Changes in calcium signaling during postembryonic dendritic growth in Manduca sexta

C. Duch, R. B. Levine

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

Activity-dependent Ca2+ influx plays crucial roles in adult and developing nervous systems through its influence on signal processing, synaptic plasticity, and neuronal differentiation. The responses to internal Ca2+ elevations vary depending on the spatial distribution of Ca2+ accumulation in different cell compartments. In this study, the mechanisms and the distribution of Ca2+ accumulation are addressed by in situ Ca2+ imaging of an identified insect motoneuron, MN5, at critical stages of postembryonic life. During metamorphosis of Manduca sexta, MN5 undergoes extensive dendritic regression followed by regrowth. The time course, amplitude, and distribution of Ca2+ accumulation within MN5 change during development. During the initial stage of rapid dendritic growth and branching, dendritic growth cones are present, and voltage-dependent Ca2+ currents are small. At this stage, activity-induced elevations of internal Ca2+ are largest in the distal dendrites, suggesting that the density of voltage-gated Ca2+ channels is highest in these regions. Later phases of dendritic growth are accompanied by the transient occurrence of prominent Ca2+ spikes. Single Ca2+ spikes cause robust Ca2+ influx of similar amplitudes and time courses in all central compartments of MN5. The resting Ca2+ levels also increase during development. Ca2+-induced Ca2+ release from intracellular stores did not contribute to the elevations measured at either stage, although Ca2+ stores are present in the dendrites. These developmental changes of the internal Ca2+ signaling are consistent with a regulatory role for activity-dependent Ca2+ influx in postembryonic dendritic growth.

Original languageEnglish (US)
Pages (from-to)1415-1425
Number of pages11
JournalJournal of neurophysiology
Volume87
Issue number3
DOIs
StatePublished - Jan 1 2002

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

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