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Characterization of alterations in basal inspiratory motor output and chemical control of breathing in two Parkinson's Disease rat models
Author(s) -
Solomon Irene C.,
Tuchinsky Jacob J.,
Brogan Anna,
Wadolowski Robert M.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.913.8
Subject(s) - medial forebrain bundle , control of respiration , parkinson's disease , basal (medicine) , respiratory system , medicine , basal ganglia , basal forebrain , endocrinology , anesthesia , neuroscience , chemistry , psychology , central nervous system , dopamine , dopaminergic , disease , insulin
Respiratory dysfunction in Parkinson's Disease (PD) patients manifests as a variety of altered breathing patterns that are suggested to result from impairment of central respiratory control. Experimental rodent (rat) PD models have been developed and studied in order to gain insight into both the motor and non‐motor symptoms that underlie PD; however, very few studies have focused on central respiratory deficits in any of these models. Ongoing work in our laboratory has begun to address this issue by characterizing the alterations in basal inspiratory motor output (tongue and/or diaphragm EMG activity) and chemical control of breathing in the 6‐hydroxydopamine (6‐OHDA) neurotoxin‐induced unilateral substantia nigra (SN)‐ and medial forebrain bundle (MFB)‐lesioned rat PD models. For these studies, experiments were conducted in spontaneously breathing urethane‐anesthetized adult female rats 2‐weeks after SN (n=6) or MFB (n=8) 6‐OHDA injections; control rats received vehicle injections (SN, n=5; MFB, n=5). Following recording of basal inspiratory‐related activity, rats were exposed to either hypoxic (12% O 2 for 90s; HVR) or hypercapnic (7% CO 2 for 5 min; HCVR) gas. Our preliminary data indicate that both SN‐ and MFB‐lesioned rats exhibited alterations in respiratory activity but the respiratory behaviors noted were not identical. Compared to control rats, SN‐lesioned rats exhibited (1) slightly higher basal breathing frequency; (2) similar HVR frequency increase; (3) attenuated HVR amplitude increase; and (4) similar HCVR frequency and amplitude increases. In contrast, MFB‐lesioned rats (compared to control rats) exhibited (1) similar basal breathing frequency; (2) slightly enhanced HVR frequency increase; (3) no change or a decrease in HVR amplitude; (4) markedly reduced or absent HCVR frequency increase; and (5) similar HCVR amplitude increase. While these 6‐OHDA site‐targeted PD models appear to exhibit differences in basal respiratory behaviors and chemical control of breathing deficits, our preliminary observations indicate that both SN‐ and MFB‐lesioned rats are viable models for studying respiratory abnormalities in PD. However, we suggest that it may be necessary to study multiple PD models to fully capture the ventilatory abnormalities seen in PD patients and identify the mechanisms that underlie these respiratory abnormalities. Support or Funding Information NIH NS101737; Thomas Hartman Center for Parkinson's Disease Research at Stony Brook University This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .