The latter delay was subtracted from the mean onset latency of whisker-evoked PSPs during the baseline period to get the pre-postpairing delay (Figures 2A, S2A, and S2B). DWE did not affect either the passive learn more membrane properties or the excitability of L2/3 pyramidal neurons as revealed by the mean number

of APs elicited by increasing current injection (Figures S3A and S3B). After induction of STD-LTP, whisker-evoked PSPs were obtained every 7.5 s for at least 10 min (mean postpairing time: 22 ± 10 min [SD], n = 54). Single trials were not included in the analysis if Rs and Rin changed by more than 30%, and if current-clamp holding potential varied more than 4mV (PW, Vm prepairing, −72.8 ± 3 [SD], Vm postpairing, −73.1 ± 2.5 [SD], n = 11; SW, Vm prepairing, −73.7 ± selleckchem 4 [SD], Vm postpairing, −74.2 ± 4 [SD], n = 14). Whisker-evoked synaptic conductances were determined using published methods by House et al. (2011) and Monier et al. (2008) in voltage clamp using whisker-induced postsynaptic currents (PSCs) recorded at 5 different holding potentials (Vh = −100, −70, −50, −30, and 0mV; 20 PSCs per Vh; 0.2 Hz). For details and discussion on voltage-clamp recordings and conductance analysis, see Supplemental Experimental Procedures. The onset latencies of EPSCs and IPSCs were determined at Vh = −100 and 0mV, respectively,

similar to the PSP onsets. GABA-A receptors and NMDARs were blocked by local and intracellular diffusion of PTX (Sigma-Aldrich; 0.1 mM) and the NMDAR open-channel blocker MK-801 (Tocris; 1 mM) in the recording pipette solution, respectively. A total of 0.1 mM of PTX in the pipette permitted similar levels of LTP as could be obtained using 50 μl PTX (50–100 nM) topically applied to the brain but largely avoided epileptic network activity (data not shown). Data are presented as the mean ± SEM, except where stated differently, e.g., for SD. All statistical tests (MATLAB statistical toolbox; MathWorks) are mentioned in the figure legends. Details of statistical comparisons are provided in the Supplemental

all Experimental Procedures. We thank Daniel Lebrecht and Alan Carleton for help with intrinsic image analysis; and Carl Petersen, Yann Humeau, Alan Carleton, and Egbert Welker for discussions and comments on the manuscript. This work was supported by the Swiss National Science Foundation (Grants 3100AO-120685, CRSI33-127289, and NCCR/SYNAPSY), the International Foundation for Research in Paraplegia (chair Alain Rossier to A.H.), and EMBO (ALTF 226-2010 to F.G.). “
“The limbic-cortical system in the brain is considered to be the neural substrate for the action of antidepressants (Mayberg, 1997; Mayberg et al., 2000). Chronic administration of antidepressant drugs in depressed patients changed regional glucose metabolism measured by positron emission tomography in the hippocampus (Kennedy et al., 2001; Mayberg et al., 2000).