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Publication : Dopamine modulation of GABA tonic conductance in striatal output neurons.

First Author  Janssen MJ Year  2009
Journal  J Neurosci Volume  29
Issue  16 Pages  5116-26
PubMed ID  19386907 Mgi Jnum  J:252956
Mgi Id  MGI:6100189 Doi  10.1523/JNEUROSCI.4737-08.2009
Citation  Janssen MJ, et al. (2009) Dopamine modulation of GABA tonic conductance in striatal output neurons. J Neurosci 29(16):5116-26
abstractText  We previously reported greater GABAA receptor-mediated tonic currents in D2+ striatopallidal than D1+ striatonigral medium spiny neurons (MSNs) are mediated by alpha5-subunit-containing receptors. Here, we used whole-cell recordings in slices from bacterial artificial chromosome transgenic mice to investigate the link between subunit composition, phosphorylation, and dopamine receptor activation. Whole-cell recordings in slices from delta-subunit knock-out mice demonstrate that while MSNs in wild-type mice do express delta-subunit-containing receptors, this receptor subtype is not responsible for tonic conductance observed in the acute slice preparation. We assessed the contribution of the beta1- and beta3-subunits expressed in MSNs by their sensitivity to etomidate, an agonist selective for beta2- or beta3-subunit-containing GABAA receptors. Although etomidate produced substantial tonic current in D2+ neurons, there was no effect in D1+ neurons. However, with internal PKA application or dopamine modulation, D1+ neurons expressed tonic conductance and responded to etomidate application. Our results suggest that distinct phosphorylation of beta3-subunits may cause larger tonic current in D2+ striatopallidal MSNs, and proper intracellular conditions can reveal tonic current in D1+ cells.
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