Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease

The underlying cause of respiratory impairments appearing in Parkinson’s disease (PD) is still far from being elucidated. To better understand the pathogenesis of respiratory disorders appearing in PD, we studied hypoglossal (HG) and phrenic (PHR) motoneuron dysfunction in a rat model evoked with re...

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Main Authors: Monika Jampolska, Kryspin Andrzejewski, Małgorzata Zaremba, Ilona Joniec-Maciejak, Katarzyna Kaczyńska
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/10/3/531
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author Monika Jampolska
Kryspin Andrzejewski
Małgorzata Zaremba
Ilona Joniec-Maciejak
Katarzyna Kaczyńska
author_facet Monika Jampolska
Kryspin Andrzejewski
Małgorzata Zaremba
Ilona Joniec-Maciejak
Katarzyna Kaczyńska
author_sort Monika Jampolska
collection DOAJ
description The underlying cause of respiratory impairments appearing in Parkinson’s disease (PD) is still far from being elucidated. To better understand the pathogenesis of respiratory disorders appearing in PD, we studied hypoglossal (HG) and phrenic (PHR) motoneuron dysfunction in a rat model evoked with reserpine administration. After reserpine, a decrease in the baseline amplitude and minute HG activity was noted, and no depressive phase of the hypoxic ventilatory response was observed. The pre-inspiratory time of HG activity along with the ratio of pre-inspiratory time to total respiratory cycle time and the ratio of pre-inspiratory to inspiratory amplitude were significantly reduced during normoxia, hypoxia, and recovery compared to sham rats. We suggest that the massive depletion of not only dopamine, but above all noradrenaline and serotonin in the brainstem observed in our study, has an impact on the pre-inspiratory activity of the HG. The shortening of the pre-inspiratory activity of the HG in the reserpine model may indicate a serious problem with maintaining the correct diameter of the upper airways in the preparation phase for inspiratory effort and explain the development of obstructive sleep apnea in some PD patients. Therapies involving the supplementation of amine depletion other than dopamine should be considered.
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spelling doaj.art-d77281e6f08f4564b19e0f0f201f01112023-12-03T12:13:05ZengMDPI AGCells2073-44092021-03-0110353110.3390/cells10030531Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s DiseaseMonika Jampolska0Kryspin Andrzejewski1Małgorzata Zaremba2Ilona Joniec-Maciejak3Katarzyna Kaczyńska4Department of Respiration Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 02-106 Warsaw, PolandDepartment of Respiration Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 02-106 Warsaw, PolandDepartment of Experimental and Clinical Pharmacology, Centre for Preclinical Research (CePT), Medical University of Warsaw, 02-091 Warsaw, PolandDepartment of Experimental and Clinical Pharmacology, Centre for Preclinical Research (CePT), Medical University of Warsaw, 02-091 Warsaw, PolandDepartment of Respiration Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 02-106 Warsaw, PolandThe underlying cause of respiratory impairments appearing in Parkinson’s disease (PD) is still far from being elucidated. To better understand the pathogenesis of respiratory disorders appearing in PD, we studied hypoglossal (HG) and phrenic (PHR) motoneuron dysfunction in a rat model evoked with reserpine administration. After reserpine, a decrease in the baseline amplitude and minute HG activity was noted, and no depressive phase of the hypoxic ventilatory response was observed. The pre-inspiratory time of HG activity along with the ratio of pre-inspiratory time to total respiratory cycle time and the ratio of pre-inspiratory to inspiratory amplitude were significantly reduced during normoxia, hypoxia, and recovery compared to sham rats. We suggest that the massive depletion of not only dopamine, but above all noradrenaline and serotonin in the brainstem observed in our study, has an impact on the pre-inspiratory activity of the HG. The shortening of the pre-inspiratory activity of the HG in the reserpine model may indicate a serious problem with maintaining the correct diameter of the upper airways in the preparation phase for inspiratory effort and explain the development of obstructive sleep apnea in some PD patients. Therapies involving the supplementation of amine depletion other than dopamine should be considered.https://www.mdpi.com/2073-4409/10/3/531Parkinson’s diseasesbiogenic aminesreserpine modelhypoxiahypoglossal nervephrenic nerve
spellingShingle Monika Jampolska
Kryspin Andrzejewski
Małgorzata Zaremba
Ilona Joniec-Maciejak
Katarzyna Kaczyńska
Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
Cells
Parkinson’s diseases
biogenic amines
reserpine model
hypoxia
hypoglossal nerve
phrenic nerve
title Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
title_full Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
title_fullStr Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
title_full_unstemmed Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
title_short Deficiency of Biogenic Amines Modulates the Activity of Hypoglossal Nerve in the Reserpine Model of Parkinson’s Disease
title_sort deficiency of biogenic amines modulates the activity of hypoglossal nerve in the reserpine model of parkinson s disease
topic Parkinson’s diseases
biogenic amines
reserpine model
hypoxia
hypoglossal nerve
phrenic nerve
url https://www.mdpi.com/2073-4409/10/3/531
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