C-fos-positive cells were quantified through z stack projections by experimenters blind to the experimental conditions. Coronal sections of 300 μm containing the vHPC were collected. Whole-cell patch-clamp recordings were made from visually identified pyramidal neurons in the CA1 region of the vHPC. BLA

terminals expressing GDC941 ChR2 were activated using a 470 nm LED. Amplitudes and onset latencies of postsynaptic potentials and currents were measured for the first pulse (Figure 4) and for the average response of each neuron (Figure S8). Group differences were detected using either one-way ANOVA with Tukey’s post hoc tests or two-way repeated-measures ANOVA with Bonferroni post hoc tests. Paired statistical comparisons were made with a one-tailed paired Student’s t test. For all results, significativity threshold was placed at p = 0.05. All data are shown as ±SEM. We thank P. Namburi for sharing

the cell-counting software, K. Kohara for the biocytin-streptavidin protocol, and all members of the Tye Laboratory for their helpful discussion. We would like to thank M. Dobbins, L.-H. Tsai, K. Jones, W. Xu, Q. Zhang, and G. Feng for providing access to their confocal microscopes. We DAPT acknowledge Dr. R.J. Samulski and the UNC Vector Core for gene transfer vectors preparation. This work was supported by funds from the JPB Foundation, Picower Institute Innovation Funds, The Whitehall Foundation, The Klingenstein Foundation, and startup funds provided by the Picower Institute for Learning and Memory and the Department of Brain and Cognitive

Sciences at MIT (K.M.T). A.B. was supported by a postdoctoral fellowship Cell press for prospective researchers from the Swiss National Science Foundation (SNSF; Project number: PBSKP3_143586). C.A.L. was supported by the MIT Summer Research Program and by HHMI undergraduate education grant. “
“The architectural and functional integrity of the mammalian neocortex requires the tight regulation of neuron production, which is primarily determined by the proliferation and differentiation of neural progenitor cells (NPCs). Perturbation of the proliferation or differentiation process results in either a reduced or excessive number of neurons, which leads to the formation of a smaller or larger brain (i.e., microcephaly or macrocephaly, respectively). In turn, this causes cortical malfunctions such as mental retardation. Cortical neurons in embryonic mouse brains are generated in the proliferative zones by two major types of NPCs: radial glial cells (RGs) (Noctor et al., 2001), and their transit-amplifying neuronal-committed progenies, intermediate progenitors (IPs) (Noctor et al., 2004). RGs located in the ventricular zone (VZ) divide asymmetrically to self-renew and give rise to either a neuron or more commonly an IP.