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Trpc3 cerebellum

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https://www.readbyqxmd.com/read/27904950/age-dependent-alpha-synuclein-accumulation-is-correlated-with-elevation-of-mitochondrial-trpc3-in-the-brains-of-monkeys-and-mice
#1
Min Chen, Jia Liu, Yongquan Lu, Chunli Duan, Lingling Lu, Ge Gao, Piu Chan, Shun Yu, Hui Yang
Aberrant α-synuclein (α-syn) accumulation has been shown to impair mitochondrial function by reducing mitochondrial membrane potential (MMP). However, the underlying mechanisms remain elusive. Transient receptor potential canonical (TRPC) channels are a diverse group of non-selective Ca(2+) channels, among which TRPC3 is the only one that is localized in mitochondria and plays a role in maintaining the normal MMP. This raises a possibility that altered TRPC3 expression may play a role in the mitochondrial dysfunction induced by α-syn accumulation...
November 30, 2016: Journal of Neural Transmission
https://www.readbyqxmd.com/read/25908616/the-mutant-moonwalker-trpc3-channel-links-calcium-signaling-to-lipid-metabolism-in-the-developing-cerebellum
#2
Anna Dulneva, Sheena Lee, Peter L Oliver, Katalin Di Gleria, Benedikt M Kessler, Kay E Davies, Esther B E Becker
The Moonwalker (Mwk) mouse is a model of dominantly inherited cerebellar ataxia caused by a gain-of-function mutation in the transient receptor potential (TRP) channel TRPC3. Here, we report impairments in dendritic growth and synapse formation early on during Purkinje cell development in the Mwk cerebellum that are accompanied by alterations in calcium signaling. To elucidate the molecular effector pathways that regulate Purkinje cell dendritic arborization downstream of mutant TRPC3, we employed transcriptomic analysis of developing Purkinje cells isolated by laser-capture microdissection...
July 15, 2015: Human Molecular Genetics
https://www.readbyqxmd.com/read/24811382/stim1-controls-neuronal-ca%C3%A2-%C3%A2-%C2%BA-signaling-mglur1-dependent-synaptic-transmission-and-cerebellar-motor-behavior
#3
Jana Hartmann, Rosa M Karl, Ryan P D Alexander, Helmuth Adelsberger, Monika S Brill, Charlotta Rühlmann, Anna Ansel, Kenji Sakimura, Yoshihiro Baba, Tomohiro Kurosaki, Thomas Misgeld, Arthur Konnerth
In central mammalian neurons, activation of metabotropic glutamate receptor type1 (mGluR1) evokes a complex synaptic response consisting of IP3 receptor-dependent Ca(2+) release from internal Ca(2+) stores and a slow depolarizing potential involving TRPC3 channels. It is largely unclear how mGluR1 is linked to its downstream effectors. Here, we explored the role of stromal interaction molecule 1 (STIM1) in regulating neuronal Ca(2+) signaling and mGluR1-dependent synaptic transmission. By analyzing mouse cerebellar Purkinje neurons, we demonstrate that STIM1 is an essential regulator of the Ca(2+) level in neuronal endoplasmic reticulum Ca(2+) stores...
May 7, 2014: Neuron
https://www.readbyqxmd.com/read/24336732/early-onset-of-ataxia-in-moonwalker-mice-is-accompanied-by-complete-ablation-of-type-ii-unipolar-brush-cells-and-purkinje-cell-dysfunction
#4
Gabriella Sekerková, Jin-Ah Kim, Maximiliano J Nigro, Esther B E Becker, Jana Hartmann, Lutz Birnbaumer, Enrico Mugnaini, Marco Martina
Transient receptor potential "canonical" cation channels (TRPC) are involved in many cellular activities, including neuronal synaptic transmission. These channels couple lipid metabolism, calcium homeostasis, and electrophysiological properties as they are calcium permeable and activated through the phospholipase C pathway and by diacylglycerol. The TRPC3 subunit is abundantly expressed in Purkinje cells (PCs), where it mediates slow metabotropic glutamate receptor-mediated synaptic responses. Recently, it has been shown that heterozygous moonwalker mice, which are a model of cerebellar ataxia, carry a dominant gain-of-function mutation (T635A) in the TRPC3 gene...
December 11, 2013: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/23408143/trpc3-channel-underlies-cerebellar-long-term-depression
#5
Sang Jeong Kim
Cerebellar long-term depression (LTD) is induced by repetitive pairing of both synaptic inputs provided by climbing fibers (CFs) and parallel fibers (PFs), especially when CF stimulation followed by burst of PFs. Metabotropic glutamate receptor type 1 (mGluR1)-dependent signaling in Purkinje cells is critically involved in the induction of cerebellar LTD. Signaling pathway of mGluR1 has two limbs: one is IP3 receptor-mediated Ca release from intracellular Ca store and the other is activation of transient receptor potential canonical (TRPC) channels...
June 2013: Cerebellum
https://www.readbyqxmd.com/read/23115168/glutamate-receptor-%C3%AE-2-associates-with-metabotropic-glutamate-receptor-1-mglur1-protein-kinase-c%C3%AE-and-canonical-transient-receptor-potential-3-and-regulates-mglur1-mediated-synaptic-transmission-in-cerebellar-purkinje-neurons
#6
Akihiko S Kato, Michael D Knierman, Edward R Siuda, John T R Isaac, Eric S Nisenbaum, David S Bredt
Cerebellar motor coordination and cerebellar Purkinje cell synaptic function require metabotropic glutamate receptor 1 (mGluR1, Grm1). We used an unbiased proteomic approach to identify protein partners for mGluR1 in cerebellum and discovered glutamate receptor δ2 (GluRδ2, Grid2, GluΔ2) and protein kinase Cγ (PKCγ) as major interactors. We also found canonical transient receptor potential 3 (TRPC3), which is also needed for mGluR1-dependent slow EPSCs and motor coordination and associates with mGluR1, GluRδ2, and PKCγ...
October 31, 2012: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/22895723/alternative-splicing-of-the-trpc3-ion-channel-calmodulin-ip3-receptor-binding-domain-in-the-hindbrain-enhances-cation-flux
#7
Youngsoo Kim, Ann Chi Yan Wong, John M Power, Sherif F Tadros, Matthias Klugmann, Andrew J Moorhouse, Paul P Bertrand, Gary D Housley
Canonical transient receptor potential (TRPC3) nonselective cation channels are effectors of G-protein-coupled receptors (GPCRs), activated via phospholipase C-diacylglycerol signaling. In cerebellar Purkinje cells, TRPC3 channels cause the metabotropic glutamate receptor (mGluR)-mediated slow EPSC (sEPSC). TRPC3 channels also provide negative feedback regulation of cytosolic Ca(2+), mediated by a C terminus "calmodulin and inositol trisphosphate receptor binding" (CIRB) domain. Here we report the alternative splicing of the TRPC3 mRNA transcript (designated TRPC3c), resulting in omission of exon 9 (approximately half of the CIRB domain) in mice, rats, and guinea pigs...
August 15, 2012: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/22207762/lack-of-kinase-regulation-of-canonical-transient-receptor-potential-3-trpc3-channel-dependent-currents-in-cerebellar-purkinje-cells
#8
Charmaine Nelson, Maike D Glitsch
Canonical transient receptor potential (TRPC) channels are widely expressed in the brain and play several roles in development and normal neuronal function. In the cerebellum, Purkinje cell TRPC3 channels underlie the slow excitatory postsynaptic potential observed after parallel fiber stimulation. In these cells TRPC3 channel opening requires stimulation of metabotropic glutamate receptor 1, activation of which can also lead to the induction of long term depression (LTD), which underlies cerebellar motor learning...
February 24, 2012: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/21976518/mutant-pkc%C3%AE-in-spinocerebellar-ataxia-type-14-disrupts-synapse-elimination-and-long-term-depression-in-purkinje-cells-in-vivo
#9
COMPARATIVE STUDY
Anton N Shuvaev, Hajime Horiuchi, Takahiro Seki, Hanna Goenawan, Tomohiko Irie, Akira Iizuka, Norio Sakai, Hirokazu Hirai
Cerebellar Purkinje cells (PCs) express a large amount of the γ isoform of protein kinase C (PKCγ) and a modest level of PKCα. The PKCγ is involved in the pruning of climbing fiber (CF) synapses from developing PCs, and PKCα plays a critical role in long-term depression (LTD) at parallel fiber (PF)-PC synapses. Moreover, the PKC signaling in PCs negatively modulates the nonselective transient receptor potential cation channel type 3 (TRPC3), the opening of which elicits slow EPSCs at PF-PC synapses. Autosomal dominant spinocerebellar ataxia type 14 (SCA14) is caused by mutations in PKCγ...
October 5, 2011: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/21558162/disruption-of-metabotropic-glutamate-receptor-signalling-is-a-major-defect-at-cerebellar-parallel-fibre-purkinje-cell-synapses-in-staggerer-mutant-mice
#10
COMPARATIVE STUDY
Kazuhiro Mitsumura, Nobutake Hosoi, Nobuhiko Furuya, Hirokazu Hirai
Staggerer mutant mice have functional loss of a transcription factor, retinoid-related orphan receptor α (RORα), which is abundantly expressed in Purkinje cells (PCs) of the cerebellum.Homozygous staggerer (sg/sg)mice show cerebellar hypoplasia and congenital ataxia. Sg/sg mice serve as an important extreme mouse model of the hereditary spinocerebellar ataxia type 1 (SCA1), since it has been shown that RORα dysfunction is strongly correlated with SCA1 pathogenesis. However, synaptic abnormalities, especially at parallel fibre (PF)-PC synapses, in SCA1-related sg/sg mice have not been examined in detail electrophysiologically...
July 1, 2011: Journal of Physiology
https://www.readbyqxmd.com/read/21441586/mglur1-trpc3-mediated-synaptic-transmission-and-calcium-signaling-in-mammalian-central-neurons
#11
REVIEW
Jana Hartmann, Horst A Henning, Arthur Konnerth
Metabotropic glutamate receptors type 1 (mGluR1s) are required for a normal function of the mammalian brain. They are particularly important for synaptic signaling and plasticity in the cerebellum. Unlike ionotropic glutamate receptors that mediate rapid synaptic transmission, mGluR1s produce in cerebellar Purkinje cells a complex postsynaptic response consisting of two distinct signal components, namely a local dendritic calcium signal and a slow excitatory postsynaptic potential. The basic mechanisms underlying these synaptic responses were clarified in recent years...
April 2011: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/21321808/candidate-screening-of-the-trpc3-gene-in-cerebellar-ataxia
#12
Esther B E Becker, Brent L Fogel, Sanjeev Rajakulendran, Anna Dulneva, Michael G Hanna, Susan L Perlman, Daniel H Geschwind, Kay E Davies
The hereditary cerebellar ataxias are a diverse group of neurodegenerative disorders primarily characterised by loss of balance and coordination due to dysfunction of the cerebellum and its associated pathways. Although many genetic mutations causing inherited cerebellar ataxia have been identified, a significant percentage of patients remain whose cause is unknown. The transient receptor potential (TRP) family member TRPC3 is a non-selective cation channel linked to key signalling pathways that are affected in cerebellar ataxia...
June 2011: Cerebellum
https://www.readbyqxmd.com/read/19741172/activation-of-native-trpc3-cation-channels-by-phospholipase-d
#13
Maike D Glitsch
In the mammalian nervous system, stimulation of G-protein-coupled type I glutamate receptors triggers various forms of neuronal plasticity, including cerebellar long-term depression and hippocampal long-term potentiation. Activation of these receptors in the cerebellum also leads to a slow excitatory postsynaptic current mediated by nonselective TRPC3 cation channels. How TRPC3 channels are opened is unknown, although it is widely thought that channel gating requires phospholipase C activation. Using the patch-clamp technique and immunohistochemistry in rat cerebellar slices, we show that metabotropic glutamate receptors activate TRPC3 channels through the small GTP-binding protein Rho and subsequent phospholipase D stimulation...
January 2010: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/19351902/a-point-mutation-in-trpc3-causes-abnormal-purkinje-cell-development-and-cerebellar-ataxia-in-moonwalker-mice
#14
Esther B E Becker, Peter L Oliver, Maike D Glitsch, Gareth T Banks, Francesca Achilli, Andrea Hardy, Patrick M Nolan, Elizabeth M C Fisher, Kay E Davies
The hereditary ataxias are a complex group of neurological disorders characterized by the degeneration of the cerebellum and its associated connections. The molecular mechanisms that trigger the loss of Purkinje cells in this group of diseases remain incompletely understood. Here, we report a previously undescribed dominant mouse model of cerebellar ataxia, moonwalker (Mwk), that displays motor and coordination defects and loss of cerebellar Purkinje cells. Mwk mice harbor a gain-of-function mutation (T635A) in the Trpc3 gene encoding the nonselective transient receptor potential cation channel, type C3 (TRPC3), resulting in altered TRPC3 channel gating...
April 21, 2009: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/19168035/trpc3-protein-is-expressed-across-the-lifespan-in-human-prefrontal-cortex-and-cerebellum
#15
Angela S Roedding, Andrew F Gao, Alex M L Wu, Peter P Li, Stephen J Kish, Jerry J Warsh
The canonical transient receptor potential type 3 (TRPC3) channel is a non-selective, voltage-independent cation channel that is expressed in both excitable and non-excitable cells. As little is known regarding its presence in human brain and the influence of age on its expression, we examined TRPC3 protein expression by immunoblotting in postmortem prefrontal cortex and cerebellum obtained from subjects (8 days to 83 years) with no history of psychiatric or neurological disorder. The expression of TRPC3 protein in the prefrontal cortex (Brodmann area A9/A10) of the neonates/infants (<2 y) was significantly higher (25%) than that in the adolescent to adult (11y-83y) age group, whereas cerebellar TRPC3 levels showed no age-related changes...
March 13, 2009: Brain Research
https://www.readbyqxmd.com/read/18983450/mechanisms-of-metabotropic-glutamate-receptor-mediated-synaptic-signaling-in-cerebellar-purkinje-cells
#16
Jana Hartmann, Arthur Konnerth
The metabotropic glutamate receptors type 1 (mGluR1s) are required for a normal function of the mammalian cerebellum. These G-protein coupled receptors are abundantly expressed in the principle cerebellar cells, namely the Purkinje neurons. Under physiological conditions, mGluR1s are activated during repetitive activity of both afferent glutamatergic synaptic inputs provided by the climbing and parallel fibers, respectively. Unlike the common ionotropic glutamate receptors that underlie rapid synaptic excitation, mGluR1s produce a complex postsynaptic response consisting of a Ca(2+) release signal from intracellular stores and a slow excitatory postsynaptic potential...
October 28, 2008: Acta Physiologica
https://www.readbyqxmd.com/read/18701065/trpc3-channels-are-required-for-synaptic-transmission-and-motor-coordination
#17
Jana Hartmann, Elena Dragicevic, Helmuth Adelsberger, Horst A Henning, Martin Sumser, Joel Abramowitz, Robert Blum, Alexander Dietrich, Marc Freichel, Veit Flockerzi, Lutz Birnbaumer, Arthur Konnerth
In the mammalian central nervous system, slow synaptic excitation involves the activation of metabotropic glutamate receptors (mGluRs). It has been proposed that C1-type transient receptor potential (TRPC1) channels underlie this synaptic excitation, but our analysis of TRPC1-deficient mice does not support this hypothesis. Here, we show unambiguously that it is TRPC3 that is needed for mGluR-dependent synaptic signaling in mouse cerebellar Purkinje cells. TRPC3 is the most abundantly expressed TRPC subunit in Purkinje cells...
August 14, 2008: Neuron
https://www.readbyqxmd.com/read/17396124/trpc-channels-promote-cerebellar-granule-neuron-survival
#18
Yichang Jia, Jian Zhou, Yilin Tai, Yizheng Wang
Channels formed by the transient receptor potential (TRP) family of proteins have a variety of physiological functions. Here we report that two members of the TRP cation channel (TRPC) subfamily, TRPC3 and 6, protected cerebellar granule neurons (CGNs) against serum deprivation-induced cell death in cultures and promoted CGN survival in rat brain. In CGN cultures, blocking TRPC channels or downregulating TRPC3 or 6 suppressed brain-derived neurotrophic factor (BDNF)-mediated protection, BDNF-triggered intracellular Ca2+ elevation and BDNF-induced CREB activation...
May 2007: Nature Neuroscience
https://www.readbyqxmd.com/read/17141310/changes-in-trpc-channel-expression-during-postnatal-development-of-cerebellar-neurons
#19
W-C Huang, J S Young, M D Glitsch
In the brain, classical (canonical) transient receptor potential (TRPC) channels are thought to be involved in different aspects of neuronal development. We investigated the developmental expression profile of TRPC channels in rat cerebellum during the first 6 weeks after birth. TRPC3 expression is significantly up-regulated whereas TRPC4 and TRPC6 expression are significantly down-regulated over this period of time. TRPC3 expression is mainly found on Purkinje cells and their dendrites, suggesting that the increase in TRPC3 expression reflects development of the dendritic tree of Purkinje cells...
July 2007: Cell Calcium
https://www.readbyqxmd.com/read/15758952/essential-role-of-trpc-channels-in-the-guidance-of-nerve-growth-cones-by-brain-derived-neurotrophic-factor
#20
Yan Li, Yi-Chang Jia, Kai Cui, Ning Li, Zai-Yu Zheng, Yi-Zheng Wang, Xiao-Bing Yuan
Brain-derived neurotrophic factor (BDNF) is known to promote neuronal survival and differentiation and to guide axon extension both in vitro and in vivo. The BDNF-induced chemo-attraction of axonal growth cones requires Ca2+ signalling, but how Ca2+ is regulated by BDNF at the growth cone remains largely unclear. Extracellular application of BDNF triggers membrane currents resembling those through TRPC (transient receptor potential canonical) channels in rat pontine neurons and in Xenopus spinal neurons. Here, we report that in cultured cerebellar granule cells, TRPC channels contribute to the BDNF-induced elevation of Ca2+ at the growth cone and are required for BDNF-induced chemo-attractive turning...
April 14, 2005: Nature
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