Local increases in intracellular calcium elicit local filopodial responses in helisoma neuronal growth cages

Davenport, Roger W.; Kater, Stanley B.

doi:10.1016/0896-6273(92)90179-h

Cited by 114 publications

(92 citation statements)

References 34 publications

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“…There are several classes of calcium channels, including those that are opened by membrane depolarization (voltage-gated channels) and those which are not. The conductance of voltage-gated channels would be increased by a reduction in membrane potential, while the conductance of nonvoltage-gated channels would be decreased (Robinson, 1985;Bedlack et al, 1992;Davenport & Kater, 1992). These properties seem to fit the requirements for a transducer of the electrical field effects we have observed.…”

Section: Galvano Tropismmentioning

confidence: 53%

Growth and guidance of the fungal hypha

Gow

1994

Microbiology

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Section: Galvano Tropismmentioning

confidence: 53%

Growth and guidance of the fungal hypha

Gow

1994

Microbiology

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“…It is likely that filopodial sprouting is an immediate consequence of a rise in intracellular Ca2+ concentration to a rather high level. This Ca requirement for the rapid filopodial sprouting is similar to that for filopodial elongation in Helisoma growth cones (Davenport and Kater, 1992;Rehder and Kater, 1992). On the contrary, it has been shown that a sustained increase in intracellular Ca2+ concentration to very high levels by repeated electrical stimulation (Cohan and Kater, 1986), or by continuous application of neurotransmitters (Haydon et al, 1984) suppressed both growth cone motility and elongation.…”

Section: Dependence On Ca2+mentioning

confidence: 78%

“…Glutamate, an excitatory neurotransmitter, induces filopodia formation in the growth cone (Cornell-Bell et al, 1990). Application of an electrical field or a K-rich solution increases the number, facilitates elongation, and induces disposition of filopodia (Davenport and Kater, 1992;Rehder and Kater, 1992). Thus, motility and structural changes of the growth cone have been extensively studied.…”

mentioning

confidence: 99%

Rapid sprouting of filopodia in nerve terminals of chromaffin cells, PC12 cells, and dorsal root neurons induced by electrical stimulation

Manivannan

Terakawa

1994

J. Neurosci.

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Rapid morphological changes induced by direct electrical stimulation of nerve terminals were studied by using video-enhanced differential interference contrast microscopy at a very high magnification (12,000x). We used mainly cultured bovine chromaffin cells, which developed neurite-like processes, and PC12 cells, which showed neuronal differentiation upon NGF treatment. In a few cases, primary neurons of the rat dorsal root ganglion were also examined. Brief pulse stimulation of the terminals and varicosities induced exocytosis accompanied by rapid formation of filopodia. These filopodia, 0.1–0.2 micron in diameter and up to 10 microns in length, formed within a few hundreds of milliseconds and then retracted within tens of seconds. They could also be induced by K depolarization. This rapid filopodial sprouting strongly depended on the presence of extracellular Ca2+ and could be abolished in a medium containing a Ca chelator (EGTA) or La2+. Anti-cytoskeletal agents colchicine and cytochalasin B failed to block this response completely but lidocaine fully suppressed it. Quantitative analysis of exocytosis and filopodial sprouting showed that they were independent events, not directly linked to each other, having different thresholds usually higher for filopodial formation. In PC12 cells, the extent of filopodial sprouting varied with the state of differentiation of the cells, suggesting a functional role of rapid sprouting during a particular phase of their differentiation. Filopodia could be induced with greater ease by repetitive stimulation. The same responses may occur at growth cones approaching the target cells or even at mature synapses particularly after repetitive electrical activity, possibly playing a role in use-dependent synapse formation or plasticity.

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“…These findings are consistent with previous studies that suggest that transient elevations in [Ca 2ϩ ] i can trigger neuronal remodeling. For example, elevations of [Ca 2ϩ ] i to hundreds of nanomolars induced by localized electric fields resulted in the transient extension of filopodia from growth cones (Davenport and Kater, 1992) or from neuritic shafts (Williams et al, 1995). However, these filopodia were transient in nature and failed to develop into persistent structures.…”

Section: Discussionmentioning

confidence: 99%

Localized and Transient Elevations of Intracellular Ca²⁺Induce the Dedifferentiation of Axonal Segments into Growth Cones

1997

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The formation of a growth cone at the tip of a severed axon is a key step in its successful regeneration. This process involves major structural and functional alterations in the formerly differentiated axonal segment. Here we examined the hypothesis that the large, localized, and transient elevation in the free intracellular calcium concentration ([Ca 2ϩ ] i ) that follows axotomy provides a signal sufficient to trigger the dedifferentiation of the axonal segment into a growth cone. Ratiometric fluorescence microscopy and electron microscopy were used to study the relations among spatiotemporal changes in [Ca 2ϩ ] i , growth cone formation, and ultrastructural alterations in axotomized and intact Aplysia californica neurons in culture. We report that, in neurons primed to grow, a growth cone forms within 10 min of axotomy near the tip of the transected axon. The nascent growth cone extends initially from a region in which peak intracellular Ca 2ϩ concentrations of 300 -500 M are recorded after axotomy. Similar [Ca 2ϩ ] i transients, produced in intact axons by focal applications of ionomycin, induce the formation of ectopic growth cones and subsequent neuritogenesis. Electron microscopy analysis reveals that the ultrastructural alterations associated with axotomy and ionomycin-induced growth cone formation are practically identical. In both cases, growth cones extend from regions in which sharp transitions are observed between axoplasm with major ultrastructural alterations and axoplasm in which the ultrastructure is unaltered. These findings suggest that transient elevations of [Ca 2ϩ ] i to 300 -500 M, such as those caused by mechanical injury, may be sufficient to induce the transformation of differentiated axonal segments into growth cones.

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Local increases in intracellular calcium elicit local filopodial responses in helisoma neuronal growth cages

Cited by 114 publications

References 34 publications

Growth and guidance of the fungal hypha

Growth and guidance of the fungal hypha

Rapid sprouting of filopodia in nerve terminals of chromaffin cells, PC12 cells, and dorsal root neurons induced by electrical stimulation

Localized and Transient Elevations of Intracellular Ca²⁺Induce the Dedifferentiation of Axonal Segments into Growth Cones

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Local increases in intracellular calcium elicit local filopodial responses in helisoma neuronal growth cages

Cited by 114 publications

References 34 publications

Growth and guidance of the fungal hypha

Growth and guidance of the fungal hypha

Rapid sprouting of filopodia in nerve terminals of chromaffin cells, PC12 cells, and dorsal root neurons induced by electrical stimulation

Localized and Transient Elevations of Intracellular Ca2+Induce the Dedifferentiation of Axonal Segments into Growth Cones

Contact Info

Product

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Localized and Transient Elevations of Intracellular Ca²⁺Induce the Dedifferentiation of Axonal Segments into Growth Cones