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The Journal of Neuroscience, January 30, 2008, 28(5):1185-1197; doi:10.1523/JNEUROSCI.3908-07.2008

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Cellular/Molecular
Differential Tonic GABA Conductances in Striatal Medium Spiny Neurons

Kristen K. Ade,^1,2 Megan J. Janssen,^1,3 Pavel I. Ortinski,^1,2,4 and Stefano Vicini^1,2

¹Department of Physiology and Biophysics, ²Interdisciplinary Program in Neuroscience, and ³Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007, and ⁴Division of Neurology, The Children's Hospital of Philadelphia, Abramson Research Center, Philadelphia, Pennsylvania 19104-4318

Correspondence should be addressed to Kristen K. Ade, Department of Physiology and Biophysics, BSB230, Georgetown University School of Medicine, 3900 Reservoir Road, Washington, DC 20007. Email: kka5{at}georgetown.edu

Medium spiny neurons (MSNs) provide the principal output for the dorsal striatum. Those that express dopamine D₂ receptors (D₂⁺) project to the globus pallidus external and are thought to inhibit movement, whereas those that express dopamine D₁ receptors (D₁⁺) project to the substantia nigra pars reticulata and are thought to facilitate movement. Whole-cell and outside-out patch recordings in slices from bacterial artificial chromosome transgenic mice examined the role of GABA_A receptor-mediated currents in dopamine receptor D₁⁺ striatonigral and D₂⁺ striatopallidal MSNs. Although inhibitory synaptic currents were similar between the two neuronal populations, D₂⁺ MSNs showed greater GABA_A receptor-mediated tonic currents. TTX application abolished the tonic current to a similar extent as GABA_A antagonists, suggesting a synaptic origin of the ambient GABA. Low GABA concentrations produced larger whole-cell responses and longer GABA channel openings in D₂⁺ than in D₁⁺ MSNs. Recordings from MSNs in 1^–/– mice and pharmacological analysis of tonic currents suggested greater expression of 5-containing GABA_A receptors in D₂⁺ than in D₁⁺ MSNs. As a number of disorders such as Parkinson's disease, Huntington's chorea, and tardive dyskinesia arise from an imbalance between these two pathways, the GABA_A receptors responsible for tonic currents in D₂⁺ MSNs may be a potential target for therapeutic intervention.

Key words: GABA_A receptors; tonic inhibition; striatum; medium spiny neurons; patch-clamp; chloride channel

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Received Aug. 27, 2007; revised Nov. 19, 2007; accepted Dec. 12, 2007.

Correspondence should be addressed to Kristen K. Ade, Department of Physiology and Biophysics, BSB230, Georgetown University School of Medicine, 3900 Reservoir Road, Washington, DC 20007. Email: kka5{at}georgetown.edu

This article has been cited by other articles:

				S. Taverna, E. Ilijic, and D. J. Surmeier Recurrent Collateral Connections of Striatal Medium Spiny Neurons Are Disrupted in Models of Parkinson's Disease J. Neurosci., May 21, 2008; 28(21): 5504 - 5512. [Abstract] [Full Text] [PDF]

				J. A. Shuen, M. Chen, B. Gloss, and N. Calakos Drd1a-tdTomato BAC Transgenic Mice for Simultaneous Visualization of Medium Spiny Neurons in the Direct and Indirect Pathways of the Basal Ganglia J. Neurosci., March 12, 2008; 28(11): 2681 - 2685. [Full Text] [PDF]

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