Several evidences suggest that obstructive sleep apnea may contribute to the development of cardiovascular diseases such as hypertension. However, the mechanisms involved and the role of carotid chemoreceptors are not clear yet. Recently we developed a method to produce obstructive apnea in rats that reproduces the respiratory effort, hypoxia, and hypercapnia observed in sleep apnea patients. In this study, we investigated the brain stem areas activated by apnea in non-anesthetized rats with or without carotid chemoreceptors. Male Wistar rats (300-350 g) were anesthetized i.p. with ketamine (100 mg/kg) and xylazine (20 mg/kg), and tracheal balloon, femoral vein cannula, and subcutaneous EKG electrodes were implanted. One week later, 14 s apneas were induced every 2 min for 1 h in 4 rats. The control group (with tracheal balloon) had no exposition to apnea protocol. Thirty min after the end of apnea rats were perfused. The brain was removed and processed for immunohistochemistry to Fos and tyrosine hydroxylase (TH) (a marker for catecholaminergic neurons). In another group of rats (n=4), the arterial chemoreceptors were inactivated 7 days after implantation of the tracheal balloon by ligation and section of the carotid body arteries. In these rats, carotid chemoreceptor function was abolished (no bradycardia after i.v. injection of 40 μg KCN). Two days after chemoreceptor inactivation, the animals were subjected to the same apnea protocol described previously. In control rats very few or no Fos was detectable. Apnea induced intense Fos expression in commissural and intermediate nucleus of the solitary tract (NTS), and in caudal and rostral ventrolateral medulla (CVLM and RVLM). With respect to the catecholaminergic groups in the brain stem, we observed Fos in 42% of the C1 neurons, 11% in the A1 neurons, 18% in the A2 neurons, and 18% in the C2 neurons. Inactivation of the carotid chemoreceptors reduced apnea-induced Fos expression in the comissural NTS (from 210 ± 5 to 153 ± 3 neurons, mean ± SEM) and intermediate NTS (from 94 ± 13 to 57 ± 7 neurons), but not in CVLM and RVLM. Fos expression in the catecholaminergic cell groups was also reduced (C1: 42% to 23%, A1: 11% to 2%, A2: 18% to 9%, C2: 18% to 4%). We conclude that apnea actives neurons in regions involved with processing the baroreceptors, chemoreceptors, pulmonary stretch receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors. Signals from carotid chemoreceptors contribute to activation in NTS region, but apnea induces additional signals that contribute to neuronal activation. This is compatible with the presence of apnea-induced pressor responses, bradycardic, and breathing effort after carotid chemoreceptor activation.