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Somatostatin-expressing interneurons induce early NO-driven and late specific astrocyte-mediated vasodilation
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Somatostatin-expressing interneurons induce early NO-driven and late specific astrocyte-mediated vasodilation
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Journal Article
Somatostatin-expressing interneurons induce early NO-driven and late specific astrocyte-mediated vasodilation
2025
Overview
Somatostatin-expressing (SST) interneurons modulate hemodynamic responses both directly and indirectly, but their precise role remains unclear. Here, we investigated the influence of SST interneurons on hemodynamic control in response to optogenetic stimulation of SST neurons and somatosensory stimulation in both awake and anesthetized mice. Prolonged optogenetic stimulation of SST neurons induces fast vasodilation through nitric oxide synthase-expressing neurons that co-express SST, and slow vasodilation mediated by astrocytes. Similar neurovascular coupling mechanisms are observed during prolonged sensory stimulation, which also induces both fast and delayed vasodilation. The delayed vasodilation, mediated by the SST neuron-astrocyte pathway, enhances the specificity of cerebral blood volume (CBV)-weighted fMRI signals to cortical layer 4, as confirmed by chemogenetic inhibition of SST neurons. Our findings indicate that the SST neuron-astrocyte-vascular pathway shapes hemodynamic responses to prolonged stimulation and is critical for achieving high-specificity, laminar-resolution fMRI, which is increasingly pursued in human cognitive studies.
The precise role of somatostatin-expressing interneurons in regulating hemodynamics remains unclear. Here, authors find that the activation of these neurons induces astrocytic calcium signaling, which subsequently drives delayed vasodilation and enhances layer-specific fMRI signals in response to prolonged sensory stimulation.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
