THE ACTIN CYTOSKELETON: Integrating Form and Function at the Synapse

Dillon, Christian; Goda, Yukiko

doi:10.1146/annurev.neuro.28.061604.135757

Cited by 386 publications

(397 citation statements)

References 160 publications

Supporting

Mentioning

380

Contrasting

Order By: Relevance

“…It activates LIM kinase (LIMK), which inhibits the actin-depolymerizing activity of n-cofilin. The dynamic remodeling of synaptic connections requires constant reorganization of actin filaments (Dillon and Goda 2005). Consequently, postnatal disruption of n-cofilin in mice leads to increased synapse density and enlargement of axospinous synapses (Rust et al 2010) with defects in long-term potentiation (LTP) and long-term depression (LTD).…”

Section: Regulation Of Dendritic Spines Glutamatergic Neurotransmissmentioning

confidence: 99%

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease

Holtzman

Herz²,

2012

Cold Spring Harbor Perspectives in Medicine

673

602

View full text Add to dashboard Cite

Section: Regulation Of Dendritic Spines Glutamatergic Neurotransmissmentioning

confidence: 99%

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease

Holtzman

Herz²,

2012

Cold Spring Harbor Perspectives in Medicine

673

602

View full text Add to dashboard Cite

“…A protein known to play a critical role in neurosecretion (Dillon and Goda, 2005), that may participate in ␣-synuclein action is actin. Actin filaments are involved in the transport of clear and dense-core vesicles along the axon and in their clustering at the plasma membrane sites where exocytosis takes place.…”

Section: Introductionmentioning

confidence: 99%

α-Synuclein and Its A30P Mutant Affect Actin Cytoskeletal Structure and Dynamics

Sousa

Bellani

Giannandrea

et al. 2009

MBoC

106

View full text Add to dashboard Cite

The function of ␣-synuclein, a soluble protein abundant in the brain and concentrated at presynaptic terminals, is still undefined. Yet, ␣-synuclein overexpression and the expression of its A30P mutant are associated with familial Parkinson's disease. Working in cell-free conditions, in two cell lines as well as in primary neurons we demonstrate that ␣-synuclein and its A30P mutant have different effects on actin polymerization. Wild-type ␣-synuclein binds actin, slows down its polymerization and accelerates its depolymerization, probably by monomer sequestration; A30P mutant ␣-synuclein increases the rate of actin polymerization and disrupts the cytoskeleton during reassembly of actin filaments. Consequently, in cells expressing mutant ␣-synuclein, cytoskeleton-dependent processes, such as cell migration, are inhibited, while exo-and endocytic traffic is altered. In hippocampal neurons from mice carrying a deletion of the ␣-synuclein gene, electroporation of wild-type ␣-synuclein increases actin instability during remodeling, with growth of lamellipodia-like structures and apparent cell enlargement, whereas A30P ␣-synuclein induces discrete actin-rich foci during cytoskeleton reassembly. In conclusion, ␣-synuclein appears to play a major role in actin cytoskeletal dynamics and various aspects of microfilament function. Actin cytoskeletal disruption induced by the A30P mutant might alter various cellular processes and thereby play a role in the pathogenesis of neurodegeneration.

show abstract

“…Finally, Actin β (Actb) becomes down-regulated, a protein forming the backbone of the dendritic compartment and spines (Urbanska, Swiech, and Jaworski, 2012). Through dynamic changes, this protein is involved in dendritic and synaptic plasticity, synapse function (Dillon and Goda, 2005) and receptor trafficking (Hanley, 2008). Masked Actin β mRNA and ribosomes are present in neuronal dendrites, allowing a local translation in response to synaptic activity (Buxbaum, Wu, and Singer, 2014).…”

Section: Discussionmentioning

confidence: 99%

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

Hertler

Buitrago

Luft

et al. 2016

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

Motor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: (1) an initial suppression of genes influencing gene transcription. (2) Expression of genes that support translation of mRNA in defined compartments. (3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24h -this is a much slower time-course when compared to hippocampusdependent learning, where peaks of gene-expression can be observed 6-12h after training ended. AbstractMotor learning is associated with plastic reorganization of neural networks in primary motor cortex (M1) that depends on changes in gene expression. Here, we investigate the temporal profile of these changes during motor memory formation in response to a skilled reaching task in rats. mRNA-levels were measured 1h, 7h and 24h after the end of a training session using microarray technique. To assure learning specificity, trained animals were compared to a control group. In response to motor learning, genes are sequentially regulated with high time-point specificity and a shift from initial suppression to later activation. The majority of regulated genes can be linked to learning-related plasticity. In the gene-expression cascade following motor learning, three different steps can be defined: 1) an initial suppression of genes influencing gene transcription. 2) Expression of genes that support translation of mRNA in defined compartments. 3) Expression of genes that immediately mediates plastic changes. Gene expression peaks after 24 hours -this is a much slower time-course when compared to hippocampus-dependent learning, where peaks of geneexpression can be observed 6 to 12 hours after training ended.3

show abstract

THE ACTIN CYTOSKELETON: Integrating Form and Function at the Synapse

Cited by 386 publications

References 160 publications

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease

α-Synuclein and Its A30P Mutant Affect Actin Cytoskeletal Structure and Dynamics

Temporal course of gene expression during motor memory formation in primary motor cortex of rats

Contact Info

Product

Resources

About