Thalamocortical (TC) connectivity is reorganized by thalamic inputs during postnatal development; however, the dynamic characteristics of TC reorganization and the underlying mechanisms remain unexplored. We addressed this question using dendritic refinement of layer 4 (L4) stellate neurons in mouse barrel cortex (barrel cells) as a model; dendritic refinement of L4 neurons is a critical component of TC reorganization through which postsynaptic L4 neurons acquire their dendritic orientation toward presynaptic TC axon termini. Simultaneous labeling of TC axons and individual barrel cell dendrites allowed in vivo time-lapse imaging of dendritic refinement in the neonatal cortex. The barrel cells reinforced the dendritic orientation toward TC axons by dynamically moving their branches. In N-methyl-D-aspartate receptor (NMDAR)-deficient barrel cells, this dendritic motility was enhanced, and the orientation bias was not reinforced. Our data suggest that L4 neurons have "fluctuating" dendrites during TC reorganization and that NMDARs cell autonomously regulate these dynamics to establish fine-tuned circuits.

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Abstract-In this paper, the design of a nonlinear observerbased fault diagnosis approach for polymer electrolyte membrane (PEM) fuel cell air feed systems is presented, taking into account a fault scenario of sudden air leak in the air supply manifold. Based on a simplified nonlinear model proposed in the literature, a modified super-twisting (ST) sliding mode algorithm is employed to the observer design. The proposed ST observer can estimate not only the system states, but also the fault signal. Then, the residual signal is computed on-line from comparisons between the oxygen excess ratio obtained from the system model and the observer system, respectively. Equivalent output error injection using the residual signal is able to reconstruct the fault signal, which is critical in both fuel cell control design and fault detection. Finally, the proposed observer-based fault diagnosis approach is implemented on the Matlab/Simulink environment in order to verify its effectiveness and robustness in the presence of load variation.

Serotonergic axons extend diffuse projections throughout various brain areas, and serotonergic system disruption causes neuropsychiatric diseases. Loss of the cytoplasmic region of protocadherin-α (Pcdh-α) family proteins, products of the diverse clustered Pcdh genes, causes unbalanced distributions (densification and sparsification) of serotonergic axons in various target regions. However, which Pcdh-α member(s) are responsible for the phenotype is unknown. Here we demonstrated that Pcdh-αC2 (αC2), a Pcdh-α isoform, was highly expressed in serotonergic neurons, and was required for normal diffusion in single-axon-level analyses of serotonergic axons. The loss of αC2 from serotonergic neurons, but not from their target brain regions, led to unbalanced distributions of serotonergic axons. Our results suggest that αC2 expressed in serotonergic neurons is required for serotonergic axon diffusion in various brain areas. The αC2 extracellular domain displays homophilic binding activity, suggesting that its homophilic interaction between serotonergic axons regulates axonal density via αC2′s cytoplasmic domain.