| First Author | Severs LJ | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 5300 |
| PubMed ID | 37652903 | Mgi Jnum | J:340554 |
| Mgi Id | MGI:7527889 | Doi | 10.1038/s41467-023-40812-x |
| Citation | Severs LJ, et al. (2023) Purinergic signaling mediates neuroglial interactions to modulate sighs. Nat Commun 14(1):5300 |
| abstractText | 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 preBotzinger complex (preBotC). 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 preBotC 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 preBotC 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 preBotC network, where the distinct modulatory responses of neurons and glia allow for both rhythms to be independently regulated. |
