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Raphe magnus nucleus is involved in ventilatory but not hypothermic response to CO₂

¹Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo; ²Department of Animal Morphology and Physiology, UNESP-São Paulo State University; and ³Department of Physiology, Dental School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil

Submitted 18 April 2007 ; accepted in final form 27 August 2007

There is evidence that serotonin [5-hydroxytryptamine (5-HT)] is involved in the physiological responses to hypercapnia. Serotonergic neurons represent the major cell type (comprising 15–20% of the neurons) in raphe magnus nucleus (RMg), which is a medullary raphe nucleus. In the present study, we tested the hypothesis 1) that RMg plays a role in the ventilatory and thermal responses to hypercapnia, and 2) that RMg serotonergic neurons are involved in these responses. To this end, we microinjected 1) ibotenic acid to promote nonspecific lesioning of neurons in the RMg, or 2) anti-SERT-SAP (an immunotoxin that utilizes a monoclonal antibody to the third extracellular domain of the serotonin reuptake transporter) to specifically kill the serotonergic neurons in the RMg. Hypercapnia caused hyperventilation and hypothermia in all groups. RMg nonspecific lesions elicited a significant reduction of the ventilatory response to hypercapnia due to lower tidal volume (VT) and respiratory frequency. Rats submitted to specific killing of RMg serotonergic neurons showed no consistent difference in ventilation during air breathing but had a decreased ventilatory response to CO₂ due to lower VT. The hypercapnia-induced hypothermia was not affected by specific or nonspecific lesions of RMg serotonergic neurons. These data suggest that RMg serotonergic neurons do not participate in the tonic maintenance of ventilation during air breathing but contribute to the ventilatory response to CO₂. Ultimately, this nucleus may not be involved in the thermal responses to CO₂.

hypercapnia; ventilation; serotonin

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