Role of serotonergic dorsal raphe neurons in hypercapnia-induced arousals

Satvinder Kaur, Roberto Luca, Mudasir A. Khanday, Sathyajit S. Bandaru, Renner C. Thomas, Rebecca Y. Broadhurst, Anne Venner, William D. Todd, Patrick M. Fuller, Elda Arrigoni and Clifford B. Saper ()
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Satvinder Kaur: Beth Israel Deaconess Medical Center and Harvard Medical School
Roberto Luca: Beth Israel Deaconess Medical Center and Harvard Medical School
Mudasir A. Khanday: Beth Israel Deaconess Medical Center and Harvard Medical School
Sathyajit S. Bandaru: Beth Israel Deaconess Medical Center and Harvard Medical School
Renner C. Thomas: Beth Israel Deaconess Medical Center and Harvard Medical School
Rebecca Y. Broadhurst: Beth Israel Deaconess Medical Center and Harvard Medical School
Anne Venner: Beth Israel Deaconess Medical Center and Harvard Medical School
William D. Todd: Beth Israel Deaconess Medical Center and Harvard Medical School
Patrick M. Fuller: Beth Israel Deaconess Medical Center and Harvard Medical School
Elda Arrigoni: Beth Israel Deaconess Medical Center and Harvard Medical School
Clifford B. Saper: Beth Israel Deaconess Medical Center and Harvard Medical School

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract During obstructive sleep apnea, elevation of CO2 during apneas contributes to awakening and restoring airway patency. We previously found that glutamatergic neurons in the external lateral parabrachial nucleus (PBel) containing calcitonin gene related peptide (PBelCGRP neurons) are critical for causing arousal during hypercapnia. However, others found that genetic deletion of serotonin (5HT) neurons in the brainstem also prevented arousal from hypercapnia. To examine interactions between the two systems, we showed that dorsal raphe (DR) 5HT neurons selectively targeted the PBel. Either genetically directed deletion or acute optogenetic silencing of DRSert neurons dramatically increased the latency of mice to arouse during hypercapnia, as did silencing DRSert terminals in the PBel. This effect was mediated by 5HT2a receptors which are expressed by PBelCGRP neurons. Our results indicate that the serotonergic input from the DR to the PBel via 5HT2a receptors is critical for modulating the sensitivity of the PBelCGRP neurons that cause arousal to rising levels of blood CO2.

Date: 2020
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DOI: 10.1038/s41467-020-16518-9

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