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Article ; Online: Synapse pathology in psychiatric and neurologic disease.

van Spronsen, Myrrhe / Hoogenraad, Casper C

Current neurology and neuroscience reports

2010 Volume 10, Issue 3, Page(s) 207–214

Abstract: Inhibitory and excitatory synapses play a fundamental role in information processing in the brain. Excitatory synapses usually are situated on dendritic spines, small membrane protrusions that harbor glutamate receptors and postsynaptic density ... ...

Abstract	Inhibitory and excitatory synapses play a fundamental role in information processing in the brain. Excitatory synapses usually are situated on dendritic spines, small membrane protrusions that harbor glutamate receptors and postsynaptic density components and help transmit electrical signals. In recent years, it has become evident that spine morphology is intimately linked to synapse function--smaller spines have smaller synapses and support reduced synaptic transmission. The relationship between synaptic signaling, spine shape, and brain function is never more apparent than when the brain becomes dysfunctional. Many psychiatric and neurologic disorders, ranging from mental retardation and autism to Alzheimer's disease and addiction, are accompanied by alterations in spine morphology and synapse number. In this review, we highlight the structure and molecular organization of synapses and discuss functional effects of synapse pathology in brain disease.
MeSH term(s)	Dendritic Spines/pathology ; Dendritic Spines/ultrastructure ; Humans ; Mental Disorders/pathology ; Models, Biological ; Nervous System Diseases/pathology ; Neuronal Plasticity/physiology ; Neurons/pathology ; Neurons/ultrastructure ; Synapses/pathology
Language	English
Publishing date	2010-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2057363-7
ISSN	1534-6293 ; 1528-4042
ISSN (online)	1534-6293
ISSN	1528-4042
DOI	10.1007/s11910-010-0104-8
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Zs.A 5549: Show issues

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Article ; Online: Kinesin-Binding Protein Controls Microtubule Dynamics and Cargo Trafficking by Regulating Kinesin Motor Activity.

Kevenaar, Josta T / Bianchi, Sarah / van Spronsen, Myrrhe / Olieric, Natacha / Lipka, Joanna / Frias, Cátia P / Mikhaylova, Marina / Harterink, Martin / Keijzer, Nanda / Wulf, Phebe S / Hilbert, Manuel / Kapitein, Lukas C / de Graaff, Esther / Ahkmanova, Anna / Steinmetz, Michel O / Hoogenraad, Casper C

Current biology : CB

2016 Volume 26, Issue 7, Page(s) 849–861

Abstract: Kinesin motor proteins play a fundamental role for normal neuronal development by controlling intracellular cargo transport and microtubule (MT) cytoskeleton organization. Regulating kinesin activity is important to ensure their proper functioning, and ... ...

Abstract	Kinesin motor proteins play a fundamental role for normal neuronal development by controlling intracellular cargo transport and microtubule (MT) cytoskeleton organization. Regulating kinesin activity is important to ensure their proper functioning, and their misregulation often leads to severe human neurological disorders. Homozygous nonsense mutations in kinesin-binding protein (KBP)/KIAA1279 cause the neurological disorder Goldberg-Shprintzen syndrome (GOSHS), which is characterized by intellectual disability, microcephaly, and axonal neuropathy. Here, we show that KBP regulates kinesin activity by interacting with the motor domains of a specific subset of kinesins to prevent their association with the MT cytoskeleton. The KBP-interacting kinesins include cargo-transporting motors such as kinesin-3/KIF1A and MT-depolymerizing motor kinesin-8/KIF18A. We found that KBP blocks KIF1A/UNC-104-mediated synaptic vesicle transport in cultured hippocampal neurons and in C. elegans PVD sensory neurons. In contrast, depletion of KBP results in the accumulation of KIF1A motors and synaptic vesicles in the axonal growth cone. We also show that KBP regulates neuronal MT dynamics by controlling KIF18A activity. Our data suggest that KBP functions as a kinesin inhibitor that modulates MT-based cargo motility and depolymerizing activity of a subset of kinesin motors. We propose that misregulation of KBP-controlled kinesin motors may represent the underlying molecular mechanism that contributes to the neuropathological defects observed in GOSHS patients.
MeSH term(s)	Animals ; Caenorhabditis elegans/metabolism ; Carrier Proteins/metabolism ; Craniofacial Abnormalities/metabolism ; Hirschsprung Disease/metabolism ; Kinesin/chemistry ; Kinesin/metabolism ; Mice ; Microtubules/metabolism ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Synaptic Vesicles/metabolism
Chemical Substances	Carrier Proteins ; KBP protein, mouse ; KIF1A protein, human ; KIFBP protein, human ; Nerve Tissue Proteins ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2016-03-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2016.01.048
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Zs.A 3208: Show issues

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Article ; Online: Mixed microtubules steer dynein-driven cargo transport into dendrites.

Kapitein, Lukas C / Schlager, Max A / Kuijpers, Marijn / Wulf, Phebe S / van Spronsen, Myrrhe / MacKintosh, Frederick C / Hoogenraad, Casper C

Current biology : CB

2010 Volume 20, Issue 4, Page(s) 290–299

Abstract: Background: To establish and maintain their polarized morphology, neurons employ active transport driven by molecular motors to sort cargo between axons and dendrites. However, the basic traffic rules governing polarized transport on neuronal ... ...

Abstract	Background: To establish and maintain their polarized morphology, neurons employ active transport driven by molecular motors to sort cargo between axons and dendrites. However, the basic traffic rules governing polarized transport on neuronal microtubule arrays are unclear. Results: Here we show that the microtubule minus-end-directed motor dynein is required for the polarized targeting of dendrite-specific cargo, such as AMPA receptors. To directly examine how dynein motors contribute to polarized dendritic transport, we established a trafficking assay in hippocampal neurons to selectively probe specific motor protein activity. This revealed that, unlike kinesins, dynein motors drive cargo selectively into dendrites, governed by their mixed microtubule array. Moreover, axon-specific cargos, such as presynaptic vesicle protein synaptophysin, are redirected to dendrites by coupling to dynein motors. Quantitative modeling demonstrated that bidirectional dynein-driven transport on mixed microtubules provides an efficient mechanism to establish a stable density of continuously renewing vesicles in dendrites. Conclusions: These results demonstrate a powerful approach to study specific motor protein activity inside living cells and imply a key role for dynein in dendritic transport. We propose that dynein establishes the initial sorting of dendritic cargo and additional motor proteins assist in subsequent delivery.
MeSH term(s)	Animals ; Biological Transport, Active/physiology ; COS Cells ; Cercopithecus aethiops ; Dendrites/metabolism ; Dyneins/metabolism ; Hippocampus/cytology ; Immunohistochemistry ; Kinesin/metabolism ; Microtubules/metabolism ; Models, Biological ; Peroxisomes/metabolism ; Receptors, AMPA/metabolism ; Synaptophysin/metabolism
Chemical Substances	Receptors, AMPA ; Synaptophysin ; Dyneins (EC 3.6.4.2) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2010-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2009.12.052
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Zs.A 3208: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Developmental and activity-dependent miRNA expression profiling in primary hippocampal neuron cultures.

van Spronsen, Myrrhe / van Battum, Eljo Y / Kuijpers, Marijn / Vangoor, Vamshidhar R / Rietman, M Liset / Pothof, Joris / Gumy, Laura F / van Ijcken, Wilfred F J / Akhmanova, Anna / Pasterkamp, R Jeroen / Hoogenraad, Casper C

PloS one

2013 Volume 8, Issue 10, Page(s) e74907

Abstract: MicroRNAs (miRNAs) are evolutionarily conserved non-coding RNAs of ∼22 nucleotides that regulate gene expression at the level of translation and play vital roles in hippocampal neuron development, function and plasticity. Here, we performed a systematic ... ...

Abstract	MicroRNAs (miRNAs) are evolutionarily conserved non-coding RNAs of ∼22 nucleotides that regulate gene expression at the level of translation and play vital roles in hippocampal neuron development, function and plasticity. Here, we performed a systematic and in-depth analysis of miRNA expression profiles in cultured hippocampal neurons during development and after induction of neuronal activity. MiRNA profiling of primary hippocampal cultures was carried out using locked nucleic-acid-based miRNA arrays. The expression of 264 different miRNAs was tested in young neurons, at various developmental stages (stage 2-4) and in mature fully differentiated neurons (stage 5) following the induction of neuronal activity using chemical stimulation protocols. We identified 210 miRNAs in mature hippocampal neurons; the expression of most neuronal miRNAs is low at early stages of development and steadily increases during neuronal differentiation. We found a specific subset of 14 miRNAs with reduced expression at stage 3 and showed that sustained expression of these miRNAs stimulates axonal outgrowth. Expression profiling following induction of neuronal activity demonstrates that 51 miRNAs, including miR-134, miR-146, miR-181, miR-185, miR-191 and miR-200a show altered patterns of expression after NMDA receptor-dependent plasticity, and 31 miRNAs, including miR-107, miR-134, miR-470 and miR-546 were upregulated by homeostatic plasticity protocols. Our results indicate that specific miRNA expression profiles correlate with changes in neuronal development and neuronal activity. Identification and characterization of miRNA targets may further elucidate translational control mechanisms involved in hippocampal development, differentiation and activity-depended processes.
MeSH term(s)	Animals ; Axons/metabolism ; Cell Differentiation ; Cells, Cultured ; Gene Expression Profiling ; Gene Regulatory Networks ; Hippocampus/cytology ; Hippocampus/growth & development ; MicroRNAs/genetics ; Neuronal Plasticity ; Neurons/cytology ; Neurons/metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism
Chemical Substances	MicroRNAs ; Receptors, N-Methyl-D-Aspartate
Language	English
Publishing date	2013-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0074907
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Article ; Online: TRAK/Milton motor-adaptor proteins steer mitochondrial trafficking to axons and dendrites.

van Spronsen, Myrrhe / Mikhaylova, Marina / Lipka, Joanna / Schlager, Max A / van den Heuvel, Dave J / Kuijpers, Marijn / Wulf, Phebe S / Keijzer, Nanda / Demmers, Jeroen / Kapitein, Lukas C / Jaarsma, Dick / Gerritsen, Hans C / Akhmanova, Anna / Hoogenraad, Casper C

Neuron

2013 Volume 77, Issue 3, Page(s) 485–502

Abstract: In neurons, the distinct molecular composition of axons and dendrites is established through polarized targeting mechanisms, but it is currently unclear how nonpolarized cargoes, such as mitochondria, become uniformly distributed over these specialized ... ...

Abstract	In neurons, the distinct molecular composition of axons and dendrites is established through polarized targeting mechanisms, but it is currently unclear how nonpolarized cargoes, such as mitochondria, become uniformly distributed over these specialized neuronal compartments. Here, we show that TRAK family adaptor proteins, TRAK1 and TRAK2, which link mitochondria to microtubule-based motors, are required for axonal and dendritic mitochondrial motility and utilize different transport machineries to steer mitochondria into axons and dendrites. TRAK1 binds to both kinesin-1 and dynein/dynactin, is prominently localized in axons, and is needed for normal axon outgrowth, whereas TRAK2 predominantly interacts with dynein/dynactin, is more abundantly present in dendrites, and is required for dendritic development. These functional differences follow from their distinct conformations: TRAK2 preferentially adopts a head-to-tail interaction, which interferes with kinesin-1 binding and axonal transport. Our study demonstrates how the molecular interplay between bidirectional adaptor proteins and distinct microtubule-based motors drives polarized mitochondrial transport.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/genetics ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Axons/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cell Polarity/genetics ; Cells, Cultured ; Dendrites/metabolism ; Embryo, Mammalian ; Green Fluorescent Proteins/metabolism ; Hippocampus/cytology ; Humans ; Kinesin/metabolism ; Kinesin/physiology ; Mitochondria/metabolism ; Models, Biological ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/ultrastructure ; Protein Binding/genetics ; Protein Conformation ; Protein Kinases/metabolism ; Protein Transport/genetics ; RNA, Small Interfering/metabolism ; Rats ; Time Factors ; Transfection
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Carrier Proteins ; KIF5A protein, human ; KIF5B protein, human ; Nerve Tissue Proteins ; RNA, Small Interfering ; TRAK1 protein, human ; TRAK2 protein, human ; Green Fluorescent Proteins (147336-22-9) ; Protein Kinases (EC 2.7.-) ; p150 protein kinase (EC 2.7.1.-) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2013-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2012.11.027
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 92: Show issues

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Article ; Online: Developmental and activity-dependent miRNA expression profiling in primary hippocampal neuron cultures.

Myrrhe van Spronsen / Eljo Y van Battum / Marijn Kuijpers / Vamshidhar R Vangoor / M Liset Rietman / Joris Pothof / Laura F Gumy / Wilfred F J van Ijcken / Anna Akhmanova / R Jeroen Pasterkamp / Casper C Hoogenraad

PLoS ONE, Vol 8, Iss 10, p e

2013 Volume 74907

Abstract	MicroRNAs (miRNAs) are evolutionarily conserved non-coding RNAs of ∼22 nucleotides that regulate gene expression at the level of translation and play vital roles in hippocampal neuron development, function and plasticity. Here, we performed a systematic and in-depth analysis of miRNA expression profiles in cultured hippocampal neurons during development and after induction of neuronal activity. MiRNA profiling of primary hippocampal cultures was carried out using locked nucleic-acid-based miRNA arrays. The expression of 264 different miRNAs was tested in young neurons, at various developmental stages (stage 2-4) and in mature fully differentiated neurons (stage 5) following the induction of neuronal activity using chemical stimulation protocols. We identified 210 miRNAs in mature hippocampal neurons; the expression of most neuronal miRNAs is low at early stages of development and steadily increases during neuronal differentiation. We found a specific subset of 14 miRNAs with reduced expression at stage 3 and showed that sustained expression of these miRNAs stimulates axonal outgrowth. Expression profiling following induction of neuronal activity demonstrates that 51 miRNAs, including miR-134, miR-146, miR-181, miR-185, miR-191 and miR-200a show altered patterns of expression after NMDA receptor-dependent plasticity, and 31 miRNAs, including miR-107, miR-134, miR-470 and miR-546 were upregulated by homeostatic plasticity protocols. Our results indicate that specific miRNA expression profiles correlate with changes in neuronal development and neuronal activity. Identification and characterization of miRNA targets may further elucidate translational control mechanisms involved in hippocampal development, differentiation and activity-depended processes.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Corticosterone alters AMPAR mobility and facilitates bidirectional synaptic plasticity.

Martin, Stéphane / Henley, Jeremy M / Holman, David / Zhou, Ming / Wiegert, Olof / van Spronsen, Myrrhe / Joëls, Marian / Hoogenraad, Casper C / Krugers, Harmen J

PloS one

2009 Volume 4, Issue 3, Page(s) e4714

Abstract: Background: The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the ... ...

Abstract	Background: The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the bidirectional effects of stress and corticosteroid hormones on synaptic efficacy and learning and memory processes. In this study we investigate the relationship between corticosterone and AMPA receptors which play a critical role in activity-dependent plasticity and hippocampal-dependent learning. Methodology/principal findings: Using immunocytochemistry and live cell imaging techniques we show that corticosterone selectively increases surface expression of the AMPAR subunit GluR2 in primary hippocampal cultures via a glucocorticoid receptor and protein synthesis dependent mechanism. In agreement, we report that corticosterone also dramatically increases the fraction of surface expressed GluR2 that undergo lateral diffusion. Furthermore, our data indicate that corticosterone facilitates NMDAR-invoked endocytosis of both synaptic and extra-synaptic GluR2 under conditions that weaken synaptic transmission. Conclusion/significance: Our results reveal that corticosterone increases mobile GluR2 containing AMPARs. The enhanced lateral diffusion properties can both facilitate the recruitment of AMPARs but under appropriate conditions facilitate the loss of synaptic AMPARs (LTD). These actions may underlie both the facilitating and suppressive effects of corticosteroid hormones on synaptic plasticity and learning and memory and suggest that these hormones accentuate synaptic efficacy.
MeSH term(s)	Adaptor Protein Complex 2/metabolism ; Animals ; Anti-Inflammatory Agents/pharmacology ; Corticosterone/pharmacology ; Electrophysiology ; Endocytosis/drug effects ; Fluorescence Recovery After Photobleaching ; Hippocampus/cytology ; Hippocampus/physiology ; N-Methylaspartate/metabolism ; Neuronal Plasticity/drug effects ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; Rats ; Receptors, AMPA/metabolism ; Receptors, Glucocorticoid/metabolism ; Synaptic Transmission/drug effects
Chemical Substances	Adaptor Protein Complex 2 ; Anti-Inflammatory Agents ; Receptors, AMPA ; Receptors, Glucocorticoid ; N-Methylaspartate (6384-92-5) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2009-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0004714
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Article ; Online: Corticosterone alters AMPAR mobility and facilitates bidirectional synaptic plasticity.

Stéphane Martin / Jeremy M Henley / David Holman / Ming Zhou / Olof Wiegert / Myrrhe van Spronsen / Marian Joëls / Casper C Hoogenraad / Harmen J Krugers

PLoS ONE, Vol 4, Iss 3, p e

2009 Volume 4714

Abstract: The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the bidirectional effects ... ...

Abstract	The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the bidirectional effects of stress and corticosteroid hormones on synaptic efficacy and learning and memory processes. In this study we investigate the relationship between corticosterone and AMPA receptors which play a critical role in activity-dependent plasticity and hippocampal-dependent learning.Using immunocytochemistry and live cell imaging techniques we show that corticosterone selectively increases surface expression of the AMPAR subunit GluR2 in primary hippocampal cultures via a glucocorticoid receptor and protein synthesis dependent mechanism. In agreement, we report that corticosterone also dramatically increases the fraction of surface expressed GluR2 that undergo lateral diffusion. Furthermore, our data indicate that corticosterone facilitates NMDAR-invoked endocytosis of both synaptic and extra-synaptic GluR2 under conditions that weaken synaptic transmission.Our results reveal that corticosterone increases mobile GluR2 containing AMPARs. The enhanced lateral diffusion properties can both facilitate the recruitment of AMPARs but under appropriate conditions facilitate the loss of synaptic AMPARs (LTD). These actions may underlie both the facilitating and suppressive effects of corticosteroid hormones on synaptic plasticity and learning and memory and suggest that these hormones accentuate synaptic efficacy.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2009-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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