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Impaired Respiratory and Body Temperature Control Upon Acute Serotonergic Neuron Inhibition
Journal article   Peer reviewed

Impaired Respiratory and Body Temperature Control Upon Acute Serotonergic Neuron Inhibition

Russell Ray, Andrea Corcoran, Rachael Brust, Jun Chul Kim, George B Richerson, Eugene Nattie and Susan M Dymecki
Science (American Association for the Advancement of Science), Vol.333(6042), pp.637-642
07/29/2011
DOI: 10.1126/science.1205295
PMCID: PMC3729433
PMID: 21798952
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3729433View
Open Access

Abstract

Physiological homeostasis is essential for organism survival. Highly responsive neuronal networks are involved but constituent neurons are just beginning to be resolved. To query brain serotonergic neurons in homeostasis, we used a synthetic GPCR (Di)-based neuronal silencing tool, mouse RC∷FPDi , designed for cell type-specific, ligand (clozapine-N-oxide, CNO)-inducible and reversible suppression of action potential firing. In mice harboring Di-expressing serotonergic neurons, CNO administration by systemic injection attenuated the chemoreflex that normally increases respiration in response to tissue CO 2 elevation and acidosis. At the cellular level, CNO suppressed firing rate increases evoked by CO 2 /acidosis. Body thermoregulation at room temperature was also disrupted following CNO triggering of Di; core temperatures plummeted, then recovered. This work establishes that serotonergic neurons regulate life-sustaining respiratory and thermoregulatory networks, and demonstrates a noninvasive tool for mapping neuron function.

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