, 2010), anti-phospho S892-GABAB2 (p-S892; Couve et al , 2001) we

, 2010), anti-phospho S892-GABAB2 (p-S892; Couve et al., 2001) were used. A monoclonal antibody anti-GABAB1 (Clone N93A/49; NeuroMab, Davis, CA, USA) and anti-GABAB2 (Clone N81/37; NeuroMab) were used. A guinea-pig polyclonal antibody anti-GIRK2 (Aguado et al., 2008) was used. A similar procedure to that described earlier (Lujan et al., 1996 and Koyrakh et al., 2005) was used. See online Supplemental Experimental Procedures for details on procedures and quantitation. Tissue punches from VTA, NAc, hippocampus, and mPFC obtained from saline- and METH-injected mice were lysed in 20 mM Tris-HCl (pH 8.0), 150 mM NaCl, 5 mM EDTA, 1% Triton X-100, 10 mM NaF, 2 mM Na3VO4, 10 mM

Na4P2O7, 10 μg/ml leupeptin, 1 μg/ml BKM120 mw aprotinin, 10 μg/ml antipain, and 250 μg/ml 4-(2-Aminoethl) benzenesulfonyl fluoride hydrochloride. Soluble material was then subjected to immunoblotting with anti-GABAB2, anti-phospho S783-GABAB2 (p-S783), anti-phospho S892-GABAB2 (p-S892), anti-GAPDH, and detected by SuperSignal West Dura Chemiluminescent Substrate (Thermo Scientific, Rockford, IL, USA). The luminescence images were captured by a Luminescent Image Analyzer (LAS3000; Fujifilm, Tokyo, Japan) and the intensity of bands were measured by Multi Gauge software (version 3; Fujifilm). We thank all members of the

Slesinger Selleckchem SNS 032 and Lüscher laboratories, as well as G.O. Hjelmstad for comments on the manuscript. This work was supported Bay 11-7085 by grants from the Salk Institute’s Catharina Foundation (Postdoctoral Fellowship to C.L.P.), the Spanish Ministry of Education and Science (BFU-2009-08404 to R.L.) and Consolider (CSD2008-00005 to R.L.), the National Institute of Neurological Disorders and Stroke (NS048045, NS051195, NS056359,

and NS054900 to S.J.M.), a Ruth L. Kirschstein National Research Service Award (F31 DA029401 to M.B.M) and the National Institute on Drug Abuse (DA019022 to P.A.S. and C.L.; DA025236 to P.A.S.). “
“Neurons are thought to encode information in a continuum of firing patterns ranging from isolated spikes to high-frequency bursts of 2–20 spikes. In place cells of the CA1 region of the hippocampus, ∼50% of spikes occur in short bursts with frequencies of >50 Hz, while the remaining spikes occur in isolation (Harris et al., 2001, Harvey et al., 2009, Jones and Wilson, 2005 and Ranck, 1973). The occurrence of spike bursts varies with behavioral state (Burgos-Robles et al., 2007, Harris et al., 2001 and Ranck, 1973) and is altered in neurological diseases (Jackson et al., 2004 and Walker et al., 2008). These properties suggest that spike-bursting patterns are functionally important for information processing by the brain, but the specific roles of spike-firing patterns in behaviors remain largely unexplored.

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