Bursting in substantia nigra pars reticulata neurons in vitro: Possible relevance for Parkinson disease
Por:
Ibáñez-Sandoval O., Carrillo-Reid L., Galarraga E., Tapia D., Mendoza E., Gomora J.C., Aceves J., Bargas J.
Publicada:
1 ene 2007
Resumen:
Projection neurons of the substantia nigra reticulata (SNr) convey basal ganglia (BG) processing to thalamocortical and brain stem circuits responsible for movement. Two models try to explain pathological BG performance during Parkinson disease (PD): the rate model, which posits an overexcitation of SNr neurons due to hyperactivity in the indirect pathway and hypoactivity of the direct pathway, and the oscillatory model, which explains PD as the product of pathological pattern generators disclosed by dopamine reduction. These models are, apparently, incompatible. We tested the predictions of the rate model by increasing the excitatory drive and reducing the inhibition on SNr neurons in vitro. This was done pharmacologically with bath application of glutamate agonist N-methyl-D-aspartate and GABAA receptor blockers, respectively. Both maneuvers induced bursting behavior in SNr neurons. Therefore synaptic changes forecasted by the rate model induce the electrical behavior predicted by the oscillatory model. In addition, we found evidence that Ca V3.2 Ca2+ channels are a critical step in generating the bursting firing pattern in SNr neurons. Other ion channels involved are: hyperpolarization-activated cation channels, high-voltage-activated Ca 2+ channels, and Ca2+-activated K+ channels. However, although these channels shape the temporal structure of bursting, only CaV3.2 Ca2+ channels are indispensable for the initiation of the bursting pattern. Copyright © 2007 The American Physiological Society.
Filiaciones:
Ibáñez-Sandoval O.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Carrillo-Reid L.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Galarraga E.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Tapia D.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Mendoza E.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Gomora J.C.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Aceves J.:
Departamento de Fisiología, Biofísica Y Neurociencias, Centro de Investigación Y Estudios Avanzados, Mexico City, Mexico
Bargas J.:
Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Instituto de Fisiología Celular, UNAM, PO Box: 70-253, México City, DF 04510, Mexico
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