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Attenuated baroreflex in a Parkinson's disease animal model coincides with impaired activation of non-C1 neurons.
Auton Neurosci. 2020 Feb 15; 225:102655.AN

Abstract

Orthostatic hypotension is one of the most common symptoms observed in Parkinson's disease (PD), a neurodegenerative disease caused by death of dopaminergic neurons in the substantia nigra pars compacta (SNc), and it is associated with denervation of the heart and impairment of the baroreflex. Here, we aimed to investigate if the impaired baroreflex was associated with lower activation of cardiovascular brainstem areas in a 6-hydroxydopamine (6-OHDA) animal model of PD. The PD model was generated with male Wistar rats by injection of 6-OHDA or vehicle into the striatum. After 20 or 60 days, the femoral vein and artery were cannulated to assess cardiovascular parameters during injection of sodium nitroprusside (SNP) or phenylephrine (Phe). Brainstem slices were submitted to immunohistochemistry and immunofluorescence. After 6-OHDA injection, 75% of the dopaminergic neurons in the SNc were absent, confirming establishment of the PD model. Intravenous (iv) injection of SNP generated reduced hypotension and tachycardia response, and the noncatecholaminergic (nonC1) neurons of the rostral ventrolateral medulla (RVLM) were less activated. Additionally, iv injection of Phe increased blood pressure and bradycardia to the same extent and activated equivalent numbers of neurons in the nucleus of the solitary tract and the caudal ventrolateral medulla as well as cholinergic neurons of the dorsal motor nucleus of the vagus and the nucleus ambiguus between control and PD animals. In summary, these data showed that in the PD model, impairment of cardiovascular autonomic control was observed only during deactivation of the baroreflex, which could be related to reduced activation of non-C1 neurons within the RVLM.

Authors+Show Affiliations

Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, Brazil.Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, Brazil.Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, Brazil. Electronic address: takakura@icb.usp.br.Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, Brazil. Electronic address: barbaraf@icb.usp.br.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32092676

Citation

Cabral, Laís M., et al. "Attenuated Baroreflex in a Parkinson's Disease Animal Model Coincides With Impaired Activation of non-C1 Neurons." Autonomic Neuroscience : Basic & Clinical, vol. 225, 2020, p. 102655.
Cabral LM, Moreira TS, Takakura AC, et al. Attenuated baroreflex in a Parkinson's disease animal model coincides with impaired activation of non-C1 neurons. Auton Neurosci. 2020;225:102655.
Cabral, L. M., Moreira, T. S., Takakura, A. C., & Falquetto, B. (2020). Attenuated baroreflex in a Parkinson's disease animal model coincides with impaired activation of non-C1 neurons. Autonomic Neuroscience : Basic & Clinical, 225, 102655. https://doi.org/10.1016/j.autneu.2020.102655
Cabral LM, et al. Attenuated Baroreflex in a Parkinson's Disease Animal Model Coincides With Impaired Activation of non-C1 Neurons. Auton Neurosci. 2020 Feb 15;225:102655. PubMed PMID: 32092676.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Attenuated baroreflex in a Parkinson's disease animal model coincides with impaired activation of non-C1 neurons. AU - Cabral,Laís M, AU - Moreira,Thiago S, AU - Takakura,Ana C, AU - Falquetto,Bárbara, Y1 - 2020/02/15/ PY - 2019/10/31/received PY - 2019/12/12/revised PY - 2020/02/14/accepted PY - 2020/2/25/pubmed PY - 2020/2/25/medline PY - 2020/2/25/entrez KW - 6-OHDA KW - Baroreflex KW - Parkinson's disease KW - fos SP - 102655 EP - 102655 JF - Autonomic neuroscience : basic & clinical JO - Auton Neurosci VL - 225 N2 - Orthostatic hypotension is one of the most common symptoms observed in Parkinson's disease (PD), a neurodegenerative disease caused by death of dopaminergic neurons in the substantia nigra pars compacta (SNc), and it is associated with denervation of the heart and impairment of the baroreflex. Here, we aimed to investigate if the impaired baroreflex was associated with lower activation of cardiovascular brainstem areas in a 6-hydroxydopamine (6-OHDA) animal model of PD. The PD model was generated with male Wistar rats by injection of 6-OHDA or vehicle into the striatum. After 20 or 60 days, the femoral vein and artery were cannulated to assess cardiovascular parameters during injection of sodium nitroprusside (SNP) or phenylephrine (Phe). Brainstem slices were submitted to immunohistochemistry and immunofluorescence. After 6-OHDA injection, 75% of the dopaminergic neurons in the SNc were absent, confirming establishment of the PD model. Intravenous (iv) injection of SNP generated reduced hypotension and tachycardia response, and the noncatecholaminergic (nonC1) neurons of the rostral ventrolateral medulla (RVLM) were less activated. Additionally, iv injection of Phe increased blood pressure and bradycardia to the same extent and activated equivalent numbers of neurons in the nucleus of the solitary tract and the caudal ventrolateral medulla as well as cholinergic neurons of the dorsal motor nucleus of the vagus and the nucleus ambiguus between control and PD animals. In summary, these data showed that in the PD model, impairment of cardiovascular autonomic control was observed only during deactivation of the baroreflex, which could be related to reduced activation of non-C1 neurons within the RVLM. SN - 1872-7484 UR - https://www.unboundmedicine.com/medline/citation/32092676/Attenuated_baroreflex_in_a_Parkinson's_disease_animal_model_coincides_with_impaired_activation_of_non-C1_neurons L2 - https://linkinghub.elsevier.com/retrieve/pii/S1566-0702(19)30266-8 DB - PRIME DP - Unbound Medicine ER -
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