Dopaminergic modulation of corticostriatal responses in medium spiny projection neurons from direct and indirect pathways
Por:
Flores-Barrera E., Vizcarra-Chacón B.J., Bargas J., Tapia D., Galarraga E.
Publicada:
1 ene 2011
Resumen:
medium spiny neurons (MSNs) from the direct and indirect pathways of the basal ganglia are different. Their differences readily distinguish D 1- and D 2-type receptor expressing MSNs in both bacterial artifcial chromosome-transgenic mice and their control littermates as well as in rats: indirect pathway neurons are more excitable than direct pathway neurons revealing autoregenerative spikes underlying their spike trains, whereas direct pathway neurons exhibit more prolonged plateau potentials and spike trains. SFK 81297, a selective agonist for D 1-class receptors enhanced corticostriatal responses in direct pathway neurons, while quinelorane, a selective agonist for D 2-class receptors reduced orthodromic and autoregenerative responses in indirect pathway neurons thus making both neuron classes similarly excitable. Because dopaminergic postsynaptic actions target Ca V1 (L) class voltage-gated calcium channels in MSNs, we hypothesized that these channels are involved and can explain a part of the dopaminergic actions on corticostriatal integration. Both 2.5 ?M nicardipine and 400 nM calciseptine, selective Ca V1 channel blockers, reduced corticostriatal responses in both D 1- and D 2-receptor expressing neurons, respectively. A previous blockade of Ca V1 channels occluded the actions of dopamine agonists in both neuronal classes. In contrast, a Ca V1 (L) channel activator, 2.5 ?M Bay K 8644, enhanced corticostriatal responses in neurons from both pathways. It is concluded that Ca V1 intrinsic currents mediate a part of the dopaminergic modulation during orthodromic synaptic integration of cortical inputs in both classes of MSNs. © 2011 Flores-Barrera, Vizcarra- Chacón, Bargas, Tapia and Galarraga.
Filiaciones:
Flores-Barrera E.:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, Federal District, Mexico
Vizcarra-Chacón B.J.:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, Federal District, Mexico
Bargas J.:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, Federal District, Mexico
Tapia D.:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, Federal District, Mexico
Galarraga E.:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México City, Federal District, Mexico
All Open Access, Gold
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