Suppression of Sleep Spindle Rhythmogenesis in Mice with Deletion of CaV3.2 and CaV3.3 T-type Ca2+ Channels | Zendy

Chiara Pellegrini | Zendy; Sandro Lecci | Zendy; Anita Lüthi | Zendy; Simone Astori | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Suppression of Sleep Spindle Rhythmogenesis in Mice with Deletion of CaV3.2 and CaV3.3 T-type Ca2+ Channels

Author(s) -

Chiara Pellegrini,

Sandro Lecci,

Anita Lüthi,

Simone Astori

Publication year - 2016

Publication title -

sleep

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.222

H-Index - 207

eISSN - 1550-9109

pISSN - 0161-8105

DOI - 10.5665/sleep.5646

Subject(s) - bursting , non rapid eye movement sleep , neuroscience , sleep spindle , neurotransmission , t type calcium channel , voltage dependent calcium channel , electrophysiology , electroencephalography , biology , medicine , calcium , receptor

Low-threshold voltage-gated T-type Ca(2+) channels (T-channels or CaV3 channels) sustain oscillatory discharges of thalamocortical (TC) and nucleus Reticularis thalami (nRt) cells. The CaV3.3 subtype dominates nRt rhythmic bursting and mediates a substantial fraction of spindle power in the NREM sleep EEG. CaV3.2 channels are also found in nRt, but whether these contribute to nRt-dependent spindle generation is unexplored. We investigated thalamic rhythmogenesis in mice lacking this subtype in isolation (CaV3.2KO mice) or in concomitance with CaV3.3 deletion (CaV3.double-knockout (DKO) mice).

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research