Literature DB >> 9496472

Role of the pons in hypoxic respiratory depression in the neonatal rat.

Y Okada1, A Kawai, K Mückenhoff, P Scheid.   

Abstract

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.

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Year:  1998        PMID: 9496472     DOI: 10.1016/s0034-5687(97)00105-9

Source DB:  PubMed          Journal:  Respir Physiol        ISSN: 0034-5687


  13 in total

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3.  Growth restriction induced by chronic prenatal hypoxia affects breathing rhythm and its pontine catecholaminergic modulation.

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4.  The vesicular glutamate transporter VGLUT3 contributes to protection against neonatal hypoxic stress.

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5.  Hypoxia-sensing properties of the newborn rat ventral medullary surface in vitro.

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Review 7.  The chemical neuroanatomy of breathing.

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10.  Ablation of Zfhx4 results in early postnatal lethality by disrupting the respiratory center in mice.

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