When i = j, ri,j was set to 1. When i≠j, ri,j was assigned according to a linear relationship between noise and signal correlation: equation(5) ri,j=avestibular×rsignal,vestibular,i,j+avisual×rsignal,visual,i,j+bri,j=avestibular×rsignal,vestibular,i,j+avisual×rsignal,visual,i,j+bWe Ceritinib manufacturer minimized the orthogonal distance between

the fit plane and the raw data using type II regression. This work was supported by grants from National Institutes of Health (EY019087 to D.E.A., and EY016178 to G.C.D.). “
“In many regions of the mammalian CNS, inhibitory microcircuits are wired with high precision, fine-tuning synaptic input and modulating neural output (Stepanyants et al., 2004). The assembly of functional inhibitory microcircuits can be considered in several independent steps: the selection of membrane subdomains on specific neuronal targets, the assignment of appropriate synaptic innervation densities, and the regulation

of transmitter phenotype and level (Williams et al., 2010). How these diverse cellular processes are orchestrated at individual synapses within defined CNS microcircuits remains unclear. One informative instance of the subcellular targeting of inhibitory synapses is found in primary sensory systems, where sensory terminals serve SKI-606 purchase both as presynaptic structures that innervate recipient CNS neurons and as the postsynaptic target of local inhibitory interneurons at axoaxonic

synapses (Rudomin, 2009). Such axoaxonic arrangements provide an anatomical substrate for selective filtering of sensory information (Rudomin and Schmidt, 1999). In the ventral spinal cord, the central terminals of proprioceptive sensory neurons are studded with numerous synaptic boutons that derive from a discrete set of GABAergic inhibitory interneurons, termed GABApre neurons (Betley et al., 2009 and Hughes et al., 2005). This set of spinal inhibitory interneurons can be distinguished by Phosphatidylinositol diacylglycerol-lyase expression of the GABA synthetic enzyme glutamic acid decarboxylase-2 (GAD2/GAD65) (Betley et al., 2009 and Hughes et al., 2005), an essential determinant of sustained GABA release (Tian et al., 1999). High-level expression of GAD65 in GABApre neurons is directed by a sensory source of brain-derived neurotrophic factor (BDNF) (Betley et al., 2009). Moreover, sensory terminals in the ventral spinal cord represent the sole target of GABApre neurons (Betley et al., 2009), implying stringent recognition specificity in the assembly and organization of this specialized inhibitory microcircuit. The molecular mediators of stringent axoaxonic specificity have remained unclear, however.