2016, Número 3
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Rev Mex Neuroci 2016; 17 (3)
Modelos clásicos de inducción de parkinsonismo y su comparación con la fisiopatología de la enfermedad de Parkinson
Velarde-Avalos A, Arias- Rincón AN, Arrezola-Tejeda FC, Castañedad-Achutigui FD
Idioma: Español
Referencias bibliográficas: 39
Paginas: 90-99
Archivo PDF: 1705.68 Kb.
RESUMEN
La enfermad de Parkinson (EP) es una enfermedad neurodegenerativa,
caracterizada principalmente por la muerte de las células
dopaminérgicas de la sustancia negra (SN) de la parts compacta
y por la disminución en los niveles de dopamina en las terminales
estriatales, responsables de la mayoría de las alteraciones motoras
características de esta enfermedad. Estas alteraciones bioquímicas
y motoras, son reproducidas por diferentes fármacos (anfetaminas,
reserpina), modelos basados en el uso de plaguicidas (rotenona
y paraquat) y modelos donde se utiliza sustancias toxicas (MPTP
y 6-hidroxidopamina). Todos estos modelos se caracterizan por
inducir modificaciones estructurales o funcionales de la transmisión
dopaminérgica nigroestriada. Sin embargo, ninguno de estos
modelos es capaz de reproducir en su totalidad todos los procesos
fisiopatológicos y las características clínicas que en este padecimiento
se presentan. Por lo que en este trabajo se hace una revisión de
los principales modelos basados en el uso de plaguicidas, modelos
farmacológicos y uso de toxinas, y su relevancia para el estudio de la
enfermedad, dando especial enfoque en los mecanismos de acción de
estos modelos.
REFERENCIAS (EN ESTE ARTÍCULO)
Mulcahy P, Walsh S, Paucard A, Rea K, Dowd E. Characterisation of a novel model of Parkinson’s disease by intra-striatal infusion of the pesticide rotenone. Neuroscience 2011; 181: 234-242.
Greenamyre JT, Cannon JR, Drolet R, Mastroberardino PG. Lessons from the rotenone model of Parkinson’s disease. Trends Pharmacol Sci 2010; 31: 141-142.
Masatoshi Inden, Yoshihisa Kitamura, Mari Abe, Aya Tamaki, Kazuyuki Takata and Takashi Taniguchi. Parkinsonian Rotenone Mouse Model: Reevaluation of Long-Term Administration of Rotenone in C57BL/6 Mice. Biol Pharm Bull 2011; 34: 92-96.
Won-Seok Choi, Richard D. Palmiter, Zhengui Xia1. Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a Parkinson’s disease model. J Cell Biol 2011; 192: 873–882.
Neha Sharma, Bimla Nehrucorresponding. Beneficial Effect of Vitamin E in Rotenone Induced Model of PD: Behavioural, Neurochemical and Biochemical Study. Exp Neurobiol 2013; 22: 214–223.
Nian Xiong, Jing Xiong, Min Jia, Ling Liu, Xiaowei Zhang, Zhenzhen Chen, et al. The role of autophagy in Parkinson’s disease: rotenone-based modeling. Behavioral and Brain Functions 2013; 9: 13.
Genaro Gabriel Ortiz, Fermín Paul Pacheco Moisés, Miguel Ángel Macías-Islas, Francisco Javier Jiménez-Gil, Alejandra G. Miranda-Díaz, Luís J. Flores-Alvarado, et. al. Toxicidad de plaguicidas y su asociación con la enfermedad de Parkinson. Arch Neurocien (Mex) 2011; 16: 33-39.
Phillip M. Rappolda, Mei Cuia, Adrianne S. Chessera, Jacqueline Tibbetta, Jonathan C. Grimaa, Lihua Duanc, et al. Paraquat neurotoxicity is mediated by the dopamine transporter and organic cation transporter-3. PNAS 2011; 108: 20766–20771.
Le W, Sayana P, Jankovic J. Animal models of Parkinson’s disease: a gateway to therapeutics?. Neurotherapeutics 2014; 11: 92-110.
R. Nisticò, B. Mehdawy, S. Piccirilli and N. Mercuri. Paraquat- and Rotenone-Induced Models of Parkinson’s Disease. International Journal of Immunopathology and Pharmacology 2011; 24: 313- 22.
C Berry, C La Vecchia, and P Nicotera. Paraquat and Parkinson’s disease. Cell Death and Differentiation 2010; 17: 1115-1125.
Jun Peng, Li Peng, Fang Feng Stevenson, Susan R. Doctrow, and Julie K. Andersen. Iron and Paraquat as Synergistic Environmental Risk Factors in Sporadic Parkinson’s Disease Accelerate Age-Related Neurodegeneration. The Journal of Neuroscience 2007; 27: 6914-6922.
Hongxia Zhou, Cao Huang, Jianbin Tong, Xu-Gang Xia. Early Exposure to Paraquat Sensitizes Dopaminergic Neurons to Subse-quent Silencing of PINK1 Gene Expression in Mice. International Journal of Biological Sciences 2011; 7: 1180-1187.
14. Arati A. Inamdar, Anathbandhu Chaudhuri, and Janis O’Donnell. The Protective Effect of Minocycline in a Paraquat-Induced Parkinson’s Disease Model in Drosophila is Modified in Altered Genetic Backgrounds. Parkinson’s Disease 2012; 2012: 938528.
Matthews M, Bondi C, Torres G, Moghaddam B. Reduced presynaptic dopamine activity in adolescent dorsal striatum. Neuropsychopharmacology 2013; 38: 1344-51.
Price MT, Fibiger HC. Apomorphine and amphetamine stereotypy after 6- hydroxydopamine lesions of the substantia nigra. Eur J Pharmacol 1974; 29: 249-252.
Abeliovich A, Schmitz Y, Farinas I, Choi-Lundberg D, Ho WH, Castillo PE, et al. Mice lacking alphasynuclein display functional deficits in the nigrostriatal dopamine system. Neuron 2000; 25: 239-52.
Przedborski S, Tieu K. 2006. Toxic animal models. InNeurodegenerative diseases (ed. Beal MF, et al.), pp. 196–221. Cambridge University Press, Cambridge.
Guillot TS, Shepherd KR, Richardson JR, Wang MZ, Li Y, Emson PC, Miller GW. Reduced vesicular storage of dopamine exacerbates methamphetamine-induced neurodegeneration and astrogliosis. J Neurochem 2008; 106: 2205–2217.
Carlsson A. The occurrence, distribution and physiological role of catecholamines in the nervous system. Pharmacol Rev 1959; 11: 490-493.
30. Carlsson A, Lindqvist M, Magnusson T. 3,4-Dihydroxyphenylalanine and 5- hydroxytryptophan as reserpine antagonists. Nature. 1957; 180: 1200.
Tieu K. A guide to neurotoxic animal models of Parkinson’s disease. Cold Spring Harb Perspect Med 2011; 1: a009316.
Heeringa M.J. & Abercrombie E.D. Biochemistry of somatodendritic dopamine release in substantia nigra: an in vivo comparison with striatal dopamine release. J. Neurochem 1995; 65: 192–200.
Benazzouz A, Breit S, Koudsie A, Pollak P, Krack P, Benabid AL. Intraoperative microrecordings of the subthalamic nucleus in Parkinson’s disease. Mov Disord 2002; 17: S145-S149.
Utley JD, Carlsson A. Relative effects of L-DOPA and its methyl ester given orally or intraperitoneally to reserpine-treated mice. Acta Pharmacol Toxicol (Copenh) 1965; 23: 189-193.
Singer TP, Castagnoli N, Jr., Ramsay RR, Trevor AJ. Biochemical events in the development of parkinsonism induced by 1-methyl-4-phenyl-1,2, 3,6- tetrahydropyridine. J Neurochem 1987; 49: 1-8.
Cohen G. Monoamine oxidase and oxidative stress at dopaminergic synapses. J Neural Transm Suppl 1990; 32: 229-238.
Ramsay RR, Kowal AT, Johnson MK, Salach JI, Singer TP. The inhibition site of MPP+, the neurotoxic bioactivation product of 1-methyl-4-phenyl-1, 2, 3,6- tetrahydropyridine is near the Q-binding site of NADH dehydrogenase. Arch Biochem Biophys 1987; 259: 645-649.
Bové J, Perier C. Neurotoxin-based models of Parkinson’s disease. Neuroscience 2012; 211:51-76.
Sedelis M, Hofele K, Auburger GW, Morgan S, Huston JP, Schwarting RK. MPTP susceptibility in the mouse: behavioral, neurochemical, and histological analysis of gender and strain differences. Behav Genet 2000; 30: 171-182.
Jackson-Lewis V, Jakowec M, Burke RE, Przedborski S. Time course and morphology of dopaminergic neuronal death caused by the neurotoxin 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine. Neurodegeneration 1995; 4: 257-69.
Hunot S, Vila M, Teismann P, Davis RJ, Hirsch EC, Przedborski S, et al. JNKmediated induction of cyclooxygenase 2 is required for neurodegeneration in a mouse model of Parkinson’s disease. Proc Natl Acad Sci 2004; 101: 665-670.
Tatton NA, Kish SJ. In situ detection of apoptotic nuclei in the substantia nigra compacta of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice using terminal deoxynucleotidyl transferase labelling and acridine orange staining. Neuroscience 1997; 77: 1037-48.
Vila M, Vukosavic S, Jackson-Lewis V, Neystat M, Jakowec M, Przedborski S. Alpha-synuclein upregulation in substantia nigra dopaminergic neurons following administration of the parkinsonian toxin MPTP. J Neurochem 2000; 74: 721-729.
Bezard E, Dovero S, Bioulac B, Gross C. Effects of different schedules of MPTP administration on dopaminergic neurodegeneration in mice. Exp Neurol 1997; 148: 288-292.
36. Bezard E, Dovero S, Bioulac B, Gross CE. Kinetics of nigral degeneration in a chronic model of MPTP-treated mice. Neurosci Lett 1997; 234: 47-50.
Thoenen H, Tranzer JP. Chemical sympathectomy by selective destruction of adrenergic nerve endings with 6-Hydroxydopamine. Naunyn Schmiedebergs Arch Exp Pathol Pharmakol 1968; 261: 271-288.
Ungerstedt, U. 6-Hydroxy-dopamine induced degeneration of central monoamine neurons. Eur. J. Pharmacol 1968; 5: 107-110.
Alarcón Aguilar Adriana, Abel Santamaría del Ángel, Mina Königsberg Fainstein. Modelos neurotóxicos de la enfermedad de parkinson y disfunción mitocondrial. REB 2010; 29: 91-99.