We computed the normalization factor in each condition by considering the average response in V1 to the balanced and biased stimulus sequences. We first apply the summation profile to the LGN input population to determine the V1 population response prior to normalization. We then compute the normalization factor as: equation(Equation 3) k=∑s(σn+∑iLisn)p(s)where find more LisLis is the prenormalization response of neuron i   to stimulus s  , and p(s)p(s) is the probability of stimulus s. The constants σ and n are not allowed to vary between the balanced and biased conditions. We thank Charu Reddy for outstanding technical support and Jeremy Freeman and Jonathan

Pillow for providing MDV3100 mouse code to fit the LNP model. This work was supported by a Royal Society Newton International Fellowship and a National Science Foundation International Research Fellowship to N.T.D. and by funding

from the Wellcome Trust and the European Research Council. M.C. holds the GlaxoSmithKline/Fight for Sight Chair in Visual Neuroscience. “
“During nervous system development, axons are directed toward their appropriate targets by guidance signals in their environment. Ephrin ligands and Eph receptor tyrosine kinases are classical axon guidance molecules with well-established roles in the assembly of various neuronal circuits. An interesting feature of ephrin ligands is their ability to signal bidirectionally. mafosfamide Ephrin trans-interactions with Eph receptors on opposing cells initiate signaling events in the Eph-expressing cell referred to as “forward” signaling, which is often repulsive. All ephrins are tethered to the plasma membrane, either by a glycosylphosphatidylinositol (GPI) anchor (ephrin-As) or through a transmembrane domain (ephrin-Bs), and are also able to elicit “reverse” signaling in the ephrin-expressing cell,

a process that can result in repulsion or attraction ( Egea and Klein, 2007). To complicate things further, in several locations ephrins and Ephs are coexpressed in the same neurons during the period of axon outgrowth. Studies from different laboratories have led to controversial conclusions about the role of coexpressed ephrins and Ephs. On the one hand, ephrins were proposed to cis-interact and inhibit Eph forward signaling, thereby fine-tuning the sensitivity of navigating axons to ephrin ligands from the target tissue presented in trans. On the other hand, Ephs and ephrins were observed to reside in separate plasma membrane microdomains and to not interact in cis, allowing the ephrins to bind Ephs in trans, which leads to parallel forward and reverse signaling within the same axon ( Carvalho et al., 2006, Hornberger et al., 1999 and Marquardt et al., 2005). Both hypotheses were largely based on in vitro findings in primary retinal ganglion cells (RGCs) and motor neurons.