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This Article Full Text Full Text (PDF) All Versions of this Article: 573/3/697    most recent jphysiol.2006.110031v1 Services Email this article to a friend Similar articles in this journal 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 Shen, K.-Z. Articles by Johnson, S. W. Search for Related Content PubMed PubMed Citation Articles by Shen, K.-Z. Articles by Johnson, S. W. Related Collections Neuroscience

¹ Department of Neurology, Oregon Health and Science University, Portland, OR 97239, USA
² Veterans Affairs Medical Center, Portland, OR 97207, USA

The subthalamic nucleus (STN) plays an important role in movement control by exerting its excitatory influence on the substantia nigra pars reticulata (SNR), a major output structure of the basal ganglia. Moreover, excessive burst firing of SNR neurons seen in Parkinson's disease has been attributed to excessive transmission in the subthalamonigral pathway. Using the ‘blind’ whole-cell patch clamp recording technique in rat brain slices, we found that focal electrical stimulation of the STN evoked complex, long-duration excitatory postsynaptic currents (EPSCs) in SNR neurons. Complex EPSCs lasted 200–500 ms and consisted of an initial monosynaptic EPSC followed by a series of late EPSCs superimposed on a slow inward shift in holding current. Focal stimulation of regions outside the STN failed to evoke complex EPSCs. The late component of complex EPSCs was markedly reduced by ionotropic glutamate receptor antagonists (2-amino-5-phosphonopentanoic acid and 6-cyano-7-nitro-quinoxalone) and by a GABA_A receptor agonist (isoguvacine) when these agents were applied directly to the STN using a fast-flow microapplicator. Moreover, the complex EPSC was greatly enhanced by bath application of the GABA_A receptor antagonists picrotoxin or bicuculline. These data suggest that recurrent glutamate synapses in the STN generate polysynaptic, complex EPSCs that are under tonic inhibition by GABA. Because complex EPSCs are expected to generate bursts of action potentials in SNR neurons, we suggest that complex EPSCs may contribute to the pathological burst firing that is associated with the symptoms of Parkinson's disease.

(Received 20 March 2006; accepted after revision 7 April 2006; first published online 13 April 2006)
Corresponding author S. W. Johnson: Portland VA Medical Center, R & D 61, 3710 SW US Veterans Hospital Road, Portland, OR 97207, USA. Email: johnsost{at}ohsu.edu

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