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Written by Liu Yongqing, editor-in-chief by Fan Minghua, plate made by Wang Sizhen, and Cha Jiaxue In mammalian brains, information from the external environment (such as sensory stimulation and social movement, e.
) continuously modulates the excitability of neural networks, thus profoundly affecting brain process.
Biological mechanisms of information processing, learning and memory [1,
Activity-dependent plasticity is the biological basis of learning and new memory formation [
Enhanced structural plasticity is closely linked to changes in the number and size of dendritic spines during learning and memo.
For example, conditioned fear training experiments increase the density of dendritic spines in hippocampal CA1 neurons [
In addition, the impairment of synaptic plasticity can lead to a series of neuropsychiatric diseases such as intellectual disability and depression [5,
Although synaptic plasticity is crucial in the physiological and pathological processes of the brain, its underlying molecular mechanisms remain poorly understo.
The maintenance of long-term synaptic plasticity and the formation of memory require changes in gene transcription in neural cells [
Epigenetic regulation is an important way to alter cellular gene expression in the presence of external environmental stimuli, suggesting that epigenetic factors are ideal candidates for regulating neural plasticity [
Reversible histone post-translational modifications, including acetylation, phosphorylation, and methylation, are important epigenetic mechanisms regulating gene expressi.
In particular, histone acetylase, histone deacetylase and acetyl-CoA synthase [9-11] are closely related to learning and memory, suggesting that histone acetylation plays an important role in cognitive functi.
On May 22, 2022, Huang Zhuo's team from Peking University School of Pharmacy published a research paper titled "JADE2 is essential for hippocampal synaptic plasticity and cognitive functions in mice" in Biological Psychiat.
This study deeply elucidates the important role and molecular mechanism of the epigenetic molecule JADE2 in hippocampal synaptic plasticity and learning and memo.
Fan Minghua and Liu Yongqing are the co-first authors of the paper, and Researcher Huang Zhuo and .
Liu Yongqing are the corresponding autho.
Professor Shang Yongfeng and Researcher Liang Jing also provided guidance and suppo.
In order to explore whether the expression levels of epigenetic factors, especially genes related to histone acetylation modification, will change during the process of neuronal excitability, the authors first stimulated primary neurons in the mouse hippocampus with high concentrations of potassium chlori.
, to detect the mRNA changes of some epigenetic facto.
The results of RT-qPCR experiments showed that the mRNA levels of most epigenetic factors were unchanged in this in vitro model, and only the mRNA level of JADE2 was significantly increased with increased neuronal excitability (F.
1.
Western blotting and WB experiments and immunofluorescence experiments also proved that in the primary neuron model stimulated by potassium chloride, the expression of JADE2 protein was significantly increased with the increase of neuronal excitabili.
In order to explore the changes of JADE2 with neuronal excitability in vivo, the authors used chemical genetics, water maze training and kaine acid-induced epilepsy model to find that when the excitability of the hippocampal neural network increased, the expression of JADE2 also increased significantly high (Figure In conclusion, the expression of JADE2 was significantly increased with the increase of neuronal excitability, indicating that JADE2 plays an important role in the activity-dependent regulation of neuronal excitabili.
Figure 1 The expression of JADE2 increases with the increase of neuronal excitability (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) In order to explore whether changes in the expression of JADE2 in adult mice will affect neuronal activity To function, the authors constructed adeno-associated (AAV) viruses in the control and JADE2 knockdown groups and injected them into the CA1 brain region of the mouse hippocamp.
Electrophysiological experiments found that JADE2 knockdown did not affect neuronal excitabili.
However, compared with control neurons, the frequency of miniature excitatory postsynaptic currents (mEPSCs) in CA1 pyramidal neurons in the JADE2 knockdown group was significantly reduced, and the amplitude was basically unchanged (F.
These results show that loss of JADE2 results in impaired glutamatergic synaptic transmissi.
Figure 2 Deletion of JADE2 causes impaired glutamatergic synaptic transmission (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) The significant decrease in mEPSC frequency reflects changes in the number of synapses or synapses Changes in the ability to release protransmitte.
To test whether JADE2 is important for the maintenance of dendritic spines, the authors first injected control or JADE2 knockdown virus in CA1, and then electrophysiologically and morphologically labeled CA1 pyramidal neurons and examined changes in dendritic spin.
Although the dendritic branching of pyramidal neurons in the JADE2 knockdown group did not change compared with the control group, their dendritic spine density was significantly reduced (F.
3.
In contrast, overexpression of JADE2 in CA1 significantly increased the number of dendritic spin.
Then the authors used paired-pulse ratios (PPRs) experiments to detect the presynaptic transmitter release capacity of the mouse hippocampal CA3-CA1 Schaffer colleteral pathw.
The experimental results showed that compared with the control group, the CA1 cones in the JADE2 knockout group The presynaptic neurotransmitter release capacity of somatic neurons was largely unchanged (F.
3.
Next, in order to explore whether JADE2 affects the synaptic plasticity function of the hippocampus, the authors detected the NMDAR/AMPAR ratio of CA1 pyramidal neurons in the mouse hippocamp.
Compared with the control group, the NMDAR/AMPAR raio of the JADE2 knockout group was significantly decreased , and the long-term potentiation (LTP) function was significantly impaired (F.
3), indicating that JADE2 is essential for the maintenance of hippocampal synaptic plastici.
Figure 3 JADE2 deletion impairs synaptic plasticity in the hippocampus (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) The authors then conducted a series of animal behavioral experiments, including open field experiments, elevated cross experiments, and novel object recognition Experiments, water maze experiments and fear memory experiments showed that the lack of JADE2 in the hippocampus had basically no effect on the motor ability and anxiety level of animals, but significantly affected the learning and memory ability of mice (Figure
Figure 4 JADE2 deletion impairs learning and memory ability in mice (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) In order to explore the molecular mechanism of JADE2-mediated learning and memory, the authors selected JADE2 knockout mice and littermates In the hippocampus of control mice, RNA-seq high-throughput sequencing experiments were performed to find the downstream regulatory genes of JADE2 related to learning and memo.
Among the downstream regulatory genes of JADE2, the authors focused on the Rac1 gene because its function is closely related to dendritic spine development and memory formation [12, 1Next, the authors wanted to explore whether JADE2-regulated synaptic plasticity and learned cognitive behavior are achieved through the expression of RACExperiments showed that when JADE2 was knocked out, the density of dendritic spines in hippocampal CA1 pyramidal neurons was significantly reduced, but when JADE2 was knocked out and RAC1 was overexpressed at the same time, the density of dendritic spines in CA1 cells returned to normal levels, which was no different from the control group ( Figure 5.
After that, electrophysiological experiments found that when JADE2 was knocked out, the frequency of cellular mEPSCs decreased significantly while the amplitude remained unchang.
When JADE2 was knocked out and RAC1 was overexpressed at the same time, the frequency of cellular mEPSCs returned to the normal level, which was not significantly different from the control gro.
In addition, overexpression of RAC1 reversed the long-term plasticity decline of the Schaffer-colleteral pathway and impaired memory in mice caused by JADE2 knockout, returning it to normal levels (F.
These experiments demonstrate that RAC1 is essential for JADE2-mediated learning and memory in mi.
Figure 5 JADE2 regulates learning and memory ability through the expression of RAC1 (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) Conclusion and discussion, inspiration and prospect Experiments in molecular biology and animal behavior have found that the epigenetic factor JADE2 is crucial in the regulation of structural plasticity and memory formati.
It is known that RAC1 dysfunction can lead to many neuropsychiatric diseases, such as intellectual disability and depression [14, 15], so the functional link between JADE2 and other neuropsychiatric diseases can be further explored in the futu.
According to previous studies [16], JADE2, as an E3 ligase, can degrade LSD1 and promote neuronal proliferation in fetal rat cerebral cortex and zebrafish embryonic cells, suggesting whether JADE2 may affect neuronal proliferation in adult mouse DG brain regions by affecting neuronal proliferati.
To regulate learning and memory, this speculation needs further experimental pro.
Taken together, our findings provide a molecular-level link between neural network excitability (environmental information) and memory formation, and suggest that JADE2 may serve as a potential target for drugs that improve learning and memory and improve cogniti.
Link to the original text: https://d.
org/11016.
biopsy.
2020021 First author Fan Minghua (left); co-first author and corresponding author Liu Yongqing (middle); corresponding author Huang Zhuo (right) (Photo provided From: Huang Zhuo Laboratory) Talent Recruitment [1] Talent Recruitment︱ "Logical Neuroscience" is looking for article interpretation/writing positions (part-time online, online office) [2] "Logical Neuroscience" is looking for associate editor/editor/operation Post (online office) selection of previous articles [1] BMC Biol︱ Wu Meilin and others reveal a new mechanism by which cannabinoids impair reinforcement learning by disrupting the normal neural activity of the striatal direct pathway [2] Neurosci Bull︱ Fang Yiru/Chen Jun team achieves dual Early Diagnosis of Phase Disorders: A Biomarker Model of Oxidative Stress Damage [3] Trends Cell Biol︱ Ming Xu's team commented on the heterogeneity and research progress of senescent cells from the single cell level [4] Nat Genet︱ Research revealed by Zhu Hongtu's group Gene association between brain function and brain diseases【5】Review of Front Cell Neurosci︱Peripheral nerve reconstruction therapy based on engineered Schwann cells【6】Acta Neuropathol︱Bovine animals and humans have similar characteristics of traumatic brain injury: Evidence from musk ox and bighorn sheep【7】Neurosci Biobehav Rev︱Virtual reality and telemedicine technology intervention research on autism patients: a systematic review of qualitative and quantitative studies【8】EMBO Rep︱DNA origami combined with topoisomerism Enzyme 1 inhibitor modulates neuroinflammation【9】Neurobiol Dis︱Yu Jin’s group reveals the neuroprotective role of microglia GPR55 in anxiety-depression-like behavior【10】Science︱Reversible CD8 T cell-neuron interaction: aging The important mechanism of inhibiting nerve regeneration High-quality scientific research training course recommendation [1] Symposium on Single-cell Sequencing and Spatial Transcriptomics Data Analysis (Tencent Online Conference on June 11-12) References (swipe up and down to read) West, AE, EC Griffith, and ME Greenberg, Regulation of transcription factors by neuronal activi.
Nature Reviews Neuroscience, 2003(12):.
921-93 West, AE and ME Greenberg, Neuronal Activity-Regulated Gene Transcription in Synapse Development and Cognitive Functi.
Cold Spring Harbor Perspectives in Biology, 201 3(6):.
a005744-a00574
Yap,.
.
and ME Greenberg, Activity-Regulated Transcription: Bridging the Gap between Neural Activity and Behavi.
Neuron, 201 100(2):.
330-34 Restivo,.
, et a.
, The Formation of Recent and Remote Memory Is Associated with Time-Dependent Formation of Dendritic Spines in the Hippocampus and Anterior Cingulate Cort.
Journal of Neuroscience, 200 29(25):.
8206-821 Kang, HJ, et a.
, Decreased expression of synapse-related genes and loss of synapses in major depressive disord.
Nature Medicine, 201 18(9):.
1413-141 Verpelli,.
, et .
,Mutations of the synapse genes and intellectual disability syndrom.
European Journal of Pharmacology, 201 719(1-3):.
112-11 Kandel, Eric.
,.
Dudai, and Mark.
Mayford, The Molecular and Systems Biology of Memo.
Cell, 201 157(1):.
163-18 Sweatt, JD, The Emerging Field of Neuroepigeneti.
Neuron, 201 80(3):.
624-63 Korzus,.
, MG Rosenfeld, and.
Mayford, CBP Histone Acetyltransferase Activity Is a Critical Component of Memory Consolidati.
Neuron, 200 42(6):.
961-971Guan,.
.
, et .
, HDAC2 negatively regulates memory formation and synaptic plastici.
Nature, 200 459(7243):.
55-61 Mews,.
, et .
, Acetyl-CoA synthetase regulates histone acetylation and hippocampal memo.
Nature, 201 546(7658): .
381-381 Costa, JF,.
Dines, and.
Lamprecht,The Role of Rac GTPase in Dendritic Spine Morphogenesis and Memo.
Frontiers in Synaptic Neuroscience, 202 11 Haditsch,.
, et .
, A central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of this paperA central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperA central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperAn Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperAn Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paper
) continuously modulates the excitability of neural networks, thus profoundly affecting brain process.
Biological mechanisms of information processing, learning and memory [1,
Activity-dependent plasticity is the biological basis of learning and new memory formation [
Enhanced structural plasticity is closely linked to changes in the number and size of dendritic spines during learning and memo.
For example, conditioned fear training experiments increase the density of dendritic spines in hippocampal CA1 neurons [
In addition, the impairment of synaptic plasticity can lead to a series of neuropsychiatric diseases such as intellectual disability and depression [5,
Although synaptic plasticity is crucial in the physiological and pathological processes of the brain, its underlying molecular mechanisms remain poorly understo.
The maintenance of long-term synaptic plasticity and the formation of memory require changes in gene transcription in neural cells [
Epigenetic regulation is an important way to alter cellular gene expression in the presence of external environmental stimuli, suggesting that epigenetic factors are ideal candidates for regulating neural plasticity [
Reversible histone post-translational modifications, including acetylation, phosphorylation, and methylation, are important epigenetic mechanisms regulating gene expressi.
In particular, histone acetylase, histone deacetylase and acetyl-CoA synthase [9-11] are closely related to learning and memory, suggesting that histone acetylation plays an important role in cognitive functi.
On May 22, 2022, Huang Zhuo's team from Peking University School of Pharmacy published a research paper titled "JADE2 is essential for hippocampal synaptic plasticity and cognitive functions in mice" in Biological Psychiat.
This study deeply elucidates the important role and molecular mechanism of the epigenetic molecule JADE2 in hippocampal synaptic plasticity and learning and memo.
Fan Minghua and Liu Yongqing are the co-first authors of the paper, and Researcher Huang Zhuo and .
Liu Yongqing are the corresponding autho.
Professor Shang Yongfeng and Researcher Liang Jing also provided guidance and suppo.
In order to explore whether the expression levels of epigenetic factors, especially genes related to histone acetylation modification, will change during the process of neuronal excitability, the authors first stimulated primary neurons in the mouse hippocampus with high concentrations of potassium chlori.
, to detect the mRNA changes of some epigenetic facto.
The results of RT-qPCR experiments showed that the mRNA levels of most epigenetic factors were unchanged in this in vitro model, and only the mRNA level of JADE2 was significantly increased with increased neuronal excitability (F.
1.
Western blotting and WB experiments and immunofluorescence experiments also proved that in the primary neuron model stimulated by potassium chloride, the expression of JADE2 protein was significantly increased with the increase of neuronal excitabili.
In order to explore the changes of JADE2 with neuronal excitability in vivo, the authors used chemical genetics, water maze training and kaine acid-induced epilepsy model to find that when the excitability of the hippocampal neural network increased, the expression of JADE2 also increased significantly high (Figure In conclusion, the expression of JADE2 was significantly increased with the increase of neuronal excitability, indicating that JADE2 plays an important role in the activity-dependent regulation of neuronal excitabili.
Figure 1 The expression of JADE2 increases with the increase of neuronal excitability (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) In order to explore whether changes in the expression of JADE2 in adult mice will affect neuronal activity To function, the authors constructed adeno-associated (AAV) viruses in the control and JADE2 knockdown groups and injected them into the CA1 brain region of the mouse hippocamp.
Electrophysiological experiments found that JADE2 knockdown did not affect neuronal excitabili.
However, compared with control neurons, the frequency of miniature excitatory postsynaptic currents (mEPSCs) in CA1 pyramidal neurons in the JADE2 knockdown group was significantly reduced, and the amplitude was basically unchanged (F.
These results show that loss of JADE2 results in impaired glutamatergic synaptic transmissi.
Figure 2 Deletion of JADE2 causes impaired glutamatergic synaptic transmission (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) The significant decrease in mEPSC frequency reflects changes in the number of synapses or synapses Changes in the ability to release protransmitte.
To test whether JADE2 is important for the maintenance of dendritic spines, the authors first injected control or JADE2 knockdown virus in CA1, and then electrophysiologically and morphologically labeled CA1 pyramidal neurons and examined changes in dendritic spin.
Although the dendritic branching of pyramidal neurons in the JADE2 knockdown group did not change compared with the control group, their dendritic spine density was significantly reduced (F.
3.
In contrast, overexpression of JADE2 in CA1 significantly increased the number of dendritic spin.
Then the authors used paired-pulse ratios (PPRs) experiments to detect the presynaptic transmitter release capacity of the mouse hippocampal CA3-CA1 Schaffer colleteral pathw.
The experimental results showed that compared with the control group, the CA1 cones in the JADE2 knockout group The presynaptic neurotransmitter release capacity of somatic neurons was largely unchanged (F.
3.
Next, in order to explore whether JADE2 affects the synaptic plasticity function of the hippocampus, the authors detected the NMDAR/AMPAR ratio of CA1 pyramidal neurons in the mouse hippocamp.
Compared with the control group, the NMDAR/AMPAR raio of the JADE2 knockout group was significantly decreased , and the long-term potentiation (LTP) function was significantly impaired (F.
3), indicating that JADE2 is essential for the maintenance of hippocampal synaptic plastici.
Figure 3 JADE2 deletion impairs synaptic plasticity in the hippocampus (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) The authors then conducted a series of animal behavioral experiments, including open field experiments, elevated cross experiments, and novel object recognition Experiments, water maze experiments and fear memory experiments showed that the lack of JADE2 in the hippocampus had basically no effect on the motor ability and anxiety level of animals, but significantly affected the learning and memory ability of mice (Figure
Figure 4 JADE2 deletion impairs learning and memory ability in mice (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) In order to explore the molecular mechanism of JADE2-mediated learning and memory, the authors selected JADE2 knockout mice and littermates In the hippocampus of control mice, RNA-seq high-throughput sequencing experiments were performed to find the downstream regulatory genes of JADE2 related to learning and memo.
Among the downstream regulatory genes of JADE2, the authors focused on the Rac1 gene because its function is closely related to dendritic spine development and memory formation [12, 1Next, the authors wanted to explore whether JADE2-regulated synaptic plasticity and learned cognitive behavior are achieved through the expression of RACExperiments showed that when JADE2 was knocked out, the density of dendritic spines in hippocampal CA1 pyramidal neurons was significantly reduced, but when JADE2 was knocked out and RAC1 was overexpressed at the same time, the density of dendritic spines in CA1 cells returned to normal levels, which was no different from the control group ( Figure 5.
After that, electrophysiological experiments found that when JADE2 was knocked out, the frequency of cellular mEPSCs decreased significantly while the amplitude remained unchang.
When JADE2 was knocked out and RAC1 was overexpressed at the same time, the frequency of cellular mEPSCs returned to the normal level, which was not significantly different from the control gro.
In addition, overexpression of RAC1 reversed the long-term plasticity decline of the Schaffer-colleteral pathway and impaired memory in mice caused by JADE2 knockout, returning it to normal levels (F.
These experiments demonstrate that RAC1 is essential for JADE2-mediated learning and memory in mi.
Figure 5 JADE2 regulates learning and memory ability through the expression of RAC1 (Source: Fan M, Liu Y, et .
, Biol Psychiatry, 2022) Conclusion and discussion, inspiration and prospect Experiments in molecular biology and animal behavior have found that the epigenetic factor JADE2 is crucial in the regulation of structural plasticity and memory formati.
It is known that RAC1 dysfunction can lead to many neuropsychiatric diseases, such as intellectual disability and depression [14, 15], so the functional link between JADE2 and other neuropsychiatric diseases can be further explored in the futu.
According to previous studies [16], JADE2, as an E3 ligase, can degrade LSD1 and promote neuronal proliferation in fetal rat cerebral cortex and zebrafish embryonic cells, suggesting whether JADE2 may affect neuronal proliferation in adult mouse DG brain regions by affecting neuronal proliferati.
To regulate learning and memory, this speculation needs further experimental pro.
Taken together, our findings provide a molecular-level link between neural network excitability (environmental information) and memory formation, and suggest that JADE2 may serve as a potential target for drugs that improve learning and memory and improve cogniti.
Link to the original text: https://d.
org/11016.
biopsy.
2020021 First author Fan Minghua (left); co-first author and corresponding author Liu Yongqing (middle); corresponding author Huang Zhuo (right) (Photo provided From: Huang Zhuo Laboratory) Talent Recruitment [1] Talent Recruitment︱ "Logical Neuroscience" is looking for article interpretation/writing positions (part-time online, online office) [2] "Logical Neuroscience" is looking for associate editor/editor/operation Post (online office) selection of previous articles [1] BMC Biol︱ Wu Meilin and others reveal a new mechanism by which cannabinoids impair reinforcement learning by disrupting the normal neural activity of the striatal direct pathway [2] Neurosci Bull︱ Fang Yiru/Chen Jun team achieves dual Early Diagnosis of Phase Disorders: A Biomarker Model of Oxidative Stress Damage [3] Trends Cell Biol︱ Ming Xu's team commented on the heterogeneity and research progress of senescent cells from the single cell level [4] Nat Genet︱ Research revealed by Zhu Hongtu's group Gene association between brain function and brain diseases【5】Review of Front Cell Neurosci︱Peripheral nerve reconstruction therapy based on engineered Schwann cells【6】Acta Neuropathol︱Bovine animals and humans have similar characteristics of traumatic brain injury: Evidence from musk ox and bighorn sheep【7】Neurosci Biobehav Rev︱Virtual reality and telemedicine technology intervention research on autism patients: a systematic review of qualitative and quantitative studies【8】EMBO Rep︱DNA origami combined with topoisomerism Enzyme 1 inhibitor modulates neuroinflammation【9】Neurobiol Dis︱Yu Jin’s group reveals the neuroprotective role of microglia GPR55 in anxiety-depression-like behavior【10】Science︱Reversible CD8 T cell-neuron interaction: aging The important mechanism of inhibiting nerve regeneration High-quality scientific research training course recommendation [1] Symposium on Single-cell Sequencing and Spatial Transcriptomics Data Analysis (Tencent Online Conference on June 11-12) References (swipe up and down to read) West, AE, EC Griffith, and ME Greenberg, Regulation of transcription factors by neuronal activi.
Nature Reviews Neuroscience, 2003(12):.
921-93 West, AE and ME Greenberg, Neuronal Activity-Regulated Gene Transcription in Synapse Development and Cognitive Functi.
Cold Spring Harbor Perspectives in Biology, 201 3(6):.
a005744-a00574
Yap,.
.
and ME Greenberg, Activity-Regulated Transcription: Bridging the Gap between Neural Activity and Behavi.
Neuron, 201 100(2):.
330-34 Restivo,.
, et a.
, The Formation of Recent and Remote Memory Is Associated with Time-Dependent Formation of Dendritic Spines in the Hippocampus and Anterior Cingulate Cort.
Journal of Neuroscience, 200 29(25):.
8206-821 Kang, HJ, et a.
, Decreased expression of synapse-related genes and loss of synapses in major depressive disord.
Nature Medicine, 201 18(9):.
1413-141 Verpelli,.
, et .
,Mutations of the synapse genes and intellectual disability syndrom.
European Journal of Pharmacology, 201 719(1-3):.
112-11 Kandel, Eric.
,.
Dudai, and Mark.
Mayford, The Molecular and Systems Biology of Memo.
Cell, 201 157(1):.
163-18 Sweatt, JD, The Emerging Field of Neuroepigeneti.
Neuron, 201 80(3):.
624-63 Korzus,.
, MG Rosenfeld, and.
Mayford, CBP Histone Acetyltransferase Activity Is a Critical Component of Memory Consolidati.
Neuron, 200 42(6):.
961-971Guan,.
.
, et .
, HDAC2 negatively regulates memory formation and synaptic plastici.
Nature, 200 459(7243):.
55-61 Mews,.
, et .
, Acetyl-CoA synthetase regulates histone acetylation and hippocampal memo.
Nature, 201 546(7658): .
381-381 Costa, JF,.
Dines, and.
Lamprecht,The Role of Rac GTPase in Dendritic Spine Morphogenesis and Memo.
Frontiers in Synaptic Neuroscience, 202 11 Haditsch,.
, et .
, A central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of this paperA central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperA central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memo.
Molecular and Cellular Neuroscience, 200 41(4):.
409-411 Tian, .
, et .
, An Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperAn Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paperAn Intellectual Disability-Related Missense Mutation in Rac1 Prevents LTP Inducti.
Frontiers in Molecular Neuroscience, 201 11 Tejada-Simon, MV, Modulation of actin dynamics by Rac1 to target cognitive functi.
Journal of Neurochemistry, 201 133(6):.
767-771 Han,.
, et .
, Destabilizing LSD1 by Jade-2 Promotes Neurogenesis: An Antibraking System in Neural Developme.
Molecular Cell, 201 55(3):.
482-49 End of paper
