit and Long-Term Memory Impairment Secondary to Repeated Ketamine Anesthesia in Young Rats

To investigate effects and possible mechanism of Ro 20-1724, a PDE4 inhibitor, on long-time learning and memory ability following repeated ketamine exposure in immature rats. Methods: Sixty 21-day-old SD rats were randomly divided into five groups (n = 12): C: Normal control group, S: Saline control group, K: Ketamine, K + Ro:?Ketamine + Ro 20-1724, K + E: Ketamine + ethanol vehicle. Ro 20-1724 (0.5 mg·kg-1) or its vehicle (ethanol) was administered intraperitoneally 30 minutes after ketamine anesthesia (70 mg·kg-1), daily for seven days. Nine weeks after birth, the Morris water maze was used to test the ability of learning and spatial localization memory on the rats. Following behavioral testing, animals’ hippocampi were removed for Western blot and electron microscopic examination. Results: In the Morris water maze test, compared with controls, the escape latency in groups exposed to ketamine or ketamine plus the ethanol vehicle were significantly prolonged (P P < 0.05), and the expression of p-CREB in the hippocampus was also decreased (P 0.05), while there was no significant difference between control groups and animals treated with Ro 20-1724 following ketamine exposure (P > 0.05). Electron microscopy demonstrated degenerative changes in hippocampal neurons of animals repetitively exposed to 70 mg·kg-1 Ketamine, which was ameliorated by Ro 20-1724 (0.5 mg·kg-1). Conclusion: The PDE-4 inhibitor Ro 20-1724 (0.5 mg·kg-1<span

On the long-term memory characteristic in land surface air temperatures:How well do CMIP6 models perform?

利用去趋势涨落分析(DFA)方法计算序列的长程记忆性(LTM),以CRUTEM5数据集的结果作为观测参照,评估了60个参与第六次国际耦合模式比较计划(CMIP6)的气候模式对地表气温LTM的再现能力.结果表明:大部分模式可以再现全球平均地表气温序列的LTM特征,其中AWI-ESM-1-1-LR和E3SM-1-0的模拟效果最好;60个模式均能模拟LTM随纬度带的变化;综合来说,全球水平上CNRM-CM6-1和HadGEM3-GC31-LL对地表气温LTM的模拟性能最好;多模式平均相比单一模式模拟性能更好;多模式平均与观测结果的偏差以及模式之间的模拟差异显著体现在赤道和沿海区域,这种偏差可能源于模式对海气耦合过程的模拟差异.

Imperative for long-term management and surveillance in Kawasaki disease

Kawasaki disease(KD)is a significant pediatric vasculitis known for its potential to cause severe coronary artery complications.Despite the effectiveness of initial treatments,such as intravenous immunoglobulin,KD patients can experience long-term cardiovascular issues,as evidenced by a recent case report of an adult who suffered a ST-segment elevation myocardial infarction due to previous KD in the World Journal of Clinical Cases.This editorial emphasizes the critical need for long-term management and regular surveillance to prevent such complications.By drawing on recent research and case studies,we advocate for a structured approach to follow-up care that includes routine cardiac evaluations and preventive measures.

The complex roles of m^(6)A modifications in neural stem cell proliferation, differentiation, and self-renewal and implications for memory and neurodegenerative diseases

N6-methyladenosine(m^(6)A), the most prevalent and conserved RNA modification in eukaryotic cells, profoundly influences virtually all aspects of mRNA metabolism. mRNA plays crucial roles in neural stem cell genesis and neural regeneration, where it is highly concentrated and actively involved in these processes. Changes in m^(6)A modification levels and the expression levels of related enzymatic proteins can lead to neurological dysfunction and contribute to the development of neurological diseases. Furthermore, the proliferation and differentiation of neural stem cells, as well as nerve regeneration, are intimately linked to memory function and neurodegenerative diseases. This paper presents a comprehensive review of the roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, as well as its implications in memory and neurodegenerative diseases. m^(6)A has demonstrated divergent effects on the proliferation and differentiation of neural stem cells. These observed contradictions may arise from the time-specific nature of m^(6)A and its differential impact on neural stem cells across various stages of development. Similarly, the diverse effects of m^(6)A on distinct types of memory could be attributed to the involvement of specific brain regions in memory formation and recall. Inconsistencies in m^(6)A levels across different models of neurodegenerative disease, particularly Alzheimer's disease and Parkinson's disease, suggest that these disparities are linked to variations in the affected brain regions. Notably, the opposing changes in m^(6)A levels observed in Parkinson's disease models exposed to manganese compared to normal Parkinson's disease models further underscore the complexity of m^(6)A's role in neurodegenerative processes. The roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, and its implications in memory and neurodegenerative diseases, appear contradictory. These inconsistencies may be attributed to the timespecific nature of m^(6)A and its varying effects on distinct brain regions and in different environments.

Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug therapy.Physical exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after stroke.In this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral ischemia.We also examined the role of exercise-induced circulating factors in these effects.Adult mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery occlusion.We found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory function.Further analysis showed that circulating adiponectin plays a critical role in these preventive effects of exercise.Agonist activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise effects.In summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice

Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.

Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis,learning,and memory in a mouse model of Alzheimer’s disease

Hippocampal neuronal loss causes cognitive dysfunction in Alzheimer’s disease.Adult hippocampal neurogenesis is reduced in patients with Alzheimer’s disease.Exercise stimulates adult hippocampal neurogenesis in rodents and improves memory and slows cognitive decline in patients with Alzheimer’s disease.However,the molecular pathways for exercise-induced adult hippocampal neurogenesis and improved cognition in Alzheimer’s disease are poorly understood.Recently,regulator of G protein signaling 6(RGS6)was identified as the mediator of voluntary running-induced adult hippocampal neurogenesis in mice.Here,we generated novel RGS6fl/fl;APP_(SWE) mice and used retroviral approaches to examine the impact of RGS6 deletion from dentate gyrus neuronal progenitor cells on voluntary running-induced adult hippocampal neurogenesis and cognition in an amyloid-based Alzheimer’s disease mouse model.We found that voluntary running in APP_(SWE) mice restored their hippocampal cognitive impairments to that of control mice.This cognitive rescue was abolished by RGS6 deletion in dentate gyrus neuronal progenitor cells,which also abolished running-mediated increases in adult hippocampal neurogenesis.Adult hippocampal neurogenesis was reduced in sedentary APP_(SWE) mice versus control mice,with basal adult hippocampal neurogenesis reduced by RGS6 deletion in dentate gyrus neural precursor cells.RGS6 was expressed in neurons within the dentate gyrus of patients with Alzheimer’s disease with significant loss of these RGS6-expressing neurons.Thus,RGS6 mediated voluntary running-induced rescue of impaired cognition and adult hippocampal neurogenesis in APP_(SWE) mice,identifying RGS6 in dentate gyrus neural precursor cells as a possible therapeutic target in Alzheimer’s disease.

Proteomic and transcriptomic analysis of visual long-term memory in Drosophila melanogaster

The fruit fly,Drosophila melanogaster,is able to discriminate visual landmarks and form visual long-term memory in a flight simulator.Studies focused on the molecular mechanism of long-term memory have shown that memory formation requires mRNA transcription and protein synthesis.However,little is known about the molecular mechanisms underlying the visual learning paradigm.The present study demonstrated that both spaced training procedure(STP)and consecutive training procedure(CTP)would induce long-term memory at 12 hour after training,and STP caused significantly higher 12-h memory scores compared with CTP.Labelfree quantification of liquid chromatography-tandem mass spectrometry(LC-MS/MS)and microarray were utilized to analyze proteomic and transcriptomic differences between the STP and CTP groups.Proteomic analysis revealed 30 up-regulated and 27 down-regulated proteins;Transcriptomic analysis revealed 145 up-regulated and 129 down-regulated genes.Among them,five candidate genes were verified by quantitative PCR,which revealed results similar to microarray.These results provide insight into the molecular components influencing visual long-term memory and facilitate further studies on the roles of identified genes in memory formation.

Formation characteristics of long-term memory in Bactrocera dorsalis

Studies on insects have contributed significantly to a better understanding of learning and memory,which is a necessary cognitive capability for all animals.Although the formation of memory has been studied in some model insects,more evidence is required to clarify the characteristics of memory formation,especially long-term memory(LTM),which is important for reliably storing information.Here,we explored this question by examining Bactrocera dorsalis,an agricultural pest with excellent learning abilities.Using the classical conditioning paradigm of the olfactory proboscis extension reflex(PER),we found that paired conditioning with multiple trials(>3)spaced with an intertrial interval(≥10 min)resulted in stable memory that lasted for at least 3 d.Furthermore,even a single conditioning trial was sufficient for the formation of a 2-d memory.With the injection of protein inhibitors,protein-synthesis-dependent memory was confirmed to start 4 h after training,and its dependence on translation and transcription differed.Moreover,the results revealed that the dependence of memory on protein translation exhibited a time-window effect(4-6 h).Our findings provide an integrated view of LTM in insects,suggesting common mechanisms in LTM formation that play a key role in the biological basis of memory.

The Screening of Genes Sensitive to Long-Term, Low-Level Microwave Exposure and Bioinformatic Analysis of Potential Correlations to Learning and Memory

Objective To gain a better understanding of gene expression changes in the brain following microwave exposure in mice. This study hopes to reveal mechanisms contributing to microwave-induced learning and memory dysfunction. Methods Mice were exposed to whole body 2100 MHz microwaves with specific absorption rates (SARs) of 0.45 W/kg, 1.8 W/kg, and 3.6 W/kg for 1 hour daily for 8 weeks. Differentially expressing genes in the brains were screened using high-density oligonucleotide arrays, with genes showing more significant differences further confirmed by RT-PCR. Results The gene chip results demonstrated that 41 genes (0.45 W/kg group), 29 genes (1.8 W/kg group), and 219 genes (3.6 W/kg group) were differentially expressed. GO analysis revealed that these differentially expressed genes were primarily involved in metabolic processes, cellular metabolic processes, regulation of biological processes, macromolecular metabolic processes, biosynthetic processes, cellular protein metabolic processes, transport, developmental processes, cellular component organization, etc. KEGG pathway analysis showed that these genes are mainly involved in pathways related to ribosome, Alzheimer's disease, Parkinson's disease, long-term potentiation, Huntington's disease, and Neurotrophin signaling. Construction of a protein interaction network identified several important regulatory genes including synbindin (sbdn), Crystallin (CryaB), PPP1CA, Ywhaq, Psap, Psmb1, Pcbp2, etc., which play important roles in the processes of learning and memory. Conclusion Long-term, low-level microwave exposure may inhibit learning and memory by affecting protein and energy metabolic processes and signaling pathways relating to neurological functions or diseases.

Attention and available long-term memory in an activation-based model

The influence of attention on memorizing related items and on available long-term memory (ALTM) was explored,showing that N400 of no-memory items was more negative than that of the memory item.The results of the category comparison task indicated that information processing under attention-driven in WM determined the availability of related long-term memory,i.e.,specific content,which was formerly concerned or ignored,yielding different indirect semantic priming effects.These indicate that the orientation of conceptual attention leads the related representations of LTM to diverse activation patterns,supporting the activation-based model.

Prediction analysis of long-term memory effect for calamity gray series

It is adequate to use the gray theory for modeling and forecasting short-term calamity series. The forecast of calamity gray series is equivalent to predicting an extraordinary event in nature. In order to look for the regularity, the calamity date series, created from the threshold for a fixed time-interval series, are studied. In this paper, the Hurst exponent is applied to defining the long-term memory effect of the simulated calamity series, and is tested for the feasibility of using it as pre-requisite information before the gray modeling and forecasting. Based on the fractional Brownian motion (fBm) model, the time series with a definite length or quantity of data are derived assuming that various kinds of memory effect exist. Different threshold values are defined to yield or to analogize the calamity date series that are required in the prediction of the gray calamity events. After case study, both of the simulated and real seismic data show that the Hurst exponents are greater than 0.5 and, therefore, indicate that the long-term memory ef-fect exists. The correlation between the Hurst exponent and the gray modeling parameter, a, provides criteria for the classification of the forecast.

Effect of moxibustion on long-term memory in vascular dementia model rats

Objective: To observe the effects on spatial long-term memory in the rats with vascular dementia(VD)treated with moxibustion for resolving stasis and promoting meridian circulation.Methods: The modified 2-vascular occlusion(2-VO) method was used to prepare VD animal model. The rats were randomized into a sham-operation group, a model group, a moxibustion group and a western medication group, 15 rats in each one. In the moxibustion group, mild warm moxibustion was applied to"Bǎihuì(百会 GV 20)" "DàZhuī(大椎 GV 14)" and "Shéntíng(神庭 GV 24)". 20 min at each point, once a day, for 3 weeks consecutively. In the western medicaion group, mouse nerve growth factor(NGF) was injected intraperitoneally, 0.18 mL/kg, once a day, for 3 weeks consecutively. Morris water maze test was used, the time of the first passing platform, the frequency of passing-platform and swimming speed in120 s were determined of the rats in each group. Western blot were used to test the protein expressions of hippocampal Nestin and DCX.Results: At the end of three courses of treatment, compared with sham-operation group, the difference was not significant statistically in swimming speed in the model group, the moxibustion group and the western medication group separately(all P>0.05). Three days after modeling, the mean of escape latency was prolonged obviously in the modeled rats compared with the rats in the shamoperation group(88.84 ± 19.94 vs 18.15 ±9.41, P< 0.01). At the end of three courses of treatment, compared with the sham-operation group(22.01 ± 10.07), the mean of escape latency was different statistically in the model group(89.18± 19.70), the moxibustion group(37.21 ±13.31) and the western medication group separately(51.50± 16.15), all P<0.01. Compared with the model group, the mean of escape latency was shortened in the moxibustion group and western medication group respectively(37.21 ± 13.31 vs89.18 ± 19.70, 51.50 ± 16.15 vs 89.18 ± 19.70, both P< 0.01). Compared with the western medication group,there was no statistical significant difference in the mean of escape latency in the moxibustion group(37.21 ± 13.31 vs 51.50 ±16.15, P> 0.05). Compared with the sham-operation group, the frequency of passing-platform was decreased in the model group(0.73 ±0.96 vs 2.60 ±1.45, P<0.01); compared with model group, the frequency of passing-platform was increased in the moxibustion group and the western medicine group and the statistically significant difference presented in the moxibustion group(2.06 ± 1.33 vs 0.73 ±0.96, P<0.01). Compared with the sham-operation group, the time of first passing-platform was prolonged in the model group(87.86 ± 33.25 vs 36.13 +29.76, P< 0.01). Compared with the model group,the time of first passing-platform was shortened in the moxibustion group and the western medicine group respectively(49.53 ±29.48 vs 87.86 ± 33.25.P< 0.01; 58.98 ± 36.22 vs 87.86 ±33.25, P< 0.05). After three courses of treatment, compared with the sham-operation group, Nestin expression was reduced in the model group,(0.33 ±0.12 vs 0.51 ±0.02, P<0.05) and was increased in the moxibustion group and the western medication group respectively(1.33 ± 0.17 vs 0.51 ± 0.02. 1.39 ± 0.10 vs 0.51 ±0.02, both P< 0.01).Compared with the model group, Nestin expression was increased in the moxibustion group and the western medication group, respectively(1.33 ± 0.17 vs 0.33±0.12. 1.39±0.10 vs 0.33 ±0.12, both P< 0.01).Compared with the western medication group, the difference was not significant statistically in the moxibustion group(1.33±0.17 vs 1.39±0.10, P>0.05). After three courses of treatment, compared with the sham-operation group, DCX expression was decreased in the model group, but without significant difference(0.44±0.20 vs 0.51 ±0.26, P> 0.05), the expression was increased in the moxibustion group and the western medication group respectively(0.98±0.25 vs 0.51±0.26. P< 0.05; 1.11±0.43 vs 0.51 ±0.26,P<0.01). Compared with the model group, DCX expression was obviously increased in the moxibustion group and the western medication group(0.98 ± 0.25 vs 0.44 ± 0.20. 1.11 ± 0.43 vs 0.44 ± 0.20, both P<0.01). The difference in DCX expression was not statistically significant between the western medication group and the moxibustion group(0.98 ± 0.25 vs 1.11 ± 0.43. P> 0.05).Conclusion: Moxibustion apparently improves the long-term memory in VD rats.

The differential requirement of mushroom body α/β subdivisions in long-term memory retrieval in Drosophila

The mushroom body(MB),a bilateral brain structure pos-sessing about 2000-2500 neurons per hemisphere,plays a central role in olfactory learning and memory in Dros-ophila melanogaster.Extensive studies have demonstrat-ed that three major types of MB neurons(α/β,α’/β’andγ)exhibit distinct functions in memory processing,including the critical role of approximately 1000 MBα/βneurons in retrieving long-term memory.Inspired by recent fi ndings that MBα/βneurons can be further divided into three subdivisions(surface,posterior and core)and wherein theα/βcore neurons play an permissive role in long-term memory consolidation,we examined the functional differ-ences of all the three morphological subdivisions of MBα/βby temporally precise manipulation of their synaptic outputs during long-term memory retrieval.We found the normal neurotransmission from a combination of MBα/βsurface and posterior neurons is necessary for retrieving both aversive and appetitive long-term memory,whereas output from MBα/βposterior or core subdivision alone is dispensable.These results imply a specifi c requirement of about 500 MBα/βneurons in supporting long-term memory retrieval and a further functional partitioning for memory processing within the MBα/βregion.

Correlating learning and memory improvements to long-term potentiation in patients with brain injury

BACKGROUND： Brain injury patients often exhibit learning and memory functional deficits. Long-term potentiation （LTP） is a representative index for studying learning and memory cellular models; the LTP index correlates to neural plasticity. OBJECTIVE： This study was designed to investigate correlations of learning and memory functions to LTP in brain injury patients, and to summarize the research advancements in mechanisms underlying brain functional improvements after rehabilitation intervention. RETRIEVAL STRATEGY： Using the terms ＂brain injuries, rehabilitation, learning and memory, long-term potentiation＂, manuscripts that were published from 2000-2007 were retrieved from the PubMed database. At the same time, manuscripts published from 2000-2007 were also retrieved from the Database of Chinese Scientific and Technical Periodicals with the same terms in the Chinese language. A total of 64 manuscripts were obtained and primarily screened. Inclusion criteria： studies on learning and memory, as well as LTP in brain injury patients, and studies focused on the effects of rehabilitation intervention on the two indices; studies that were recently published or in high-impact journals. Exclusion criteria： repetitive studies. LITERATURE EVALUATION： The included manuscripts primarily focused on correlations between learning and memory and LTP, the effects of brain injury on learning and memory, as well as LTP, and the effects of rehabilitation intervention on learning and memory after brain injury. The included 39 manuscripts were clinical, basic experimental, or review studies. DATA SYNTHESIS： Learning and memory closely correlates to LTP. The neurobiological basis of learning and memory is central nervous system plasticity, which involves neural networks, neural circuits, and synaptic connections, in particular, synaptic plasticity. LTP is considered to be an ideal model for studying synaptic plasticity, and it is also a classic model for studying neural plasticity of learning and memory. Brain injury patients clinically present with various manifestations, such as paralysis and sensory disability, which closely correlate to injured regions. In addition, learning and memory abilities decrease in brain injury patients and LTP decreases following brain injury. Brain tissue injury will lead to brain functional deficits. Hippocampal LTP is very sensitive. Difficulties in LTP induction are apparent even prior to morphological changes in brain tissue. There are no specific treatments for learning and memory functional deficits following brain injury. At present, behavioral and compensative therapies are the typical forms of rehabilitation. These results indicate that rehabilitation promotes learning and memory functional recovery in brain injury patients by speeding up LTP formation in the hippocampal CA3 region. CONCLUSION： Rehabilitation intervention increases LTP formation in the hippocampal CA3 region and recovers learning and memory functions in brain injury patients.

Analyses of fear memory in Arc/Arg3.1-deficient mice: intact short-term memory and impaired long-term and remote memory

Activity-regulated cytoskeleton-associated protein (Arc/Arg3.1) was originally identified in patients with seizures. It is densely distributed in the hip-pocampus and amygdala in particular. Because the expression of Arc/Arg3.1 is regulated by nerve in-puts, it is thought to be an immediate early gene. As shown both in vitro and in vivo, Arc/Arg3.1 is in-volved in synaptic consolidation and regulates some forms of learning and memory in rats and mice [1,2]. Furthermore, a recent study suggests that Arc/Arg3.1 may play a significant role in signal transmission via AMPA-type glutamate receptors [3-5]. Therefore, we conducted a detailed analysis of fear memory in Arc/Arg3.1-deficient mice. As previously reported, the knockout animals exhib-ited impaired fear memory in both contextual and cued test situations. Although Arc/Arg3.1-deficient mice showed almost the same performance as wild-type littermates 4 hr after a conditioning trial, their performance was impaired in the retention test after 24 hr or longer, either with or without reconsolidation. Immunohistochemical analyses showed an abnormal density of GluR1 in the hip-pocampus of Arc/Arg3.1-deficient mice;however, an application of AMPA potentiator did not improve memory performance in the mutant mice. Memory impairment in Arc/Arg3.1-deficient mice is so ro-bust that the mice provide a useful tool for devel-oping treatments for memory impairment.

Long-term spatial memory and morphological changes in hippocampus of Wistar rats exposed to smoke from Carica papaya leaves

Objective:To investigate the effects of smoking of dried leaves of Carica papaya(pawpaw)based on ethnopharmacological information which indicated that smoking of papaya leaves could influence motor performance and learning.Methods:Twenty-four rats were used for the study,and were grouped into four groups.Groups 1served as the control(not exposed to papaya leaves smoke),while Groups 2,3 and 4 were exposed to smoke from 6.25 g,12.50 g and 18.75 g of dry pawpaw leaves respectively in a smoking chamber twice daily for 21 d with each exposure lasting for 3 min.Lastly,hippocampus was harvested in each group for histological study.Result:The results showed that there were significant(P<0.05)increases in mean of recall latencies of long-term spatial memory in the animal administered the high dose while the other groups had significantly(P<0.05)lower frequencies.Histological investigation showed signs of mild neural degeneration in high dose group and hypochromic appcarance of the Nissl substance in all treated groups.Conclusions:In conclusion,the findings from this study has demonstrated that smoking of papaya leaves has the ability to maintain an intact long-term spatial memory at all doses but retrieving such memory is faster with the low and medium dosages.