English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Glial-neuronal signaling at synapses is widely studied, but how glia interact with neuronal somas to regulate their activity is unclear.  Drosophila  cortex glia are restricted to brain regions devoid of synapses, providing an opportunity to characterize interactions with neuronal somas. Mutations in the cortex glial  NCKX zydeco   elevate basal Ca 2+ , predisposing animals to seizure-like behavior. To determine how cortex glial Ca 2+  signaling controls neuronal excitability, we performed an in vivo modifier screen of the  NCKX zydeco   seizure phenotype. We show that elevation of glial Ca 2+  causes hyperactivation of calcineurin-dependent endocytosis and accumulation of early endosomes. Knockdown of sandman, a K 2P  channel, recapitulates  NCKX zydeco   seizures. Indeed, sandman expression on cortex glial membranes is substantially reduced in  NCKX zydeco   mutants, indicating enhanced internalization of sandman predisposes animals to seizures. These data provide an unexpected link between glial Ca 2+  signaling and the well-known role of glia in K +  buffering as a key mechanism for regulating neuronal excitability.

Glial Ca 2+ signaling links endocytosis to K + buffering around neuronal somas to regulate excitability