Distinct calcium signaling within neuronal growth cones and filopodia

Davenport, Roger W.; Dou, Ping; Mills, Linda R.; Kater, Stanley B.

doi:10.1002/(sici)1097-4695(199609)31:1<1::aid-neu1>3.0.co;2-6

Cited by 28 publications

(24 citation statements)

References 65 publications

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“…In support of this, it has been shown that mitochondria stalling at the axon branching sites are necessary for efficient branching, an actinpolymerization-dependent process (Spillane et al, 2013). However, we cannot exclude a role for mitochondria in filopodial Ca 2+ regulation (Davenport et al, 1996) or other signaling events leading to filopodia formation.…”

Section: Discussionmentioning

confidence: 74%

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Shneyer

Ušaj

Henn

2016

Journal of Cell Science

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Mitochondria respond to environmental cues and stress conditions. Additionally, the disruption of the mitochondrial network dynamics and its distribution is implicated in a variety of neurodegenerative diseases. Here, we reveal a new function for Myo19 in mitochondrial dynamics and localization during the cellular response to glucose starvation. Ectopically expressed Myo19 localized with mitochondria to the tips of starvation-induced filopodia. Corollary to this, RNA interference (RNAi)-mediated knockdown of Myo19 diminished filopodia formation without evident effects on the mitochondrial network. We analyzed the Myo19-mitochondria interaction, and demonstrated that Myo19 is uniquely anchored to the outer mitochondrial membrane (OMM) through a 30-45-residue motif, indicating that Myo19 is a stably attached OMM molecular motor. Our work reveals a new function for Myo19 in mitochondrial positioning under stress.

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Section: Discussionmentioning

confidence: 74%

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Shneyer

Ušaj

Henn

2016

Journal of Cell Science

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“…In addition to the regulatory influence on ion fluxes in neural signal transmission, [21][22][23] changes in intracellular calcium can modify events such as release of neurotransmitters, 24 axon sprouting, 25 and neuronal survival. 26 Increased intracellular level of free Ca 2ϩ is considered a major pathogenic mechanism in ischemic brain damage, 15,27 and excessive Ca 2ϩ influx is suggested to be important in excitotoxic neuronal cell death.…”

Section: Discussionmentioning

confidence: 99%

High Expression of Stanniocalcin in Differentiated Brain Neurons

Zhang

Westberg

Paetau

et al. 1998

The American Journal of Pathology

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“…Further, even the type of channel through which calcium may enter the neuron can differentially influence neurite growth and branching (Heng et al 1999). Additionally, growth cones and their associated filopodia may be differentially sensitive to calcium compared to shaft filopodia (Davenport et al 1996;Portera-Cailliau et al 2003). Clearly, the status of the local environment as well as the nature of the local event may be factors that determine neuronal responses to changes in calcium.…”

Section: Calcium and Neuronal Maturationmentioning

confidence: 99%

Effects of Disrupting Calcium Homeostasis on Neuronal Maturation: Early Inhibition and Later Recovery

et al. 2008

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It has become increasingly clear that agents that disrupt calcium homeostasis may also be toxic to developing neurons. Using isolated primary neurons, we sought to understand the neurotoxicity of agents such as MK801 (which blocks ligand-gated calcium entry), BAPTA (which chelates intracellular calcium), and thapsigargin (TG; which inhibits the endoplasmic reticulum Ca 2+ -ATPase pump). Thus, E18 at cotical neuons wee grown for 1 day in vitro (DIV) and then exposed to vehicle (0.1% DMSO), MK801 (0.01-20 μM), BAPTA (0.1-20 μM), or TG (0.001-1 μM) for 24 h. We found that all three agents could profoundly influence early neuronal maturation (growth cone expansion, neurite length, neurite complexity), with the order of potency being MK801 < BAPTA < TG. We next asked if cultures exposed to these agents were able to re-establish their developmental program once the agent was removed. When we examined network maturity at 4 and 7 DIV, the order of recovery was MK801 > BAPTA > TG. Thus, mechanistically distinct ways of disrupting calcium homeostasis differentially influenced both short-term and long-term neuronal maturation. These observations suggest that agents that act by altering intracellular calcium and are used in obstetrics or neonatology may be quite harmful to the still-developing human brain.

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Distinct calcium signaling within neuronal growth cones and filopodia

Cited by 28 publications

References 65 publications

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia

High Expression of Stanniocalcin in Differentiated Brain Neurons

Effects of Disrupting Calcium Homeostasis on Neuronal Maturation: Early Inhibition and Later Recovery

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