This week, Kanemaru et al. explore the signaling pathway between spontaneous Ca2+ oscillations in cultured astrocytes and the promotion of neurite growth. Their results reveal a role for the membrane-bound adhesion molecule N-cadherin.
The authors blocked Ca2+ oscillations by preventing IP3 signaling with retroviral-mediated expression of IP3 5-phosphatase (5ppase). This molecule hydrolyzes IP3 and thus prevented spontaneous astrocytic Ca2+ oscillations. Growth cone motility was compromised in hippocampal neurons cultured with 5ppase-expressing astrocytes. Interference with neurotransmitter-evoked astrocytic Ca2+ transients did not affect neurite outgrowth. The messenger was not diffusible because direct contact with an astrocyte deficient in spontaneous Ca2+ signaling arrested growth cone advancement. Surface expression of the growth-promoting molecule N-cadherin was downregulated in 5ppase-expressing astrocytes, and neuronal growth cone advancement was rescued by extrinsic expression of N-cadherin on astrocytes. -Society for Neuroscience
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