Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon technologies

Colicos, Michael A.; Syed, Naweed I.

doi:10.1242/jeb.02163

Cited by 22 publications

(20 citation statements)

References 41 publications

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“…Rat hippocampal neurons taken from postnatal day 0 (P0) pups were grown on silicon wafers as previously described (Colicos et al, 2001;Colicos and Syed, 2006;Goda and Colicos, 2006). Neuronal cultures were grown until DIV 4, at which time they were transfected using Lipofectamine 2000 (Invitrogen, Burlington, ON, Canada) and stimulated 3-4 d later.…”

Section: Photoconductive Stimulation and Quantificationmentioning

confidence: 99%

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Arstikaitis

Gauthier-Campbell

Herrera

et al. 2008

MBoC

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Dendritic filopodia are thought to participate in neuronal contact formation and development of dendritic spines; however, molecules that regulate filopodia extension and their maturation to spines remain largely unknown. Here we identify paralemmin-1 as a regulator of filopodia induction and spine maturation. Paralemmin-1 localizes to dendritic membranes, and its ability to induce filopodia and recruit synaptic elements to contact sites requires protein acylation. Effects of paralemmin-1 on synapse maturation are modulated by alternative splicing that regulates spine formation and recruitment of AMPA-type glutamate receptors. Paralemmin-1 enrichment at the plasma membrane is subject to rapid changes in neuronal excitability, and this process controls neuronal activity-driven effects on protrusion expansion. Knockdown of paralemmin-1 in developing neurons reduces the number of filopodia and spines formed and diminishes the effects of Shank1b on the transformation of existing filopodia into spines. Our study identifies a key role for paralemmin-1 in spine maturation through modulation of filopodia induction. INTRODUCTIONDuring CNS excitatory synapse development, the formation of spines, bulbous protrusions enriched with F-actin, is essential for proper synaptic transmission and neuronal function (Hall and Nobes, 2000;Yuste and Bonhoeffer, 2004;Halpain et al., 2005;Matus, 2005;. Spines contain a plethora of proteins including neurotransmitter receptors, cytoskeleton-associated proteins, and cell adhesion molecules. Spines are pleomorphic protrusions that can be modified by changes in neuronal activity, which regulate actin-based motility (Fischer et al., 1998;Portera-Cailliau et al., 2003;Matus, 2005). Defects in spine maturation and function have been associated with several forms of mental retardation including Down, Rett, Fragile X, and fetal alcohol syndromes. Some of these disorders exhibit a reduction in spine size and density and the formation of long, thin filopodia-like structures (Hering and Sheng, 2001;Zoghbi, 2003).Although our knowledge of molecules that control the morphology and functional properties of dendritic spines has expanded, information about the structures from which spines emerge is lacking. Dendritic filopodia, thin protrusions ranging in length from 2 to 35 m, are thought to participate in synaptogenesis, dendritic branching and the development of spines. During synaptogenesis, filopodia decorate the dendrites of neurons. Studies show that dendritic filopodia exhibit highly dynamic protrusive motility during periods of active synaptogenesis (Dailey and Smith, 1996;Ziv and Smith, 1996;Marrs et al., 2001). Thus, filopodia are thought to function by extending and probing the environment for appropriate presynaptic partners, thereby aiding in synapse formation. These results are further supported by electron microscopy studies which show that synapses can be formed at the tip and base of dendritic filopodia (Fiala et al., 1998;Kirov et al., 2004). As synapses form, the number of filopodia d...

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Section: Photoconductive Stimulation and Quantificationmentioning

confidence: 99%

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Arstikaitis

Gauthier-Campbell

Herrera

et al. 2008

MBoC

Self Cite

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“…Synaptic plasticity refers to any change, increase or decrease, in the strength of synaptic transmission and is determined for example by changes in neurotransmitter release or changes at the level of the post-synaptic receptor, which ultimately should lead to changes in the activity of specific neuronal networks (Neves et al, 2008). Moreover, the strength of connectivity between neurons may result from changes in the strength or efficiency of existing synapses or by alteration in the number of synapses (Colicos and Syed, 2006).…”

Section: Synaptic Plasticitymentioning

confidence: 99%

Lipid rafts, synaptic transmission and plasticity: Impact in age-related neurodegenerative diseases

et al. 2013

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“…The synapse, or connection between neurons, has the interesting capability of altering the strength of the connection between the adjacent neurons [63,64]. This is known as synaptic plasticity.…”

Section: Neural Codingmentioning

confidence: 99%

Toward in vivo nanoscale communication networks: utilizing an active network architecture

Bush

2011

Front. Comput. Sci. China

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A safe and reliable in vivo nanoscale communication network will be of great benefit for medical diagnosis and monitoring as well as medical implant communication. This review article provides a brief introduction to nanoscale and molecular networking in general and provides opinions on the role of active networking for in vivo nanoscale information transport. While there are many in vivo communication mechanisms that can be leveraged, for example, forms of cell signaling, gap junctions, calcium and ion signaling, and circulatory borne communication, this review examines two in particular: molecular motor transport and neuronal information communication. Molecular motors transport molecules representing information and neural coding operates by means of the action potential; these mechanisms are reviewed within the theoretical framework of an active network. This review suggests that an active networking paradigm is necessary at the nanoscale along with a new communication constraint, namely, minimizing the communication impact upon the living environment. The goal is to assemble efficient nanoscale and molecular communication channels while minimizing disruption to the host organism.

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Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon technologies

Cited by 22 publications

References 41 publications

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Paralemmin-1, a Modulator of Filopodia Induction Is Required for Spine Maturation

Lipid rafts, synaptic transmission and plasticity: Impact in age-related neurodegenerative diseases

Toward in vivo nanoscale communication networks: utilizing an active network architecture

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