Effect of 6-OHDA on hypercapnic ventilatory response in the rat model of Parkinson's disease
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
30628829
DOI
10.33549/physiolres.933949
PII: 933949
Knihovny.cz E-resources
- MeSH
- Medial Forebrain Bundle drug effects physiology MeSH
- Hypercapnia physiopathology MeSH
- Rats MeSH
- Oxidopamine toxicity MeSH
- Parkinsonian Disorders chemically induced physiopathology MeSH
- Pulmonary Ventilation drug effects physiology MeSH
- Rats, Wistar MeSH
- Sympatholytics toxicity MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Oxidopamine MeSH
- Sympatholytics MeSH
Breathing impairments, such as an alteration in breathing pattern, dyspnoea, and sleep apnoea, are common health deficits recognised in Parkinson's disease (PD). The mechanism that underlies these disturbances, however, remains unclear. We investigated the effect of the unilateral damage to the rat nigrostriatal pathway on the central ventilatory response to hypercapnia, evoked by administering 6-hydroxydopamine (6-OHDA) into the right medial forebrain bundle (MFB). The respiratory experiments were carried out in conscious animals in the plethysmography chamber. The ventilatory parameters were studied in normocapnic and hyperoxic hypercapnia before and 14 days after the neurotoxin injection. Lesion with the 6-OHDA produced an increased tidal volume during normoxia. The magnified response of tidal volume and a decrease of breathing frequency to hypercapnia were observed in comparison to the pre-lesion and sham controls. Changes in both respiratory parameters resulted in an increase of minute ventilation of the response to CO(2) by 28% in comparison to the pre-lesion state at 60 s. Our results demonstrate that rats with implemented unilateral PD model presented an altered respiratory pattern most often during a ventilatory response to hypercapnia. Preserved noradrenaline and specific changes in dopamine and serotonin characteristic for this model could be responsible for the pattern of breathing observed during hypercapnia.
References provided by Crossref.org
Respiratory Function and Dysfunction in Parkinson-Type Neurodegeneration