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Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model.
Brain Pathol 2015; 25(4):377-90BP

Abstract

The administration of reserpine to rodents was one of the first models used to investigate the pathophysiology and screening for potential treatments of Parkinson's disease (PD). The reserpine model was critical to the understanding of the role of monoamine system in the regulation of motor and affective disorders, as well as the efficacy of current PD treatments, such as L-DOPA and dopamine agonists. Nevertheless, with the introduction of toxin-induced and genetic models of PD, reserpine became underused. The main rationale to this drawback was the supposed absence of reserpine construct validity with PD. Here, we highlight classical and recent experimental findings that support the face, pharmacological, and construct validity of reserpine PD model and reason against the current rationale for its underuse. We also aim to shed a new perspective upon the model by discussing the main challenges and potentials for the reserpine model of PD.

Authors+Show Affiliations

Memory Studies Laboratory, Department of Physiology, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil.Memory Studies Laboratory, Department of Physiology, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil.Biology Department, Universidade Federal de Sergipe, São Cristóvão, SE, Brazil.Memory Studies Laboratory, Department of Physiology, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil. Department of Biosciences, Universidade Federal de São Paulo, Santos, SP, Brazil.Memory Studies Laboratory, Department of Physiology, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil. Behavioral Neuroscience Laboratory, Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP, Brazil.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25726735

Citation

Leão, Anderson H F F., et al. "Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model." Brain Pathology (Zurich, Switzerland), vol. 25, no. 4, 2015, pp. 377-90.
Leão AH, Sarmento-Silva AJ, Santos JR, et al. Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model. Brain Pathol. 2015;25(4):377-90.
Leão, A. H., Sarmento-Silva, A. J., Santos, J. R., Ribeiro, A. M., & Silva, R. H. (2015). Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model. Brain Pathology (Zurich, Switzerland), 25(4), pp. 377-90. doi:10.1111/bpa.12253.
Leão AH, et al. Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model. Brain Pathol. 2015;25(4):377-90. PubMed PMID: 25726735.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinson's Disease: New Perspectives to a Long-Standing Model. AU - Leão,Anderson H F F, AU - Sarmento-Silva,Aldair J, AU - Santos,José R, AU - Ribeiro,Alessandra M, AU - Silva,Regina H, Y1 - 2015/04/22/ PY - 2014/11/18/received PY - 2015/02/23/accepted PY - 2015/3/3/entrez PY - 2015/3/3/pubmed PY - 2016/3/16/medline KW - Parkinson's disease KW - animal model KW - dopamine KW - reserpine KW - rodent SP - 377 EP - 90 JF - Brain pathology (Zurich, Switzerland) JO - Brain Pathol. VL - 25 IS - 4 N2 - The administration of reserpine to rodents was one of the first models used to investigate the pathophysiology and screening for potential treatments of Parkinson's disease (PD). The reserpine model was critical to the understanding of the role of monoamine system in the regulation of motor and affective disorders, as well as the efficacy of current PD treatments, such as L-DOPA and dopamine agonists. Nevertheless, with the introduction of toxin-induced and genetic models of PD, reserpine became underused. The main rationale to this drawback was the supposed absence of reserpine construct validity with PD. Here, we highlight classical and recent experimental findings that support the face, pharmacological, and construct validity of reserpine PD model and reason against the current rationale for its underuse. We also aim to shed a new perspective upon the model by discussing the main challenges and potentials for the reserpine model of PD. SN - 1750-3639 UR - https://www.unboundmedicine.com/medline/citation/25726735/Molecular_Neurochemical_and_Behavioral_Hallmarks_of_Reserpine_as_a_Model_for_Parkinson's_Disease:_New_Perspectives_to_a_Long_Standing_Model_ L2 - https://doi.org/10.1111/bpa.12253 DB - PRIME DP - Unbound Medicine ER -