keyword
https://read.qxmd.com/read/36135748/stimulation-of-neurite-outgrowth-in-cerebrocortical-neurons-by-sodium-channel-activator-brevetoxin-2-requires-both-n-methyl-d-aspartate-receptor-2b-glun2b-and-p21-protein-cdc42-rac-activated-kinase-1-pak1
#1
JOURNAL ARTICLE
Suneet Mehrotra, Marsha L Pierce, Shashank M Dravid, Thomas F Murray
N-methyl-D-aspartate (NMDA) receptors play a critical role in activity-dependent dendritic arborization, spinogenesis, and synapse formation by stimulating calcium-dependent signaling pathways. Previously, we have shown that brevetoxin 2 (PbTx-2), a voltage-gated sodium channel (VGSC) activator, produces a concentration-dependent increase in intracellular sodium [Na+ ]I and increases NMDA receptor (NMDAR) open probabilities and NMDA-induced calcium (Ca2+ ) influxes. The objective of this study is to elucidate the downstream signaling mechanisms by which the sodium channel activator PbTx-2 influences neuronal morphology in murine cerebrocortical neurons...
August 31, 2022: Marine Drugs
https://read.qxmd.com/read/35831873/transient-neuroinflammation-following-surgery-contributes-to-long-lasting-cognitive-decline-in-elderly-rats-via-dysfunction-of-synaptic-nmda-receptor
#2
JOURNAL ARTICLE
Bo Chen, Guangcheng Qin, Jingyu Xiao, Xiaoyuan Deng, Aolei Lin, Hongliang Liu
BACKGROUND: Perioperative neurocognitive disorders (PNDs) are considered the most common postoperative complication in geriatric patients. However, its pathogenesis is not fully understood. Surgery-triggered neuroinflammation is a major contributor to the development of PNDs. Neuroinflammation can influence N-methyl-D-aspartate receptor (NMDAR) expression or function which is closely associated with cognition. We, therefore, hypothesized that the persistent changes in NMDAR expression or function induced by transient neuroinflammation after surgery were involved in the development of PNDs...
July 13, 2022: Journal of Neuroinflammation
https://read.qxmd.com/read/34161760/bmpr-2-gates-activity-dependent-stabilization-of-primary-dendrites-during-mitral-cell-remodeling
#3
JOURNAL ARTICLE
Shuhei Aihara, Satoshi Fujimoto, Richi Sakaguchi, Takeshi Imai
Developing neurons initially form excessive neurites and then remodel them based on molecular cues and neuronal activity. Developing mitral cells in the olfactory bulb initially extend multiple primary dendrites. They then stabilize single primary dendrites while eliminating others. However, the mechanisms underlying selective dendrite remodeling remain elusive. Using CRISPR-Cas9-based knockout screening combined with in utero electroporation, we identify BMPR-2 as a key regulator for selective dendrite stabilization...
June 22, 2021: Cell Reports
https://read.qxmd.com/read/32321746/molecular-mechanisms-of-non-ionotropic-nmda-receptor-signaling-in-dendritic-spine-shrinkage
#4
JOURNAL ARTICLE
Ivar S Stein, Deborah K Park, Juan C Flores, Jennifer N Jahncke, Karen Zito
Structural plasticity of dendritic spines is a key component of the refinement of synaptic connections during learning. Recent studies highlight a novel role for the NMDA receptor (NMDAR), independent of ion flow, in driving spine shrinkage and LTD. Yet little is known about the molecular mechanisms that link conformational changes in the NMDAR to changes in spine size and synaptic strength. Here, using two-photon glutamate uncaging to induce plasticity at individual dendritic spines on hippocampal CA1 neurons from mice and rats of both sexes, we demonstrate that p38 MAPK is generally required downstream of non-ionotropic NMDAR signaling to drive both spine shrinkage and LTD...
May 6, 2020: Journal of Neuroscience
https://read.qxmd.com/read/30953439/fmrp-modulates-activity-dependent-spine-plasticity-by-binding-cofilin1-mrna-and-regulating-localization-and-local-translation
#5
JOURNAL ARTICLE
Jonas Feuge, Franziska Scharkowski, Kristin Michaelsen-Preusse, Martin Korte
Multiple variants of intellectual disability, e.g., the Fragile X Syndrome are associated with alterations in dendritic spine morphology, thereby pointing to dysregulated actin dynamics during development and processes of synaptic plasticity. Surprisingly, although the necessity of spine actin remodeling was demonstrated repeatedly, the importance and precise role of actin regulators is often undervalued. Here, we provide evidence that structural and functional plasticity are severely impaired after NMDAR-dependent LTP in the hippocampus of Fmr1 KO mice...
April 6, 2019: Cerebral Cortex
https://read.qxmd.com/read/30483111/hippocampal-long-term-depression-in-the-presence-of-calcium-permeable-ampa-receptors
#6
JOURNAL ARTICLE
Feng Cao, Zikai Zhou, Sammy Cai, Wei Xie, Zhengping Jia
The GluA2 subunit of AMPA glutamate receptors (AMPARs) has been shown to be critical for the expression of NMDA receptor (NMDAR)-dependent long-term depression (LTD). However, in young GluA2 knockout (KO) mice, this form of LTD can still be induced in the hippocampus, suggesting that LTD mechanisms may be modified in the presence of GluA2-lacking, Ca2+ permeable AMPARs. In this study, we examined LTD at the CA1 synapse in GluA2 KO mice by using several well-established inhibitory peptides known to block LTD in wild type (WT) rodents...
2018: Frontiers in Synaptic Neuroscience
https://read.qxmd.com/read/28993724/plpp-cin-regulates-seizure-activity-by-the-differential-modulation-of-calsenilin-binding-to-glun1-and-kv4-2-in-mice
#7
JOURNAL ARTICLE
Ji-Eun Kim, Hye-Won Hyun, Su-Ji Min, Duk-Shin Lee, A Ran Jeon, Min Ju Kim, Tae-Cheon Kang
Calsenilin (CSEN) binds to Kv4.2 (an A-type K(+) channel) as well as N-methyl-D-aspartate receptor (NMDAR), and modulates their activities. However, the regulatory mechanisms for CSEN-binding to Kv4.2 or NMDAR remain elusive. Here, we demonstrate the novel role of pyridoxal-5'-phosphate phosphatase/chronophin (PLPP/CIN), one of the cofilin-mediated F-actin regulators, in the CSEN binding to Kv4.2 or GluN1 (an NMDAR subunit). PLPP/CIN dephosphorylated CSEN in competition with casein kinase 1, independent of cofilin dephosphorylation...
2017: Frontiers in Molecular Neuroscience
https://read.qxmd.com/read/28973019/beta-arrestin-1-regulation-of-reward-motivated-behaviors-and-glutamatergic-function
#8
JOURNAL ARTICLE
Nitish Mittal, Ani Minasyan, Nicole Romaneschi, Joshua K Hakimian, Gabriel Gonzalez-Fernandez, Ralph Albert, Nina Desai, Ian A Mendez, Timothy Schallert, Sean B Ostlund, Wendy Walwyn
The two highly homologous non-visual arrestins, beta-arrestin 1 and 2, are ubiquitously expressed in the central nervous system, yet knowledge of their disparate roles is limited. While beta-arrestin 2 (βarr2) has been implicated in several aspects of reward-related learning and behavior, very little is known about the behavioral function of beta-arrestin 1 (βarr1). Using mice lacking βarr1, we focused on the role of this scaffolding and signal transduction protein in reward-motivated behaviors and in striatal glutamatergic function...
2017: PloS One
https://read.qxmd.com/read/27372643/partial-amelioration-of-synaptic-and-cognitive-deficits-by-inhibiting-cofilin-dephosphorylation-in-an-animal-model-of-alzheimer-s-disease
#9
JOURNAL ARTICLE
Yulei Deng, Jing Wei, Jia Cheng, Ping Zhong, Zhe Xiong, Aiyi Liu, Lin Lin, Shengdi Chen, Zhen Yan
The loss of synaptic structure and function has been linked to the cognitive impairment of Alzheimer's disease (AD). Dysregulation of the actin cytoskeleton, which plays a key role in regulating the integrity of synapses and the transport of synaptic proteins, has been suggested to contribute to the pathology of AD. In this study, we found that glutamate receptor surface expression and synaptic function in frontal cortical neurons were significant diminished in a familial AD (FAD) model, which was correlated with the reduction of phosphorylated cofilin, a key protein regulating the dynamics of actin filaments...
June 28, 2016: Journal of Alzheimer's Disease: JAD
https://read.qxmd.com/read/26027926/autism-like-deficits-in-shank3-deficient-mice-are-rescued-by-targeting-actin-regulators
#10
JOURNAL ARTICLE
Lara J Duffney, Ping Zhong, Jing Wei, Emmanuel Matas, Jia Cheng, Luye Qin, Kaijie Ma, David M Dietz, Yuji Kajiwara, Joseph D Buxbaum, Zhen Yan
Haploinsufficiency of the Shank3 gene, which encodes a scaffolding protein at glutamatergic synapses, is a highly prevalent and penetrant risk factor for autism. Using combined behavioral, electrophysiological, biochemical, imaging, and molecular approaches, we find that Shank3-deficient mice exhibit autism-like social deficits and repetitive behaviors, as well as the significantly diminished NMDA receptor (NMDAR) synaptic function and synaptic distribution in prefrontal cortex. Concomitantly, Shank3-deficient mice have a marked loss of cortical actin filaments, which is associated with the reduced Rac1/PAK activity and increased activity of cofilin, the major actin depolymerizing factor...
June 9, 2015: Cell Reports
https://read.qxmd.com/read/25721396/essential-role-of-glud1-in-dendritic-spine-development-and-glun2b-to-glun2a-nmdar-subunit-switch-in-the-cortex-and-hippocampus-reveals-ability-of-glun2b-inhibition-in-correcting-hyperconnectivity
#11
JOURNAL ARTICLE
Subhash C Gupta, Roopali Yadav, Ratnamala Pavuluri, Barbara J Morley, Dustin J Stairs, Shashank M Dravid
The glutamate delta-1 (GluD1) receptor is highly expressed in the forebrain. We have previously shown that loss of GluD1 leads to social and cognitive deficits in mice, however, its role in synaptic development and neurotransmission remains poorly understood. Here we report that GluD1 is enriched in the medial prefrontal cortex (mPFC) and GluD1 knockout mice exhibit a higher dendritic spine number, greater excitatory neurotransmission as well as higher number of synapses in mPFC. In addition abnormalities in the LIMK1-cofilin signaling, which regulates spine dynamics, and a lower ratio of GluN2A/GluN2B expression was observed in the mPFC in GluD1 knockout mice...
June 2015: Neuropharmacology
https://read.qxmd.com/read/25394486/oligomeric-a%C3%AE-induced-synaptic-dysfunction-in-alzheimer-s-disease
#12
REVIEW
Shichun Tu, Shu-ichi Okamoto, Stuart A Lipton, Huaxi Xu
Alzheimer's disease (AD) is a devastating disease characterized by synaptic and neuronal loss in the elderly. Compelling evidence suggests that soluble amyloid-β peptide (Aβ) oligomers induce synaptic loss in AD. Aβ-induced synaptic dysfunction is dependent on overstimulation of N-methyl-D-aspartate receptors (NMDARs) resulting in aberrant activation of redox-mediated events as well as elevation of cytoplasmic Ca2+, which in turn triggers downstream pathways involving phospho-tau (p-tau), caspases, Cdk5/dynamin-related protein 1 (Drp1), calcineurin/PP2B, PP2A, Gsk-3β, Fyn, cofilin, and CaMKII and causes endocytosis of AMPA receptors (AMPARs) as well as NMDARs...
November 14, 2014: Molecular Neurodegeneration
https://read.qxmd.com/read/25297090/a%C3%AE-selectively-impairs-mglur7-modulation-of-nmda-signaling-in-basal-forebrain-cholinergic-neurons-implication-in-alzheimer-s-disease
#13
JOURNAL ARTICLE
Zhenglin Gu, Jia Cheng, Ping Zhong, Luye Qin, Wenhua Liu, Zhen Yan
Degeneration of basal forebrain (BF) cholinergic neurons is one of the early pathological events in Alzheimer's disease (AD) and is thought to be responsible for the cholinergic and cognitive deficits in AD. The functions of this group of neurons are highly influenced by glutamatergic inputs from neocortex. We found that activation of metabotropic glutamate receptor 7 (mGluR7) decreased NMDAR-mediated currents and NR1 surface expression in rodent BF neurons via a mechanism involving cofilin-regulated actin dynamics...
October 8, 2014: Journal of Neuroscience
https://read.qxmd.com/read/24089484/shank3-deficiency-induces-nmda-receptor-hypofunction-via-an-actin-dependent-mechanism
#14
JOURNAL ARTICLE
Lara J Duffney, Jing Wei, Jia Cheng, Wenhua Liu, Katharine R Smith, Josef T Kittler, Zhen Yan
Shank3, which encodes a scaffolding protein at glutamatergic synapses, is a genetic risk factor for autism. In this study, we examined the impact of Shank3 deficiency on the NMDA-type glutamate receptor, a key player in cognition and mental illnesses. We found that knockdown of Shank3 with a small interfering RNA (siRNA) caused a significant reduction of NMDAR-mediated ionic or synaptic current, as well as the surface expression of NR1 subunits, in rat cortical cultures. The effect of Shank3 siRNA on NMDAR currents was blocked by an actin stabilizer, and was occluded by an actin destabilizer, suggesting the involvement of actin cytoskeleton...
October 2, 2013: Journal of Neuroscience
https://read.qxmd.com/read/23765104/spin90-dephosphorylation-is-required-for-cofilin-mediated-actin-depolymerization-in-nmda-stimulated-hippocampal-neurons
#15
JOURNAL ARTICLE
In Ha Cho, Min Jung Lee, Dae Hwan Kim, Bora Kim, Jeomil Bae, Kyu Yeong Choi, Seon-Myung Kim, Yun Hyun Huh, Kun Ho Lee, Chong-Hyun Kim, Woo Keun Song
Actin plays a fundamental role in the regulation of spine morphology (both shrinkage and enlargement) upon synaptic activation. In particular, actin depolymerization is crucial for the spine shrinkage in NMDAR-mediated synaptic depression. Here, we define the role of SPIN90 phosphorylation/dephosphorylation in regulating actin depolymerization via modulation of cofilin activity. When neurons were treated with NMDA, SPIN90 was dephosphorylated by STEP61 (striatal-enriched protein tyrosine phosphatase) and translocated from the spines to the dendritic shafts...
November 2013: Cellular and Molecular Life Sciences: CMLS
https://read.qxmd.com/read/23153583/molecular-mechanisms-coordinating-functional-and-morphological-plasticity-at-the-synapse-role-of-glua2-n-cadherin-interaction-mediated-actin-signaling-in-mglur-dependent-ltd
#16
REVIEW
Suhail Asrar, Zhengping Jia
Long-lasting synaptic plasticity involves changes in both synaptic morphology and electrical signaling (here referred to as structural and functional plasticity). Recent studies have revealed a myriad of molecules and signaling processes that are critical for each of these two forms of plasticity, but whether and how they are mechanistically linked to achieve coordinated changes remain controversial. It is well accepted that functional plasticity at the excitatory synapse is dependent upon the activities of glutamate receptors...
February 2013: Cellular Signalling
https://read.qxmd.com/read/22308427/cofilin-under-control-of-%C3%AE-arrestin-2-in-nmda-dependent-dendritic-spine-plasticity-long-term-depression-ltd-and-learning
#17
JOURNAL ARTICLE
Crystal G Pontrello, Min-Yu Sun, Alice Lin, Todd A Fiacco, Kathryn A DeFea, Iryna M Ethell
Dendritic spines are dynamic, actin-rich structures that form the postsynaptic sites of most excitatory synapses in the brain. The F-actin severing protein cofilin has been implicated in the remodeling of dendritic spines and synapses under normal and pathological conditions, by yet unknown mechanisms. Here we report that β-arrestin-2 plays an important role in NMDA-induced remodeling of dendritic spines and synapses via translocation of active cofilin to dendritic spines. NMDAR activation triggers cofilin activation through calcineurin and phosphatidylinositol 3-kinase (PI3K)-mediated dephosphorylation and promotes cofilin translocation to dendritic spines that is mediated by β-arrestin-2...
February 14, 2012: Proceedings of the National Academy of Sciences of the United States of America
https://read.qxmd.com/read/22287544/regulation-of-n-methyl-d-aspartic-acid-nmda-receptors-by-metabotropic-glutamate-receptor-7
#18
JOURNAL ARTICLE
Zhenglin Gu, Wenhua Liu, Jing Wei, Zhen Yan
Emerging evidence suggests that metabotropic glutamate receptors (mGluRs) are potential novel targets for brain disorders associated with the dysfunction of prefrontal cortex (PFC), a region critical for cognitive and emotional processes. Because N-methyl-D-aspartic acid receptor (NMDAR) dysregulation has been strongly associated with the pathophysiology of mental illnesses, we examined the possibility that mGluRs might be involved in modulating PFC functions by targeting postsynaptic NMDARs. We found that application of prototypical group III mGluR agonists significantly reduced NMDAR-mediated synaptic and ionic currents in PFC pyramidal neurons, which was mediated by mGluR7 localized at postsynaptic neurons and involved the β-arrestin/ERK signaling pathway...
March 23, 2012: Journal of Biological Chemistry
https://read.qxmd.com/read/19770351/phosphatidylinositol-4-5-bisphosphate-regulation-of-n-methyl-d-aspartate-receptor-channels-in-cortical-neurons
#19
JOURNAL ARTICLE
Madhuchhanda Mandal, Zhen Yan
The membrane phospholipid phosphatidylinositol (4,5)-bisphosphate (PIP(2)) has been implicated in the regulation of several ion channels and transporters. In this study, we examined the impact of PIP(2) on N-methyl-D-aspartate receptors (NMDARs) in cortical neurons. Blocking PIP(2) synthesis by inhibiting phosphoinositide-4 kinase, or stimulating PIP(2) hydrolysis via activation of phospholipase C (PLC), or blocking PIP(2) function with an antibody caused a significant reduction of NMDAR-mediated currents. On the other hand, inhibition of PLC or application of PIP(2) caused an enhancement of NMDAR currents...
December 2009: Molecular Pharmacology
https://read.qxmd.com/read/17360908/natural-oligomers-of-the-alzheimer-amyloid-beta-protein-induce-reversible-synapse-loss-by-modulating-an-nmda-type-glutamate-receptor-dependent-signaling-pathway
#20
COMPARATIVE STUDY
Ganesh M Shankar, Brenda L Bloodgood, Matthew Townsend, Dominic M Walsh, Dennis J Selkoe, Bernardo L Sabatini
Alzheimer's disease (AD) is characterized by decreased synapse density in hippocampus and neocortex, and synapse loss is the strongest anatomical correlate of the degree of clinical impairment. Although considerable evidence supports a causal role for the amyloid-beta protein (Abeta) in AD, a direct link between a specific form of Abeta and synapse loss has not been established. We demonstrate that physiological concentrations of naturally secreted Abeta dimers and trimers, but not monomers, induce progressive loss of hippocampal synapses...
March 14, 2007: Journal of Neuroscience
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