Data are reported as mean ± SD. The significance of differences between the connectivity found in the experiment and models of random connectivity was assessed using Monte Carlo methods. The first model represents the simplest case: connections between neurons are formed independently of each other based on the connection probabilities pE and pC, and independent of other parameters. This model is called the “uniform random” model, because the probabilities pE and pC are uniform with respect to distance. The second model is called the “nonuniform random” model, because the probabilities of electrical and chemical connections click here are distance

dependent and determined by the experimentally measured distribution of pE and pC versus the intersomatic distance between recorded cells (Figures 2A and 2B). Where appropriate, the p values were SB431542 corrected for multiple hypothesis comparisons using the Bonferroni method. Further details are available in the Supplemental Experimental Procedures. We are grateful to Beverley Clark, Martha Havenith, Adam Packer, Christoph Schmidt-Hieber, Srini Turaga, and Christian Wilms for helpful discussions; to Charlotte Arlt, Peter Latham, Adam Packer, and Srini

Turaga for comments on the manuscript; and to Maja Boznakova and Arifa Naeem for assistance with histology and reconstructions. This work was supported by grants from the Wellcome Trust, ERC, European Union (FP7 HEALTH-F2-2009-241498 Eurospin), and the Gatsby Charitable Foundation and by a PhD scholarship to S.R. from the Boehringer Ingelheim Fonds. “
“(Neuron 81, 787–799; February 19, 2014) In the version of this article published early online, the citation for Alle et al. (2011) was incorrectly deleted during the production stage, and the corresponding reference

was Dichloromethane dehalogenase omitted. The corrected article, including the citation and matching reference, now appears online and in print. The journal apologizes for this error. “
“A lot is being asked of the genetic analysis of major depression (MD): to find the biological underpinnings of one of the commonest psychiatric illnesses and one of the world’s leading causes of morbidity. While lifetime prevalence estimates vary, from 3% in Japan to 16.9% in the U.S., in all countries the disorder is common, with a frequency typically varying from 8% to 12% (Demyttenaere et al., 2004 and Kessler et al., 2003). In the U.S., MD has the greatest impact of all biomedical diseases on disability; in Europe, it is the third leading cause of disability (Alonso et al., 2004b, Nierenberg et al., 2001, Penninx et al., 2001 and Ustün et al., 2004). Despite its prevalence and MD’s enormous burden on our health care systems (Scott et al., 2003), our treatments are almost entirely symptomatic. There is even dispute about the value of medication (Khin et al., 2011, Kirsch et al., 2008, Turner et al.