16 results on '"Si-Qiang Ren"'
Search Results
2. Regulation of spike timing-dependent plasticity of olfactory inputs in mitral cells in the rat olfactory bulb.
- Author
-
Teng-Fei Ma, Xiao-Lei Zhao, Lei Cai, Nan Zhang, Si-Qiang Ren, Fang Ji, Tian Tian, and Wei Lu
- Subjects
Medicine ,Science - Abstract
The recent history of activity input onto granule cells (GCs) in the main olfactory bulb can affect the strength of lateral inhibition, which functions to generate contrast enhancement. However, at the plasticity level, it is unknown whether and how the prior modification of lateral inhibition modulates the subsequent induction of long-lasting changes of the excitatory olfactory nerve (ON) inputs to mitral cells (MCs). Here we found that the repetitive stimulation of two distinct excitatory inputs to the GCs induced a persistent modification of lateral inhibition in MCs in opposing directions. This bidirectional modification of inhibitory inputs differentially regulated the subsequent synaptic plasticity of the excitatory ON inputs to the MCs, which was induced by the repetitive pairing of excitatory postsynaptic potentials (EPSPs) with postsynaptic bursts. The regulation of spike timing-dependent plasticity (STDP) was achieved by the regulation of the inter-spike-interval (ISI) of the postsynaptic bursts. This novel form of inhibition-dependent regulation of plasticity may contribute to the encoding or processing of olfactory information in the olfactory bulb.
- Published
- 2012
- Full Text
- View/download PDF
3. TBR2 coordinates neurogenesis expansion and precise microcircuit organization via Protocadherin 19 in the mammalian cortex
- Author
-
Zhizhong Li, Anjin Xianyu, Si-Qiang Ren, Tanay Ghosh, Qiangqiang Zhang, Matthias Groszer, Peng Gao, Xin-Jun Zhang, Susan Lin, Yang Yu, Song-Hai Shi, Xiaohui Lv, Zhongfu Shen, Apollo - University of Cambridge Repository, Memorial Sloane Kettering Cancer Center [New York], Tsinghua University [Beijing] (THU), Institut du Fer à Moulin, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Sorbonne Université (SU), University of Cambridge [UK] (CAM), and Weill Medical College of Cornell University [New York]
- Subjects
0301 basic medicine ,[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,Science ,Neurogenesis ,General Physics and Astronomy ,Protocadherin ,Mice, Transgenic ,02 engineering and technology ,Biology ,Article ,General Biochemistry, Genetics and Molecular Biology ,Synapse ,03 medical and health sciences ,Cortex (anatomy) ,medicine ,Animals ,Humans ,lcsh:Science ,Neural stem cells ,Regulation of gene expression ,Cerebral Cortex ,Mice, Knockout ,Neurons ,Multidisciplinary ,Gene Expression Profiling ,HEK 293 cells ,Gene Expression Regulation, Developmental ,General Chemistry ,021001 nanoscience & nanotechnology ,Cadherins ,Protocadherins ,030104 developmental biology ,medicine.anatomical_structure ,HEK293 Cells ,Cerebral cortex ,Synapses ,Excitatory postsynaptic potential ,lcsh:Q ,RNA Interference ,0210 nano-technology ,T-Box Domain Proteins ,Neuroscience - Abstract
Cerebral cortex expansion is a hallmark of mammalian brain evolution; yet, how increased neurogenesis is coordinated with structural and functional development remains largely unclear. The T-box protein TBR2/EOMES is preferentially enriched in intermediate progenitors and supports cortical neurogenesis expansion. Here we show that TBR2 regulates fine-scale spatial and circuit organization of excitatory neurons in addition to enhancing neurogenesis in the mouse cortex. TBR2 removal leads to a significant reduction in neuronal, but not glial, output of individual radial glial progenitors as revealed by mosaic analysis with double markers. Moreover, in the absence of TBR2, clonally related excitatory neurons become more laterally dispersed and their preferential synapse development is impaired. Interestingly, TBR2 directly regulates the expression of Protocadherin 19 (PCDH19), and simultaneous PCDH19 expression rescues neurogenesis and neuronal organization defects caused by TBR2 removal. Together, these results suggest that TBR2 coordinates neurogenesis expansion and precise microcircuit assembly via PCDH19 in the mammalian cortex., The T-box protein TBR2 is involved in cortical neurogenesis expansion during neurodevelopment and is preferentially enriched in intermediate progenitors. The authors show that TBR2 coordinates neurogenesis expansion and precise microcircuit assembly in the mouse cortex via PCDH19.
- Published
- 2019
4. Precise Long-Range Microcircuit-to-Microcircuit Communication Connects the Frontal and Sensory Cortices in the Mammalian Brain
- Author
-
Susan Lin, Si-Qiang Ren, Zhizhong Li, Matteo Bergami, and Song-Hai Shi
- Subjects
0301 basic medicine ,media_common.quotation_subject ,Sensory system ,Biology ,Article ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Neural Stem Cells ,Perception ,Cortex (anatomy) ,Inhibitory neuron ,Neural Pathways ,medicine ,Premovement neuronal activity ,Animals ,Sensory cortex ,media_common ,Neurons ,Brain Mapping ,General Neuroscience ,Motor Cortex ,Somatosensory Cortex ,Mammalian brain ,Frontal Lobe ,Neuroanatomical Tract-Tracing Techniques ,030104 developmental biology ,medicine.anatomical_structure ,Cerebral cortex ,Synapses ,Neuroscience ,030217 neurology & neurosurgery - Abstract
The frontal area of the cerebral cortex provides long-range inputs to sensory areas to modulate neuronal activity and information processing. These long-range circuits are crucial for accurate sensory perception and complex behavioral control; however, little is known about their precise circuit organization. Here we specifically identified the presynaptic input neurons to individual excitatory neuron clones as a unit that constitutes functional microcircuits in the mouse sensory cortex. Interestingly, the long-range input neurons in the frontal but not contralateral sensory area are spatially organized into discrete vertical clusters and preferentially form synapses with each other over nearby non-input neurons. Moreover, the assembly of distant presynaptic microcircuits in the frontal area depends on the selective synaptic communication of excitatory neuron clones in the sensory area that provide inputs to the frontal area. These findings suggest that highly precise long-range reciprocal microcircuit-to-microcircuit communication mediates frontal-sensory area interactions in the mammalian cortex.
- Published
- 2019
- Full Text
- View/download PDF
5. Vascular Influence on Ventral Telencephalic Progenitors and Neocortical Interneuron Production
- Author
-
Wei Shi, Wenying Angela Liu, Zhizhong Li, Keith N. Brown, Xin Tan, Xin-Jun Zhang, Si-Qiang Ren, and Song-Hai Shi
- Subjects
Telencephalon ,0301 basic medicine ,Interkinetic nuclear migration ,Interneuron ,Green Fluorescent Proteins ,Gestational Age ,Mice, Transgenic ,Neocortex ,Inhibitory postsynaptic potential ,Article ,General Biochemistry, Genetics and Molecular Biology ,Mice ,03 medical and health sciences ,Glutamatergic ,0302 clinical medicine ,Neural Stem Cells ,Interneurons ,Pregnancy ,medicine ,Animals ,Molecular Biology ,Embryonic Stem Cells ,biology ,Integrin beta1 ,musculoskeletal, neural, and ocular physiology ,fungi ,Neurogenesis ,Median Eminence ,Cell Biology ,Anatomy ,Preoptic Area ,Recombinant Proteins ,Parvalbumins ,030104 developmental biology ,medicine.anatomical_structure ,nervous system ,biology.protein ,GABAergic ,Female ,Somatostatin ,Neuroglia ,Neuroscience ,030217 neurology & neurosurgery ,Parvalbumin ,Developmental Biology - Abstract
The neocortex contains glutamatergic excitatory neurons and γ-aminobutyric acid (GABA)ergic inhibitory interneurons. Extensive studies have revealed substantial insights into excitatory neuron production. However, our knowledge of the generation of GABAergic interneurons remains limited. Here we show that periventricular blood vessels selectively influence neocortical interneuron progenitor behavior and neurogenesis. Distinct from those in the dorsal telencephalon, radial glial progenitors (RGPs) in the ventral telencephalon responsible for producing neocortical interneurons progressively grow radial glial fibers anchored to periventricular vessels. This progenitor-vessel association is robust and actively maintained as RGPs undergo interkinetic nuclear migration and divide at the ventricular zone surface. Disruption of this association by selective removal of INTEGRIN β1 in RGPs leads to a decrease in progenitor division, a loss of PARVALBUMIN and SOMATOSTATIN-expressing interneurons, and defective synaptic inhibition in the neocortex. These results highlight a prominent interaction between RGPs and periventricular vessels important for proper production and function of neocortical interneurons.
- Published
- 2016
6. Amyloid β causes excitation/inhibition imbalance through dopamine receptor 1-dependent disruption of fast-spiking GABAergic input in anterior cingulate cortex
- Author
-
Chunhui Jin, Si-Qiang Ren, Shui Yu, Wen Yao, Zaohuo Cheng, Jianmin Yuan, Jing-Zhi Yan, and Jiajun Yin
- Subjects
0301 basic medicine ,Cingulate cortex ,Male ,lcsh:Medicine ,Neurotransmission ,Inhibitory postsynaptic potential ,Gyrus Cinguli ,Article ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Dopamine receptor D1 ,Dopamine ,Interneurons ,medicine ,Animals ,GABAergic Neurons ,lcsh:Science ,Anterior cingulate cortex ,gamma-Aminobutyric Acid ,Analysis of Variance ,Multidisciplinary ,Amyloid beta-Peptides ,Microscopy, Confocal ,Chemistry ,Pyramidal Cells ,Receptors, Dopamine D1 ,lcsh:R ,Excitatory Postsynaptic Potentials ,Synaptic Potentials ,030104 developmental biology ,medicine.anatomical_structure ,Excitatory postsynaptic potential ,GABAergic ,lcsh:Q ,Neuroscience ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. At the early stages of AD development, the soluble β-amyloid (Aβ) induces synaptic dysfunction, perturbs the excitation/inhibition balance of neural circuitries, and in turn alters the normal neural network activity leading to cognitive decline, but the underlying mechanisms are not well established. Here by using whole-cell recordings in acute mouse brain slices, we found that 50 nM Aβ induces hyperexcitability of excitatory pyramidal cells in the cingulate cortex, one of the most vulnerable areas in AD, via depressing inhibitory synaptic transmission. Furthermore, by simultaneously recording multiple cells, we discovered that the inhibitory innervation of pyramidal cells from fast-spiking (FS) interneurons instead of non-FS interneurons is dramatically disrupted by Aβ, and perturbation of the presynaptic inhibitory neurotransmitter gamma-aminobutyric acid (GABA) release underlies this inhibitory input disruption. Finally, we identified the increased dopamine action on dopamine D1 receptor of FS interneurons as a key pathological factor that contributes to GABAergic input perturbation and excitation/inhibition imbalance caused by Aβ. Thus, we conclude that the dopamine receptor 1-dependent disruption of FS GABAergic inhibitory input plays a critical role in Aβ-induced excitation/inhibition imbalance in anterior cingulate cortex.
- Published
- 2017
7. Aβ induces acute depression of excitatory glutamatergic synaptic transmission through distinct phosphatase-dependent mechanisms in rat CA1 pyramidal neurons
- Author
-
Si-Qiang Ren, Wen Yao, Da Sun, and Hao-Jun Zou
- Subjects
Male ,Patch-Clamp Techniques ,Calcineurin Inhibitors ,Glutamic Acid ,Hippocampus ,Hippocampal formation ,Neurotransmission ,Synaptic Transmission ,Tacrolimus ,Rats, Sprague-Dawley ,Glutamatergic ,Organ Culture Techniques ,Postsynaptic potential ,Animals ,CA1 Region, Hippocampal ,Molecular Biology ,Amyloid beta-Peptides ,Chemistry ,Calcineurin ,Pyramidal Cells ,General Neuroscience ,fungi ,Excitatory Postsynaptic Potentials ,food and beverages ,Protein phosphatase 2 ,Peptide Fragments ,Rats ,Synaptic fatigue ,Excitatory postsynaptic potential ,Neurology (clinical) ,Neuroscience ,Developmental Biology - Abstract
Beta-amyloid peptide (Aβ) has a causal role in the pathophysiology of Alzheimer's disease (AD). Recent studies indicate that Aβ can disrupt excitatory glutamatergic synaptic function at synaptic level. However, the underlying mechanisms remain obscure. In this study, we recorded evoked and spontaneous EPSCs in hippocampal CA1 pyramidal neurons via whole-cell voltage-clamping methods and found that 1 μM Aβ can induce acute depression of basal glutamatergic synaptic transmission through both presynaptic and postsynaptic dysfunction. Moreover, we also found that Aβ-induced both presynaptic and postsynaptic dysfunction can be reversed by the inhibitor of protein phosphatase 2B (PP2B), FK506, whereas only postsynaptic disruption can be ameliorated by the inhibitor of PP1/PP2A, Okadaic acid (OA). These results indicate that PP1/PP2A and PP2B have overlapping but not identical functions in Aβ-induced acute depression of excitatory glutamatergic synaptic transmission of hippocampal CA1 pyramidal neurons.
- Published
- 2013
8. PKCλ is critical in AMPA receptor phosphorylation and synaptic incorporation during LTP
- Author
-
Jing-Zhi Yan, Si-Qiang Ren, Wei-Wei Pan, Wei Lu, Wen Yao, Xiao-Yan Zhang, Tian Tian, and Yun-Fei Bu
- Subjects
Scaffold protein ,General Immunology and Microbiology ,musculoskeletal, neural, and ocular physiology ,General Neuroscience ,Long-term potentiation ,AMPA receptor ,Phosphatidylinositol 3-Kinases ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Cell biology ,chemistry.chemical_compound ,nervous system ,Biochemistry ,chemistry ,Phosphorylation ,Phosphatidylinositol ,Signal transduction ,Molecular Biology ,Protein kinase C - Abstract
Direct phosphorylation of GluA1 by PKC controls α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor (AMPAR) incorporation into active synapses during long-term potentiation (LTP). Numerous signalling molecules that involved in AMPAR incorporation have been identified, but the specific PKC isoform(s) participating in GluA1 phosphorylation and the molecule triggering PKC activation remain largely unknown. Here, we report that the atypical isoform of PKC, PKCλ, is a critical molecule that acts downstream of phosphatidylinositol 3-kinase (PI3K) and is essential for LTP expression. PKCλ activation is required for both GluA1 phosphorylation and increased surface expression of AMPARs during LTP. Moreover, p62 interacts with both PKCλ and GluA1 during LTP and may serve as a scaffolding protein to place PKCλ in close proximity to facilitate GluA1 phosphorylation by PKCλ. Thus, we conclude that PKCλ is the critical signalling molecule responsible for GluA1-containing AMPAR phosphorylation and synaptic incorporation at activated synapses during LTP expression.
- Published
- 2013
9. Protein Kinase C Promotes N-Methyl-d-aspartate (NMDA) Receptor Trafficking by Indirectly Triggering Calcium/Calmodulin-dependent Protein Kinase II (CaMKII) Autophosphorylation
- Author
-
Bin Hu, Zhuo Xu, Jing-Zhi Yan, Wen Yao, Su-Yi Liu, Si-Qiang Ren, Shan-Hui Wang, and Wei Lu
- Subjects
Male ,Long-Term Potentiation ,Synaptic Membranes ,AMPA receptor ,Biology ,Receptors, N-Methyl-D-Aspartate ,Biochemistry ,Rats, Sprague-Dawley ,Neurobiology ,Ca2+/calmodulin-dependent protein kinase ,mental disorders ,Animals ,Phosphorylation ,Molecular Biology ,Protein Kinase C ,Protein kinase C ,musculoskeletal, neural, and ocular physiology ,Autophosphorylation ,Long-term potentiation ,Cell Biology ,Rats ,Cell biology ,Enzyme Activation ,Protein Transport ,nervous system ,Synaptic plasticity ,NMDA receptor ,biological phenomena, cell phenomena, and immunity ,Signal transduction ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,psychological phenomena and processes ,Signal Transduction - Abstract
Regulation of neuronal NMDA receptor (NMDAR) is critical in synaptic transmission and plasticity. Protein kinase C (PKC) promotes NMDAR trafficking to the cell surface via interaction with NMDAR-associated proteins (NAPs). Little is known, however, about the NAPs that are critical to PKC-induced NMDAR trafficking. Here, we showed that calcium/calmodulin-dependent protein kinase II (CaMKII) could be a NAP that mediates the potentiation of NMDAR trafficking by PKC. PKC activation promoted the level of autophosphorylated CaMKII and increased association with NMDARs, accompanied by functional NMDAR insertion, at postsynaptic sites. This potentiation, along with PKC-induced long term potentiation of the AMPA receptor-mediated response, was abolished by CaMKII antagonist or by disturbing the interaction between CaMKII and NR2A or NR2B. Further mutual occlusion experiments demonstrated that PKC and CaMKII share a common signaling pathway in the potentiation of NMDAR trafficking and long-term potentiation (LTP) induction. Our results revealed that PKC promotes NMDA receptor trafficking and induces synaptic plasticity through indirectly triggering CaMKII autophosphorylation and subsequent increased association with NMDARs.
- Published
- 2011
10. Role of Glycine Receptors in Glycine-Induced LTD in Hippocampal CA1 Pyramidal Neurons
- Author
-
Fang Ji, Wen Yao, Su-Yi Liu, Rongqing Chen, Shan-Hui Wang, Wei Lu, Jing-Zhi Yan, Jing-Jing Wang, Si-Qiang Ren, and Zheng Chen
- Subjects
Male ,Glycine ,Glycine Plasma Membrane Transport Proteins ,Biology ,Synaptic Transmission ,Rats, Sprague-Dawley ,Glycine transporter ,chemistry.chemical_compound ,Organ Culture Techniques ,Receptors, Glycine ,Animals ,Long-term depression ,CA1 Region, Hippocampal ,Glycine receptor ,Pharmacology ,Long-Term Synaptic Depression ,Pyramidal Cells ,musculoskeletal, neural, and ocular physiology ,Excitatory Postsynaptic Potentials ,Neural Inhibition ,Strychnine ,Rats ,Psychiatry and Mental health ,nervous system ,chemistry ,Synaptic plasticity ,Excitatory postsynaptic potential ,Biophysics ,NMDA receptor ,Original Article ,Neuroscience - Abstract
Glycine in the hippocampus can exert its effect on both synaptic NMDA receptors (NMDARs) and extrasynaptic functional glycine receptors (GlyRs) via distinct binding sites. Previous studies have reported that glycine induces long-term potentiation (LTP) through the activation of synaptic NMDARs. However, little is known about the potential role of the activated GlyRs that are largely located in extrasynaptic regions. We report here that relatively high levels of glycine achieved either by exogenous glycine application or by the elevation of endogenous glycine accumulation with an antagonist of the glycine transporter induced long-term depression (LTD) of excitatory postsynaptic currents (EPSCs) in hippocampal CA1 pyramidal neurons. The co-application of glycine with the selective GlyR antagonist strychnine changed glycine-induced LTD (Gly-LTD) to LTP. Blocking the postsynaptic GlyR-gated net chloride flux by manipulating intracellular chloride concentrations failed to elicit any changes in EPSCs. These results suggest that GlyRs are involved in Gly-LTD. Furthermore, this new form of chemical LTD was accompanied by the internalization of postsynaptic AMPA receptors and required the activation of NMDARs. Therefore, our present findings reveal an important function of GlyR activation and modulation in gating the direction of synaptic plasticity.
- Published
- 2011
11. Glycine exerts dual roles in ischemic injury through distinct mechanisms
- Author
-
Xiao-Yan Zhang, Wei Lu, Su-Yi Liu, Si-Qiang Ren, Nan Zhang, Fang Ji, Wen Yao, and Zheng Chen
- Subjects
Male ,Patch-Clamp Techniques ,Long-Term Potentiation ,Ischemia ,Glycine ,Pharmacology ,Neuroprotection ,Hippocampus ,Receptors, N-Methyl-D-Aspartate ,Brain Ischemia ,Rats, Sprague-Dawley ,Stereotaxic Techniques ,Receptors, Glycine ,Quinoxalines ,medicine ,Animals ,Patch clamp ,Hypoxia, Brain ,Glycine receptor ,Advanced and Specialized Nursing ,Dose-Response Relationship, Drug ,business.industry ,Long-term potentiation ,Infarction, Middle Cerebral Artery ,medicine.disease ,Rats ,Glucose ,2-Amino-5-phosphonovalerate ,Anesthesia ,Stereotaxic technique ,Viruses ,NMDA receptor ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,business - Abstract
Background and Purpose— We characterized the differential effects of glycine at different levels in the induction of postischemic long-term potentiation, as well as in the neuronal damage induced by focal ischemia. Methods— Whole-cell patch clamp recordings were obtained from rat hippocampal slice preparations. In vitro ischemia and postischemic long-term potentiation were induced by oxygen and glucose deprivation. In vivo ischemia was induced by transient middle cerebral artery occlusion. Results— In both in vitro and in vivo ischemia models, glycine at low level exerts deleterious effects in postischemic long-term potentiation and ischemic neuronal injury by modulation of the N-methyl- d -aspartate receptor coagonist site; whereas glycine at high level exerts neuroprotective effects by activation of glycine receptor and subsequent differential regulation of N-methyl- d -aspartate receptor subunit components. Conclusions— Our results provide a molecular basis for the dual roles of glycine in ischemic injury through distinct mechanisms, and they suggest that glycine receptors could be a potential target for clinical treatment of stroke.
- Published
- 2012
12. Regulation of Spike Timing-Dependent Plasticity of Olfactory Inputs in Mitral Cells in the Rat Olfactory Bulb
- Author
-
Si-Qiang Ren, Fang Ji, Nan Zhang, Tengfei Ma, Lei Cai, Xiao-Lei Zhao, Tian Tian, and Wei Lu
- Subjects
Central Nervous System ,Anatomy and Physiology ,Olfactory Nerve ,lcsh:Medicine ,Neurophysiology ,Action Potentials ,Biology ,In Vitro Techniques ,Inhibitory postsynaptic potential ,Biochemistry ,Neurological System ,GABA Antagonists ,Rats, Sprague-Dawley ,Learning and Memory ,Olfactory nerve ,Developmental Neuroscience ,Postsynaptic potential ,Lateral inhibition ,Animals ,GABAergic Neurons ,lcsh:Science ,GABA Agonists ,Neurons ,Olfactory System ,Multidisciplinary ,Neuronal Plasticity ,Post-tetanic potentiation ,Spike-timing-dependent plasticity ,lcsh:R ,Excitatory Postsynaptic Potentials ,Neurochemistry ,Neural Inhibition ,Anatomy ,Olfactory Bulb ,Sensory Systems ,Electric Stimulation ,Olfactory bulb ,Rats ,Pyridazines ,Synapses ,Excitatory postsynaptic potential ,Medicine ,lcsh:Q ,Isonicotinic Acids ,Neuroscience ,Research Article ,Synaptic Plasticity - Abstract
The recent history of activity input onto granule cells (GCs) in the main olfactory bulb can affect the strength of lateral inhibition, which functions to generate contrast enhancement. However, at the plasticity level, it is unknown whether and how the prior modification of lateral inhibition modulates the subsequent induction of long-lasting changes of the excitatory olfactory nerve (ON) inputs to mitral cells (MCs). Here we found that the repetitive stimulation of two distinct excitatory inputs to the GCs induced a persistent modification of lateral inhibition in MCs in opposing directions. This bidirectional modification of inhibitory inputs differentially regulated the subsequent synaptic plasticity of the excitatory ON inputs to the MCs, which was induced by the repetitive pairing of excitatory postsynaptic potentials (EPSPs) with postsynaptic bursts. The regulation of spike timing-dependent plasticity (STDP) was achieved by the regulation of the inter-spike-interval (ISI) of the postsynaptic bursts. This novel form of inhibition-dependent regulation of plasticity may contribute to the encoding or processing of olfactory information in the olfactory bulb.
- Published
- 2012
13. Glycine Exerts Dual Roles in Ischemic Injury Through Distinct Mechanisms.
- Author
-
Wen Yao, Fang Ji, Zheng Chen, Nan Zhang, Si-Qiang Ren, Xiao-Yan Zhang, Su-Yi Liu, and Wei Lu
- Published
- 2012
- Full Text
- View/download PDF
14. Role of Glycine Receptors in Glycine-Induced LTD in Hippocampal CA1 Pyramidal Neurons.
- Author
-
Rong-Qing Chen, Shan-Hui Wang, Wen Yao, Jing-Jing Wang, Fang Ji, Jing-Zhi Yan, Si-Qiang Ren, Zheng Chen, Su-Yi Liu, and Wei Lu
- Subjects
GLYCINE ,MENTAL depression ,DRUG synergism ,DRUG receptors ,NEUROPLASTICITY ,STRYCHNINE - Abstract
Glycine in the hippocampus can exert its effect on both synaptic NMDA receptors (NMDARs) and extrasynaptic functional glycine receptors (GlyRs) via distinct binding sites. Previous studies have reported that glycine induces long-term potentiation (LTP) through the activation of synaptic NMDARs. However, little is known about the potential role of the activated GlyRs that are largely located in extrasynaptic regions. We report here that relatively high levels of glycine achieved either by exogenous glycine application or by the elevation of endogenous glycine accumulation with an antagonist of the glycine transporter induced long-term depression (LTD) of excitatory postsynaptic currents (EPSCs) in hippocampal CA1 pyramidal neurons. The co-application of glycine with the selective GlyR antagonist strychnine changed glycine-induced LTD (Gly-LTD) to LTP. Blocking the postsynaptic GlyR-gated net chloride flux by manipulating intracellular chloride concentrations failed to elicit any changes in EPSCs. These results suggest that GlyRs are involved in Gly-LTD. Furthermore, this new form of chemical LTD was accompanied by the internalization of postsynaptic AMPA receptors and required the activation of NMDARs. Therefore, our present findings reveal an important function of GlyR activation and modulation in gating the direction of synaptic plasticity. [ABSTRACT FROM AUTHOR]
- Published
- 2011
- Full Text
- View/download PDF
15. Distinct Roles of PKCι/λ and PKMζ in the Initiation and Maintenance of Hippocampal Long-Term Potentiation and Memory
- Author
-
Tao Sheng, Si-Qiang Ren, Tian Tian, Wei Lu, and Shaoli Wang
- Subjects
Male ,0301 basic medicine ,Memory, Long-Term ,Time Factors ,Dorsal hippocampus ,Green Fluorescent Proteins ,Long-Term Potentiation ,Biology ,Hippocampal formation ,Hippocampus ,General Biochemistry, Genetics and Molecular Biology ,Rats, Sprague-Dawley ,Tissue Culture Techniques ,03 medical and health sciences ,0302 clinical medicine ,Genes, Reporter ,Animals ,Fear conditioning ,RNA, Small Interfering ,lcsh:QH301-705.5 ,Protein Kinase C ,Regulation of gene expression ,Gene knockdown ,PKCS ,Long-term potentiation ,Fear ,Microtomy ,Rats ,Isoenzymes ,Memory, Short-Term ,030104 developmental biology ,Gene Expression Regulation ,lcsh:Biology (General) ,Molecular mechanism ,Neuroscience ,030217 neurology & neurosurgery ,Molecular Chaperones - Abstract
SummaryPKMζ has been proposed to be essential for maintenance of long-term potentiation (LTP) and long-term memory (LTM). However, recent data from PKMζ-knockout mice has called this role into question. Instead, the other atypical isoform, protein kinase C iota/lambda (PKCι/λ), has emerged as a potential alternative player. Therefore, the nature of the “memory molecule” maintaining learned information remains uncertain. Here, we report knockdown (KD) of PKCι/λ and PKMζ in the dorsal hippocampus and find deficits in early expression and late maintenance, respectively, during both LTP and hippocampus-dependent LTM. Sequential increases in the active form of PKCι/λ and PKMζ are detected during LTP or fear conditioning. Importantly, PKMζ, but not PKCι/λ, KD disrupts previously established LTM. Thus, PKCι/λ and PKMζ have distinct functions in LTP and memory, with PKMζ playing a specific role in memory maintenance. This relaying pattern may represent a precise molecular mechanism by which atypical PKCs regulate the different stages of memory.
- Full Text
- View/download PDF
16. Protein Kinase C Promotes N-Methyl-D-aspartate (NMDA) Receptor Trafficking by Indirectly Triggering Calcium/ Calmodulin-dependent Protein Kinase II (CaMKII) Autophosphorylation.
- Author
-
Jing-Zhi Yan, Zhuo Xu, Si-Qiang Ren, Bin Hu, Wen Yao, Shan-Hui Wang, Su-Yi Liu, and Wei Lu
- Subjects
- *
PROTEIN kinases , *PHOSPHORYLATION , *CELL membranes , *CALCIUM , *NEURAL transmission - Abstract
Regulation of neuronal NMDA receptor (NMDAR) is critical in synaptic transmission and plasticity. Protein kinase C (PKC) promotes NMDAR trafficking to the cell surface via interaction with NMDAR-associated proteins (NAPs). Little is known, however, about the NAPs that are critical to PKC-induced NMDAR trafficking. Here, we showed that calcium/calmodulin-dependent protein kinase II (CaMKII) could be a NAP that mediates the potentiation of NMDAR trafficking by PKC. PKC activation promoted the level of autophosphorylated CaMKII and increased association with NMDARs, accompanied by functional NMDAR insertion, at postsynaptic sites. This potentiation, along with PKC-induced long term potentiation of the AMPA receptor-mediated response, was abolished by CaMI(II antagonist or by disturbing the interaction between CaMI(II and NR2A or NR2B. Further mutual occlusion experiments demonstrated that PKC and CaMKII share a common signaling pathway in the potentiation of NMDAR trafficking and longterm potentiation (LTP) induction. Our results revealed that PKC promotes NMDA receptor trafficking and induces synaptic plasticity through indirectly triggering CaMKII autophosphorylation and subsequent increased association with NMDARs. [ABSTRACT FROM AUTHOR]
- Published
- 2011
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.