Substance P regulates Tacr1 neurons, which control nitric oxide-mediated neurovascular coupling in the mouse cortex.

Authors

Fernanda Juarez Anaya, Jiwon Kim, Sarah E Ross, Alberto L Vazquez

Published in

Science advances. Volume 12. Issue 27. Pages eadx5109. Jul 03, 2026. Epub Jul 03, 2026.

Abstract

Neuronal activity-driven increases in cerebral blood flow (CBF), known as neurovascular coupling (NVC), are crucial for sustaining the metabolic demands of the brain. Our group has found that Tacr1 neurons, a subset of somatostatin neurons expressing the substance P (SP) receptor and neuronal nitric oxide synthase (nNOS), exert a disproportionately large regulation of CBF. Here, we use two-photon imaging to show that Tacr1 neurons regulate CBF through nitric oxide (NO) release and SP-receptor signaling . We identify astrocytic calcium (Ca²⁺) transients as a secondary response to vasodilation. To identify potential sources of SP in somatosensory cortex, viral mapping revealed Tac1-positive neurons locally, predominantly among parvalbumin (PV) neurons, as well as Tac1-positive long-range projections from perirhinal cortex. Functional analyses indicate that PV neurons regulate CBF through a Tacr1 neuron dependent pathway. These findings suggest a sequential mechanism whereby Tacr1 neurons respond to SP to release NO, inducing vasodilation and driving astrocytic Ca²⁺ signaling.

PMID:
42397904
Bibliographic data and abstract were imported from PubMed on 04 Jul 2026.

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