Ca2+/calmodulin-dependent protein kinases II and IV both promote survival but differ in their effects on axon growth in spiral ganglion neurons

Marlan R Hansen; Jinwoong Bok; Anand K Devaiah; Xiang-Ming Zha; Steven H Green

doi:10.1002/jnr.10551

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Ca2+/calmodulin-dependent protein kinases II and IV both promote survival but differ in their effects on axon growth in spiral ganglion neurons

Journal article

Peer reviewed

Ca2+/calmodulin-dependent protein kinases II and IV both promote survival but differ in their effects on axon growth in spiral ganglion neurons

Marlan R Hansen, Jinwoong Bok, Anand K Devaiah, Xiang-Ming Zha and Steven H Green

Journal of neuroscience research, Vol.72(2), pp.169-184

04/15/2003

DOI: 10.1002/jnr.10551

PMID: 12671991

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Abstract

Spiral ganglion neuron (SGN) survival in vitro can be maintained by neurotrophins, permeant cAMP analogs, and depolarization in an additive manner, with depolarization being the most efficacious. Therefore, we used cultured SGNs to determine the mechanism by which depolarization promotes neuronal survival. Our data implicate Ca(2+)/calmodulin-dependent protein kinase (CaMK) activity by showing that it is induced by depolarization, that CaMK activity is necessary for at least part of the survival-promoting effect of depolarization, and that CaMKII or CamKIV activity suffices to support neuronal survival in the absence of other trophic stimuli. First, that depolarization of SGNs activates CaMKs is evidenced by observation of increased CaMKII phosphorylation and of CaMK-dependent CREB phosphorylation. Second, the requirement for CaMKs is shown by a reduction of SGN survival under depolarizing conditions in the presence of CaMK inhibitors. Third, transfection of COOH-terminal-truncated (lacking regulatory domain), constitutively active CaMKII or CaMKIV, but not of normal, full-length CAMKs, promotes SGN survival in the absence of other trophic stimuli, indicating that CaMK activity is sufficient to promote survival. The survival-promoting effect of truncated CaMKs is additive with that of depolarization, neurotrophins, or cyclic AMP. Although both CaMKII and CaMKIV activities converge in promoting survival, their actions on axon growth are markedly different: Transfection of truncated CaMKII, but not of truncated CaMKIV, into SGNs prevents axon outgrowth.

Spiral Ganglion - enzymology

Sequence Deletion

Phosphorylation

Calcium Signaling - physiology

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives

Axons - physiology

Spiral Ganglion - cytology

Protein-Serine-Threonine Kinases - antagonists & inhibitors

Calcium-Calmodulin-Dependent Protein Kinase Type 2

Cell Survival - physiology

Protein-Serine-Threonine Kinases - metabolism

Membrane Potentials - drug effects

Amino Acid Sequence

Cell Survival - drug effects

Peptide Fragments - metabolism

Calcium-Calmodulin-Dependent Protein Kinases - genetics

Cells, Cultured

Enzyme Inhibitors - pharmacology

Protein-Serine-Threonine Kinases - genetics

Rats

Imidazoles - pharmacology

Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors

Membrane Potentials - physiology

Calcium-Calmodulin-Dependent Protein Kinase Kinase

Peptide Fragments - chemistry

Animals

Signal Transduction - drug effects

Calcium Signaling - drug effects

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology

Neurons - enzymology

Protein Isoforms

Cyclic AMP Response Element-Binding Protein - metabolism

Signal Transduction - physiology

Calcium-Calmodulin-Dependent Protein Kinases - metabolism

Details

Title: Subtitle: Ca2+/calmodulin-dependent protein kinases II and IV both promote survival but differ in their effects on axon growth in spiral ganglion neurons
Creators: Marlan R Hansen - Department of Biological Sciences, University of Iowa, Iowa City 52242-1324, USA
Jinwoong Bok
Anand K Devaiah
Xiang-Ming Zha
Steven H Green
Resource Type: Journal article
Publication Details: Journal of neuroscience research, Vol.72(2), pp.169-184
DOI: 10.1002/jnr.10551
PMID: 12671991
NLM abbreviation: J Neurosci Res
ISSN: 0360-4012
eISSN: 1097-4547
Publisher: United States
Grant note: T32 DC000040 / NIDCD NIH HHS DK25295 / NIDDK NIH HHS DC00040 / NIDCD NIH HHS DC02961 / NIDCD NIH HHS R01 DC002961 / NIDCD NIH HHS
Language: English
Date published: 04/15/2003
Academic Unit: Molecular Physiology and Biophysics; Biology; Neurosurgery; Otolaryngology
Record Identifier: 9984007176202771

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