Spontaneous Astrocytic Ca2+ Oscillations and Neurite Growth
Kazunori Kanemaru, Yohei Okubo, Kenzo Hirose, and Masamitsu Iino
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.
Yutaka Furutani, Hitomi Matsuno, Miwa Kawasaki, Takehiko Sasaki, Kensaku Mori, and Yoshihiro Yoshihara
Before synapses form between axons and dendrites, even before dendritic spines take shape, dendritic filopodia are out there, poking and prodding and exploring their surroundings. In this weeks Journal, Furutani et al. searched for intracellular binding partners for telencephalin (TLCN), atelencephalon- and dendrite-specific cell adhesion molecule that is expressed in filopodia. A yeast two-hybrid screen revealed interactions with ezrin, radixin, and moesin of the so-called ERM family; these adaptors link membrane proteins to the actin cytoskeleto
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