Brain endothelial gap junction coupling enables rapid vasodilation propagation during neurovascular coupling, 2025, Krolak et al.

[SNT Gatchaman]

Brain endothelial gap junction coupling enables rapid vasodilation propagation during neurovascular coupling
Trevor Krolak; Luke Kaplan; Kathleen Navas; Lujing Chen; Austin Birmingham; Daniel Ryvkin; Victoria Izsa; Megan Powell; Zhuhao Wu; Benjamin E. Deverman; Chenghua Gu

To meet the brain's moment-to-moment energy demand, neural activation rapidly increases local blood flow. This process, known as neurovascular coupling, involves rapid, coordinated vasodilation of the brain's arterial network.

Here, we demonstrate that endothelial gap junction coupling enables long-range propagation of vasodilation signals through the vasculature during neurovascular coupling. The molecular composition of these gap junctions is zonated along the arterio-venous axis, with arteries being the most strongly coupled segment. Using optogenetics and visual stimuli in awake mice, we found that acute, arterial endothelial cell type-specific deletion of Cx37 and Cx40 abolishes arterial gap junction coupling and results in impaired vasodilation. Specifically, we demonstrated that arterial endothelial gap junction coupling determines both the speed and the spatial extent of vasodilation propagation elicited by neural activity.

These findings indicate that endothelial gap junctions serve as a signaling highway for neurovascular coupling, enabling flexible and efficient distribution of limited energetic resources.

HIGHLIGHTS
• Non-invasive tracing method for in vivo visualization of gap junction coupling

• Connexin expression and cell-cell coupling strength vary along the arterio-venous axis

• Arterial gap junction coupling enables neurally evoked long-range dilations

• Endothelial gap junctions set the speed and spatial extent of vasodilation spread

Web | PDF | Cell | Open Access

 

[Utsikt]

Do we known the genes involved here?

Using optogenetics and visual stimuli in awake mice, we found that acute, arterial endothelial cell type-specific deletion of Cx37 and Cx40 abolishes arterial gap junction coupling and results in impaired vasodilation.

 

[Creekside]

My question is: how large of an effect is involved? With neurovascular coupling shut down, were the mice seriously impaired, or did they simply score slightly less on maze-wandering or some such thing?