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The Journal of Neuroscience, March 15, 1999, 19(6):1940-1951
Akt-Dependent Potentiation of L Channels by Insulin-Like Growth Factor-1 Is Required for Neuronal Survival
Leslie A. C. Blair1, Kendra K. Bence-Hanulec1, 2, Sunil Mehta1, Thomas Franke3, David Kaplan4, and John Marshall1 1 Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island 02912, 2 Department of Physiology and Biophysics, Cornell Medical College, New York, New York 10021, 3 Department of Pharmacology, Columbia University, New York, New York 10032, and 4 Brain Tumor Research Center, McGill University, Montréal, Québec, Canada H3G 1Y6
The insulin-like growth factor-1 (IGF-1)/receptor tyrosine kinase recently has been shown to mediate neuronal survival and potentiate the activity of specific calcium channel subtypes; survival requires Akt, a serine/threonine kinase. We demonstrate here that Akt mediates the IGF-1-induced potentiation of L channel currents, but not that of N channels. Transient expression of wild-type, dominant-negative, and constitutively active forms of Akt in cerebellar granule neurons causes, respectively, no change in IGF-1/L channel potentiation, complete inhibition of potentiation, and a dramatic increase in basal L currents accompanied by the loss of ability to induce further increases. In no case is the IGF-1 potentiation of N currents affected. We additionally find that IGF-1 partially mediates granule neuron survival via L channel activity and that Akt-dependent L channel modulation is a necessary component. Interestingly, very brief exposure (1 min) to IGF-1 triggers nearly complete survival and requires L channel activity. These results strongly suggest that neuronal receptor tyrosine kinases can control long-term calcium-dependent processes via the rapid control of voltage-sensitive channels.
Key words: IGF-1; RTK; L channel; modulation; granule neurons; apoptosis; survival
Copyright © 1999 Society for Neuroscience 0270-6474/99/1961940-12$05.00/0
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