News tips from the Journal of Ne...( Spontaneous Astrocytic Ca 2+ Oscil...)

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.

Forming Filopodia
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
'/>"/>