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This Article Full Text Full Text (PDF) All Versions of this Article: 94/6/3893    most recent 00211.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science 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 ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Endo, T. Articles by Isa, T. Search for Related Content PubMed PubMed Citation Articles by Endo, T. Articles by Isa, T.

Nicotinic Acetylcholine Receptor Subtypes Involved in Facilitation of GABAergic Inhibition in Mouse Superficial Superior Colliculus

¹Department of Developmental Physiology, National Institute for Physiological Sciences, Myodaiji, Okazaki; ²Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi; ³Core Research for Evolutional Science and Technology and ⁴Solution Oriented Research for Science and Technology of the Japan Science and Technology Corporation, Kawaguchi; ⁵Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Wako; and ⁶The Graduate University for Advanced Studies, Hayama, Kanagawa, Japan

Submitted 28 February 2005; accepted in final form 10 August 2005

The superficial superior colliculus (sSC) is a key station in the sensory processing related to visual salience. The sSC receives cholinergic projections from the parabigeminal nucleus, and previous studies have revealed the presence of several different nicotinic acetylcholine receptor (nAChR) subunits in the sSC. In this study, to clarify the role of the cholinergic inputs to the sSC, we examined current responses induced by ACh in GABAergic and non-GABAergic sSC neurons using in vitro slice preparations obtained from glutamate decarboxylase 67-green fluorescent protein (GFP) knock-in mice in which GFP is specifically expressed in GABAergic neurons. Brief air pressure application of acetylcholine (ACh) elicited nicotinic inward current responses in both GABAergic and non-GABAergic neurons. The inward current responses in the GABAergic neurons were highly sensitive to a selective antagonist for 32- and 62-containing receptors, -conotoxin MII (CtxMII). A subset of these neurons exhibited a faster -bungarotoxin-sensitive inward current component, indicating the expression of 7-containing nAChRs. We also found that the activation of presynaptic nAChRs induced release of GABA, which elicited a burst of miniature inhibitory postsynaptic currents mediated by GABA_A receptors in non-GABAergic neurons. This ACh-induced GABA release was mediated mainly by CtxMII-sensitive nAChRs and resulted from the activation of voltage-dependent calcium channels. Morphological analysis revealed that recorded GFP-positive neurons are interneurons and GFP-negative neurons include projection neurons. These findings suggest that nAChRs are involved in the regulation of GABAergic inhibition and modulate visual processing in the sSC.

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