Impaired Respiratory and Body Temperature Control Upon Acute Serotonergic Neuron Inhibition

• DOI: 10.1126/science.1205295
• Publication Date: 2011-07-28T19:20:38Z
• Authors: Russell S. Ray; Andrea E. Corcoran; Rachael D. Brust; Jun Chul Kim; George B. Richerson; Eugene Nattie; Susan M. Dymecki
• Keywords: Homeostasis

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