Purinergic signaling mediates neuroglial interactions to modulate sighs

Liza J. Severs (), Nicholas E. Bush, Lely A. Quina, Skyler Hidalgo-Andrade, Nicholas J. Burgraff, Tatiana Dashevskiy, Andy Y. Shih, Nathan A. Baertsch and Jan-Marino Ramirez ()
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Liza J. Severs: Seattle Children’s Research Institute
Nicholas E. Bush: Seattle Children’s Research Institute
Lely A. Quina: Seattle Children’s Research Institute
Skyler Hidalgo-Andrade: Seattle Children’s Research Institute
Nicholas J. Burgraff: Seattle Children’s Research Institute
Tatiana Dashevskiy: Seattle Children’s Research Institute
Andy Y. Shih: Seattle Children’s Research Institute
Nathan A. Baertsch: Seattle Children’s Research Institute
Jan-Marino Ramirez: Seattle Children’s Research Institute

Nature Communications, 2023, vol. 14, issue 1, 1-14

Abstract: Abstract Sighs prevent the collapse of alveoli in the lungs, initiate arousal under hypoxic conditions, and are an expression of sadness and relief. Sighs are periodically superimposed on normal breaths, known as eupnea. Implicated in the generation of these rhythmic behaviors is the preBötzinger complex (preBötC). Our experimental evidence suggests that purinergic signaling is necessary to generate spontaneous and hypoxia-induced sighs in a mouse model. Our results demonstrate that driving calcium increases in astrocytes through pharmacological methods robustly increases sigh, but not eupnea, frequency. Calcium imaging of preBötC slices corroborates this finding with an increase in astrocytic calcium upon application of sigh modulators, increasing intracellular calcium through g-protein signaling. Moreover, photo-activation of preBötC astrocytes is sufficient to elicit sigh activity, and this response is blocked with purinergic antagonists. We conclude that sighs are modulated through neuron-glia coupling in the preBötC network, where the distinct modulatory responses of neurons and glia allow for both rhythms to be independently regulated.

Date: 2023
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DOI: 10.1038/s41467-023-40812-x

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