Role of the pons in hypoxic respiratory depression in the neonatal rat.
The main purpose of this study was to evaluate the role of the pons in hypoxic respiratory depression (HRD) of the neonatal rat. Experiments were conducted using the isolated brainstem-spinal cord preparation of the neonatal rat (1-3 days old). The brainstem was transected at various levels. We found that ablation of the diencephalon decreased respiratory frequency (fR), and conversely, that ablation of the midbrain or pons increased fR. In the preparation with the pons intact (without the midbrain), hypoxia (superfusate PO2 = 56 mmHg) caused strong depression of respiratory activity, which was characterized by a steady decrease in fR and in integrated inspiratory burst amplitude (integral of Phr). In the preparation with the intact ventral pons (without midbrain and dorsal pons) we observed similar, though weaker, HRD. When the entire pons was ablated, integral of Phr was little depressed by hypoxia and thus, HRD was further attenuated. We conclude that the pons contributes importantly to the induction of hypoxic respiratory depression in the neonatal rat. Both the ventral and dorsal portions of the pons are involved in the control of hypoxic respiratory depression. In addition, we show that the respiratory modulatory functions of the diencephalon (facilitating) and midbrain (inhibitory) are already expressed at the time of birth.
Okada
Y
Y
Institut für Physiologie, Ruhr-Universität Bochum, Germany. neuron@nic.med.keio.ac.jp
Kawai
A
A
Mückenhoff
K
K
Scheid
P
P
D000818:Animals; D000831:Animals, Newborn; D001933:Brain Stem / Q000502:physiology / Q000601:surgery; D004027:Diencephalon / Q000502:physiology / Q000601:surgery; D004594:Electrophysiology; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008636:Mesencephalon / Q000502:physiology / Q000601:surgery; D011149:Pons / Q000502:physiology* / Q000601:surgery; D012123:Pulmonary Ventilation / Q000502:physiology*; D051381:Rats; D012131:Respiratory Insufficiency / Q000503:physiopathology*