Synaptic-like transmission between neural axons and arteriolar smooth muscle cells drives cerebral neurovascular coupling.
Nat Neurosci
; 27(2): 232-248, 2024 Feb.
Article
in En
| MEDLINE
| ID: mdl-38168932
ABSTRACT
Neurovascular coupling (NVC) is important for brain function and its dysfunction underlies many neuropathologies. Although cell-type specificity has been implicated in NVC, how active neural information is conveyed to the targeted arterioles in the brain remains poorly understood. Here, using two-photon focal optogenetics in the mouse cerebral cortex, we demonstrate that single glutamatergic axons dilate their innervating arterioles via synaptic-like transmission between neural-arteriolar smooth muscle cell junctions (NsMJs). The presynaptic parental-daughter bouton makes dual innervations on postsynaptic dendrites and on arteriolar smooth muscle cells (aSMCs), which express many types of neuromediator receptors, including a low level of glutamate NMDA receptor subunit 1 (Grin1). Disruption of NsMJ transmission by aSMC-specific knockout of GluN1 diminished optogenetic and whisker stimulation-caused functional hyperemia. Notably, the absence of GluN1 subunit in aSMCs reduced brain atrophy following cerebral ischemia by preventing Ca2+ overload in aSMCs during arteriolar constriction caused by the ischemia-induced spreading depolarization. Our findings reveal that NsMJ transmission drives NVC and open up a new avenue for studying stroke.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Neurovascular Coupling
Limits:
Animals
Language:
En
Journal:
Nat Neurosci
Year:
2024
Document type:
Article