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The Journal of Neuroscience, May 24, 2006, 26(21):5656-5664; doi:10.1523/JNEUROSCI.0675-06.2006

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Development/Plasticity/Repair
Ca²⁺ Influx through Mechanosensitive Channels Inhibits Neurite Outgrowth in Opposition to Other Influx Pathways and Release from Intracellular Stores

Bridget T. Jacques-Fricke,^1,2 Yiqi Seow,³ Philip A. Gottlieb,⁴ Frederick Sachs,⁴ and Timothy M. Gomez^1,2

¹Department of Anatomy and ²Neuroscience Training Program, University of Wisconsin, Madison, Wisconsin 53706, ³Institute of Molecular and Cell Biology, Singapore, 138673, and ⁴Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, New York 14214

Correspondence should be addressed to Timothy M. Gomez, University of Wisconsin, 257 Bardeen Labs, 1300 University Avenue, Madison, WI 53706. Email: tmgomez{at}wisc.edu

Ca²⁺ signals are known to be important regulators of neurite outgrowth and steering. Here we show that inhibiting Ca²⁺ influx through stretch-activated channels using various compounds, including a highly specific peptide isolated from Grammostola spatulata spider venom (GsMTx4), strongly accelerates the rate of neurite extension on diverse substrata and within the intact spinal cord. Consistent with the presence of stretch-activated channels, we show that Ca²⁺ influx is triggered by hypotonic solutions, which can be partially blocked by GsMTx4. Finally, chelating local, but not global, Ca²⁺ signals prevents the acceleration that is normally produced by GsMTx4. Blocking Ca²⁺ influx through other channel types has little or opposite effects, but release from intracellular stores is required for maximal acceleration. Together, our data suggest that Ca²⁺ functions at distinct microdomains in growth cones, with influx through mechanosensitive channels acting to inhibit outgrowth in opposition to influx through other plasma membrane channels and release from stores.

Key words: pathfinding; axon guidance; stretch activated channels; TRP; IP₃, ryanodine; spinal cord

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Received Feb. 15, 2006; revised April 14, 2006; accepted April 16, 2006.

Correspondence should be addressed to Timothy M. Gomez, University of Wisconsin, 257 Bardeen Labs, 1300 University Avenue, Madison, WI 53706. Email: tmgomez{at}wisc.edu

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