D3 dopamine receptors interact with dopamine D1 but not D4 receptors in the GABAergic terminals of the SNr of the rat
Por:
Cruz-Trujillo R., Avalos-Fuentes A., Rangel-Barajas C., Paz-Bermúdez F., Sierra A., Escartín-Perez E., Aceves J., Erlij D., Florán B.
Publicada:
1 abr 2013
Resumen:
The firing rate of substantia nigra reticulata (SNr) neurons is
modulated by GABA release from striatonigral and pallidonigral
projections. This release is, in turn, modulated by dopamine acting on
dopamine D1 receptors at striatonigral terminals and D4 receptors at
pallidonigral terminals. In addition, striatal neurons that express D1
receptors also express D3 receptors. In this study we analyzed the
possible significance of D3 and D1 receptor colocalization in
striatonigral projections. We found that these receptors coprecipitate
in SNr synaptosomes suggesting their close association in this
structure. D1 agonist SKF 38393 administered alone increased mIPSC
frequency in SNr slices and cAMP production in SNr synaptosomes,
however, the selective D3 agonist PD 128,907 increased mIPSC frequency
and cAMP production only when D1 receptors were concurrently stimulated.
The D1 antagonist SCH 23390 blocked completely the effects of the
concurrent administration of these agonists while the selective D3
antagonist GR 103691 blocked only the potentiating effects of PD
128,907. These findings further indicate that D1 and D3 receptors are
localized in the same structure. The D4 agonist PD 168,077 decreased
mIPSCs frequency without changing amplitude, an effect that was blocked
by the selective D4 antagonist L 745,870. The effects of D4 receptor
stimulation disappeared after lesioning the globus pallidus. D3 agonist
PD 128,907 did not reduce mIPSC frequency even in neurons that responded
to D4 agonist. In sum, activation of D3 receptors in SNr potentiates the
stimulation of transmitter release and cAMP production caused by D1
receptor activation of striatonigral projections while it is without
effects in terminals, probably of pallidal origin, that are inhibited by
activation of D4 receptors. (C) 2012 Elsevier Ltd. All rights reserved.
Filiaciones:
Cruz-Trujillo R.:
Department of Pharmacology, CINVESTAV-IPN, Mexico
Avalos-Fuentes A.:
Department of Pharmacology, CINVESTAV-IPN, Mexico
Rangel-Barajas C.:
Department of Physiology, Biophysics and Neurosciences, CINVESTAV-IPN, Av. IPN # 2508, San-Pedro Zacatenco, México 07360, Mexico
Paz-Bermúdez F.:
Department of Physiology, Biophysics and Neurosciences, CINVESTAV-IPN, Av. IPN # 2508, San-Pedro Zacatenco, México 07360, Mexico
Sierra A.:
Department of Physiology, Biophysics and Neurosciences, CINVESTAV-IPN, Av. IPN # 2508, San-Pedro Zacatenco, México 07360, Mexico
Escartín-Perez E.:
Univ Nacl Autonoma Mexico, IZTACALA, FES, Mexico City, DF, Mexico
Aceves J.:
Department of Physiology, Biophysics and Neurosciences, CINVESTAV-IPN, Av. IPN # 2508, San-Pedro Zacatenco, México 07360, Mexico
Erlij D.:
Department of Physiology, SUNY Downstate Medical Center, NY, United States
Florán B.:
Department of Physiology, Biophysics and Neurosciences, CINVESTAV-IPN, Av. IPN # 2508, San-Pedro Zacatenco, México 07360, Mexico
|