Impaired Breathing During Exposure to Hypoxia and Carotid Body Dysfunction in an Animal Model of Parkinson's Disease
Impaired Breathing During Exposure to Hypoxia and Carotid Body Dysfunction in an Animal Model of Parkinson's Disease
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Original abstract
ABSTRACTBackgroundParkinson's disease (PD) manifestations involve respiratory dysfunction and motor disability. Previous research on PD has mainly focused on central dopamine (DA) deficits and their effect on ventilation.ObjectivesThe purpose of the study was to analyze the function of carotid bodies (CB), sensors of blood O2, by studying the hypoxic ventilatory response (HVR) and measuring biogenic amine content in the CB of a 6‐hydroxydopamine (6‐OHDA) induced PD model. We also investigated the effects of supplementation with the DA biosynthesis precursor L‐DOPA on HVR and central DA depletion on hypoxic phrenic (PHR) and hypoglossal (HG) nerve activity.MethodsAfter 6‐OHDA intrastriatal injection, awake Wistar rats were tested in a plethysmographic chamber to study the HVR (8% O2) before and after L‐DOPA treatment. Registration of PHR and HG under acute hypoxia (8% O2) was performed in anesthetized rats.ResultsThe 6‐OHDA rats showed reduced normoxic ventilation and HVR, eliminated by L‐DOPA treatment. Increased HG activity during hypoxia in the form of increased amplitude and pre‐inspiratory amplitude was observed. In addition to decreased striatal levels of DA, serotonin (5‐HT) and noradrenaline (NA), reduced NA (42%) and 5‐HT (52%) were found in CB of 6‐OHDA rats. The open‐field test showed a decrease in motor activity 2 weeks after the lesion.ConclusionsOur results showed NA and 5‐HT deficits in CB in the PD model, which may be responsible for impaired HVR. L‐DOPA treatment, replenishing DA deficiency in the striatum, stimulated HVR. Increased pre‐inspiratory HG activity indicates modifications to the central mechanisms controlling their activity.