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This Article Full Text Full Text (PDF) All Versions of this Article: 98/4/2311    most recent 00620.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ibáñez-Sandoval, O. Articles by Bargas, J. Search for Related Content PubMed PubMed Citation Articles by Ibáñez-Sandoval, O. Articles by Bargas, J.

Bursting in Substantia Nigra Pars Reticulata Neurons In Vitro: Possible Relevance for Parkinson Disease

¹Departamento de Biofísica, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México; and ²Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y Estudios Avanzados, Mexico City, Mexico

Submitted 5 June 2007; accepted in final form 16 August 2007

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 GABA_A 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 Ca²⁺ channels, and Ca²⁺-activated K⁺ channels. However, although these channels shape the temporal structure of bursting, only Ca_V3.2 Ca²⁺ channels are indispensable for the initiation of the bursting pattern.

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