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IGF-1 modulates N and L calcium channels in a PI 3-kinase-dependent manner.

Abstract：

:Receptor tyrosine kinases (RTKs) have long been associated with proliferation in non-neural cells, although they are also expressed in postmitotic neurons. We demonstrate that insulin-like growth factor-1 (IGF-1) induces within seconds a large, tyrosine-kinase-dependent increase in calcium channel currents in cerebellar granule neurons. Separation of channel subtypes reveals that, while P, Q, and R channels are unaffected, N and L channel activities are strongly potentiated at specific membrane voltages: N currents triple at depolarized potentials, while L currents rapidly increase 4-fold at hyperpolarized potentials. Moreover, transient expression of dominant-negative and wild-type phosphatidylinositol 3-OH kinase (PI 3-kinase) subunits, as well as application of specific inhibitors, demonstrates that PI 3-kinase is an essential and rate-limiting messenger in this signaling pathway. Our results indicate that N and L calcium channels are downstream targets of neuronal RTKs and suggest that RTK modulation may control calcium-dependent processes, such as neurotransmitter release and IGF-1-dependent differentiation or survival.

journal_name

Neuron

journal_title

Neuron

authors

Blair LA,Marshall J

doi

10.1016/s0896-6273(00)80950-2

subject

Has Abstract

pub_date

1997-08-01 00:00:00

pages

421-9

issue

2

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(00)80950-2

journal_volume

19

pub_type

杂志文章

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