title: GABAergic synaptic transmission onto striatal cholinergic interneurons in dopamine D2 receptor knock-out mice.
abstract: Whole-cell or cell-attached analysis was carried out in dopamine (DA) D2 receptor (D2R) knock-out (KO) mice to elucidate the function of this receptor in the regulation of GABAergic synaptic transmission onto striatal cholinergic interneurons as well as their spontaneous firing. In slice preparation obtained from wild-type mice, evoked GABAergic inhibitory postsynaptic currents (IPSCs) showed frequency-dependent suppression, and this suppression significantly decreased in the presence of a D2-like receptor antagonist or in D2R KO mice. Contribution of N-type calcium channel was also significantly reduced in the striatal cholinergic interneurons of the D2R KO mice compared with that in the wild-type mice. Spontaneous firing of striatal cholinergic interneurons was inhibited by 5- or 10-Hz stimulation, and the suppression was decreased in the presence of a D2-like receptor antagonist or in D2R KO mice. These findings substantiate the physiological role of D2R in the regulation of GABAergic synaptic transmission onto striatal cholinergic interneurons as well as their excitability, confirming the tight coupling between D2R and N-type calcium channels in the regulation of GABA release.
authors.affiliation: Department of Laboratory Animal Science, Kitasato University School of Medicine, Sagamihara 252-0374, Japan; National Institute for Basic Biology, Okazaki 444-8585, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.affiliation: Department of Laboratory Animal Science, Kitasato University School of Medicine, Sagamihara 252-0374, Japan; National Institute for Basic Biology, Okazaki 444-8585, Japan; Department of Comparative and Experimental Medicine, Center for Bioresource-based Researches, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sasaoka
authors.affiliation: Department of Pharmacology, Jikei University School of Medicine, Tokyo 105-8461, Japan; Department of Pharmacology, Keio University Faculty of Pharmacy, Tokyo 105-8512, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nishijo
authors.affiliation: Department of Pharmacology, Jikei University School of Medicine, Tokyo 105-8461, Japan. Electronic address: tmomi@jikei.ac.jp.
authors.forename: T
authors.initials: T
authors.lastname: Momiyama
mesh_terms: D000818:Animals; D020864:Calcium Channels, N-Type / Q000378:metabolism; D059329:Cholinergic Neurons / Q000502:physiology*; D003342:Corpus Striatum / Q000502:physiology*; D053444:Inhibitory Postsynaptic Potentials; D007395:Interneurons / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D020864:Calcium Channels, N-Type; D017448:Receptors, Dopamine D2; D005680:gamma-Aminobutyric Acid
keywords: GABAergic synapse; cholinergic neuron; dopamine receptors; knock-out mice; striatum