@article{12875, abstract = {The superior colliculus (SC) in the mammalian midbrain is essential for multisensory integration and is composed of a rich diversity of excitatory and inhibitory neurons and glia. However, the developmental principles directing the generation of SC cell-type diversity are not understood. Here, we pursued systematic cell lineage tracing in silico and in vivo, preserving full spatial information, using genetic mosaic analysis with double markers (MADM)-based clonal analysis with single-cell sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron types, even at the stage of terminal division. While individual clonal units show no pre-defined cellular composition, the establishment of appropriate relative proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively, our findings provide an inaugural framework at the single-RGP/-cell level of the mammalian SC ontogeny.}, author = {Cheung, Giselle T and Pauler, Florian and Koppensteiner, Peter and Krausgruber, Thomas and Streicher, Carmen and Schrammel, Martin and Özgen, Natalie Y and Ivec, Alexis and Bock, Christoph and Shigemoto, Ryuichi and Hippenmeyer, Simon}, issn = {0896-6273}, journal = {Neuron}, number = {2}, pages = {230--246.e11}, publisher = {Elsevier}, title = {{Multipotent progenitors instruct ontogeny of the superior colliculus}}, doi = {10.1016/j.neuron.2023.11.009}, volume = {112}, year = {2024}, } @article{14843, abstract = {The coupling between Ca2+ channels and release sensors is a key factor defining the signaling properties of a synapse. However, the coupling nanotopography at many synapses remains unknown, and it is unclear how it changes during development. To address these questions, we examined coupling at the cerebellar inhibitory basket cell (BC)-Purkinje cell (PC) synapse. Biophysical analysis of transmission by paired recording and intracellular pipette perfusion revealed that the effects of exogenous Ca2+ chelators decreased during development, despite constant reliance of release on P/Q-type Ca2+ channels. Structural analysis by freeze-fracture replica labeling (FRL) and transmission electron microscopy (EM) indicated that presynaptic P/Q-type Ca2+ channels formed nanoclusters throughout development, whereas docked vesicles were only clustered at later developmental stages. Modeling suggested a developmental transformation from a more random to a more clustered coupling nanotopography. Thus, presynaptic signaling developmentally approaches a point-to-point configuration, optimizing speed, reliability, and energy efficiency of synaptic transmission.}, author = {Chen, JingJing and Kaufmann, Walter and Chen, Chong and Arai, Itaru and Kim, Olena and Shigemoto, Ryuichi and Jonas, Peter M}, issn = {1097-4199}, journal = {Neuron}, publisher = {Elsevier}, title = {{Developmental transformation of Ca2+ channel-vesicle nanotopography at a central GABAergic synapse}}, doi = {10.1016/j.neuron.2023.12.002}, year = {2024}, } @article{9793, abstract = {Astrocytes extensively infiltrate the neuropil to regulate critical aspects of synaptic development and function. This process is regulated by transcellular interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes coordinate developmental processes among one another to parse out the synaptic neuropil and form non-overlapping territories is unknown. Here we identify a molecular mechanism regulating astrocyte-astrocyte interactions during development to coordinate astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked, astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for territory and morphological complexity in the developing mouse cortex. Furthermore, conditional deletion of Hepacam from developing astrocytes significantly impairs gap junction coupling between astrocytes and disrupts the balance between synaptic excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy with subcortical cysts in humans. Therefore, our findings suggest that disruption of astrocyte self-organization mechanisms could be an underlying cause of neural pathology.}, author = {Baldwin, Katherine T. and Tan, Christabel X. and Strader, Samuel T. and Jiang, Changyu and Savage, Justin T. and Elorza-Vidal, Xabier and Contreras, Ximena and Rülicke, Thomas and Hippenmeyer, Simon and Estévez, Raúl and Ji, Ru-Rong and Eroglu, Cagla}, issn = {1097-4199}, journal = {Neuron}, number = {15}, pages = {2427--2442.e10}, publisher = {Elsevier}, title = {{HepaCAM controls astrocyte self-organization and coupling}}, doi = {10.1016/j.neuron.2021.05.025}, volume = {109}, year = {2021}, } @article{11054, abstract = {In recent years, the nuclear pore complex (NPC) has emerged as a key player in genome regulation and cellular homeostasis. New discoveries have revealed that the NPC has multiple cellular functions besides mediating the molecular exchange between the nucleus and the cytoplasm. In this review, we discuss non-transport aspects of the NPC focusing on the NPC-genome interaction, the extreme longevity of the NPC proteins, and NPC dysfunction in age-related diseases. The examples summarized herein demonstrate that the NPC, which first evolved to enable the biochemical communication between the nucleus and the cytoplasm, now doubles as the gatekeeper of cellular identity and aging.}, author = {Cho, Ukrae H. and HETZER, Martin W}, issn = {0896-6273}, journal = {Neuron}, keywords = {General Neuroscience}, number = {6}, pages = {899--911}, publisher = {Elsevier}, title = {{Nuclear periphery takes center stage: The role of nuclear pore complexes in cell identity and aging}}, doi = {10.1016/j.neuron.2020.05.031}, volume = {106}, year = {2020}, } @article{7472, abstract = {Temporally organized reactivation of experiences during awake immobility periods is thought to underlie cognitive processes like planning and evaluation. While replay of trajectories is well established for the hippocampus, it is unclear whether the medial prefrontal cortex (mPFC) can reactivate sequential behavioral experiences in the awake state to support task execution. We simultaneously recorded from hippocampal and mPFC principal neurons in rats performing a mPFC-dependent rule-switching task on a plus maze. We found that mPFC neuronal activity encoded relative positions between the start and goal. During awake immobility periods, the mPFC replayed temporally organized sequences of these generalized positions, resembling entire spatial trajectories. The occurrence of mPFC trajectory replay positively correlated with rule-switching performance. However, hippocampal and mPFC trajectory replay occurred independently, indicating different functions. These results demonstrate that the mPFC can replay ordered activity patterns representing generalized locations and suggest that mPFC replay might have a role in flexible behavior.}, author = {Käfer, Karola and Nardin, Michele and Blahna, Karel and Csicsvari, Jozsef L}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {P154--165.e6}, publisher = {Elsevier}, title = {{Replay of behavioral sequences in the medial prefrontal cortex during rule switching}}, doi = {10.1016/j.neuron.2020.01.015}, volume = {106}, year = {2020}, } @article{7546, abstract = {The extent to which behavior is shaped by experience varies between individuals. Genetic differences contribute to this variation, but the neural mechanisms are not understood. Here, we dissect natural variation in the behavioral flexibility of two Caenorhabditis elegans wild strains. In one strain, a memory of exposure to 21% O2 suppresses CO2-evoked locomotory arousal; in the other, CO2 evokes arousal regardless of previous O2 experience. We map that variation to a polymorphic dendritic scaffold protein, ARCP-1, expressed in sensory neurons. ARCP-1 binds the Ca2+-dependent phosphodiesterase PDE-1 and co-localizes PDE-1 with molecular sensors for CO2 at dendritic ends. Reducing ARCP-1 or PDE-1 activity promotes CO2 escape by altering neuropeptide expression in the BAG CO2 sensors. Variation in ARCP-1 alters behavioral plasticity in multiple paradigms. Our findings are reminiscent of genetic accommodation, an evolutionary process by which phenotypic flexibility in response to environmental variation is reset by genetic change.}, author = {Beets, Isabel and Zhang, Gaotian and Fenk, Lorenz A. and Chen, Changchun and Nelson, Geoffrey M. and Félix, Marie-Anne and de Bono, Mario}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {106--121.e10}, publisher = {Cell Press}, title = {{Natural variation in a dendritic scaffold protein remodels experience-dependent plasticity by altering neuropeptide expression}}, doi = {10.1016/j.neuron.2019.10.001}, volume = {105}, year = {2020}, } @article{8001, abstract = {Post-tetanic potentiation (PTP) is an attractive candidate mechanism for hippocampus-dependent short-term memory. Although PTP has a uniquely large magnitude at hippocampal mossy fiber-CA3 pyramidal neuron synapses, it is unclear whether it can be induced by natural activity and whether its lifetime is sufficient to support short-term memory. We combined in vivo recordings from granule cells (GCs), in vitro paired recordings from mossy fiber terminals and postsynaptic CA3 neurons, and “flash and freeze” electron microscopy. PTP was induced at single synapses and showed a low induction threshold adapted to sparse GC activity in vivo. PTP was mainly generated by enlargement of the readily releasable pool of synaptic vesicles, allowing multiplicative interaction with other plasticity forms. PTP was associated with an increase in the docked vesicle pool, suggesting formation of structural “pool engrams.” Absence of presynaptic activity extended the lifetime of the potentiation, enabling prolonged information storage in the hippocampal network.}, author = {Vandael, David H and Borges Merjane, Carolina and Zhang, Xiaomin and Jonas, Peter M}, issn = {10974199}, journal = {Neuron}, number = {3}, pages = {509--521}, publisher = {Elsevier}, title = {{Short-term plasticity at hippocampal mossy fiber synapses is induced by natural activity patterns and associated with vesicle pool engram formation}}, doi = {10.1016/j.neuron.2020.05.013}, volume = {107}, year = {2020}, } @article{8162, abstract = {In mammalian genomes, a subset of genes is regulated by genomic imprinting, resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development, but prevalence and functional impact in individual cells is unclear. Here, we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental chromosome disomy (UPD) containing two copies of either the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold overexpressed or not expressed. By genetic labeling of UPD, we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single-cell resolution. We discovered an unexpected degree of cell-type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally, our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell-type diversity.}, author = {Laukoter, Susanne and Pauler, Florian and Beattie, Robert J and Amberg, Nicole and Hansen, Andi H and Streicher, Carmen and Penz, Thomas and Bock, Christoph and Hippenmeyer, Simon}, issn = {0896-6273}, journal = {Neuron}, number = {6}, pages = {1160--1179.e9}, publisher = {Elsevier}, title = {{Cell-type specificity of genomic imprinting in cerebral cortex}}, doi = {10.1016/j.neuron.2020.06.031}, volume = {107}, year = {2020}, } @article{8261, abstract = {Dentate gyrus granule cells (GCs) connect the entorhinal cortex to the hippocampal CA3 region, but how they process spatial information remains enigmatic. To examine the role of GCs in spatial coding, we measured excitatory postsynaptic potentials (EPSPs) and action potentials (APs) in head-fixed mice running on a linear belt. Intracellular recording from morphologically identified GCs revealed that most cells were active, but activity level varied over a wide range. Whereas only ∼5% of GCs showed spatially tuned spiking, ∼50% received spatially tuned input. Thus, the GC population broadly encodes spatial information, but only a subset relays this information to the CA3 network. Fourier analysis indicated that GCs received conjunctive place-grid-like synaptic input, suggesting code conversion in single neurons. GC firing was correlated with dendritic complexity and intrinsic excitability, but not extrinsic excitatory input or dendritic cable properties. Thus, functional maturation may control input-output transformation and spatial code conversion.}, author = {Zhang, Xiaomin and Schlögl, Alois and Jonas, Peter M}, issn = {0896-6273}, journal = {Neuron}, number = {6}, pages = {1212--1225}, publisher = {Elsevier}, title = {{Selective routing of spatial information flow from input to output in hippocampal granule cells}}, doi = {10.1016/j.neuron.2020.07.006}, volume = {107}, year = {2020}, } @article{7473, abstract = {How structural and functional properties of synapses relate to each other is a fundamental question in neuroscience. Electrophysiology has elucidated mechanisms of synaptic transmission, and electron microscopy (EM) has provided insight into morphological properties of synapses. Here we describe an enhanced method for functional EM (“flash and freeze”), combining optogenetic stimulation with high-pressure freezing. We demonstrate that the improved method can be applied to intact networks in acute brain slices and organotypic slice cultures from mice. As a proof of concept, we probed vesicle pool changes during synaptic transmission at the hippocampal mossy fiber-CA3 pyramidal neuron synapse. Our findings show overlap of the docked vesicle pool and the functionally defined readily releasable pool and provide evidence of fast endocytosis at this synapse. Functional EM with acute slices and slice cultures has the potential to reveal the structural and functional mechanisms of transmission in intact, genetically perturbed, and disease-affected synapses.}, author = {Borges Merjane, Carolina and Kim, Olena and Jonas, Peter M}, issn = {0896-6273}, journal = {Neuron}, pages = {992--1006}, publisher = {Elsevier}, title = {{Functional electron microscopy (“Flash and Freeze”) of identified cortical synapses in acute brain slices}}, doi = {10.1016/j.neuron.2019.12.022}, volume = {105}, year = {2020}, } @article{7099, author = {Kasugai, Yu and Vogel, Elisabeth and Hörtnagl, Heide and Schönherr, Sabine and Paradiso, Enrica and Hauschild, Markus and Göbel, Georg and Milenkovic, Ivan and Peterschmitt, Yvan and Tasan, Ramon and Sperk, Günther and Shigemoto, Ryuichi and Sieghart, Werner and Singewald, Nicolas and Lüthi, Andreas and Ferraguti, Francesco}, issn = {0896-6273}, journal = {Neuron}, number = {4}, pages = {781--794.e4}, publisher = {Elsevier}, title = {{Structural and functional remodeling of amygdala GABAergic synapses in associative fear learning}}, doi = {10.1016/j.neuron.2019.08.013}, volume = {104}, year = {2019}, } @article{6454, abstract = {Adult neural stem cells and multiciliated ependymalcells are glial cells essential for neurological func-tions. Together, they make up the adult neurogenicniche. Using both high-throughput clonal analysisand single-cell resolution of progenitor division pat-terns and fate, we show that these two componentsof the neurogenic niche are lineally related: adult neu-ral stem cells are sister cells to ependymal cells,whereas most ependymal cells arise from the termi-nal symmetric divisions of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation, GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells. Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and identify the Geminin familymembers as key regulators of the initial pool of adultneural stem cells.}, author = {Ortiz-Álvarez, G and Daclin, M and Shihavuddin, A and Lansade, P and Fortoul, A and Faucourt, M and Clavreul, S and Lalioti, ME and Taraviras, S and Hippenmeyer, Simon and Livet, J and Meunier, A and Genovesio, A and Spassky, N}, issn = {1097-4199}, journal = {Neuron}, number = {1}, pages = {159--172.e7}, publisher = {Elsevier}, title = {{Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members}}, doi = {10.1016/j.neuron.2019.01.051}, volume = {102}, year = {2019}, } @article{8015, abstract = {The neural code of cortical processing remains uncracked; however, it must necessarily rely on faithful signal propagation between cortical areas. In this issue of Neuron, Joglekar et al. (2018) show that strong inter-areal excitation balanced by local inhibition can enable reliable signal propagation in data-constrained network models of macaque cortex. }, author = {Stroud, Jake P. and Vogels, Tim P}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {8--9}, publisher = {Elsevier}, title = {{Cortical signal propagation: Balance, amplify, transmit}}, doi = {10.1016/j.neuron.2018.03.028}, volume = {98}, year = {2018}, } @article{7698, abstract = {Motor output varies along the rostro-caudal axis of the tetrapod spinal cord. At limb levels, ∼60 motor pools control the alternation of flexor and extensor muscles about each joint, whereas at thoracic levels as few as 10 motor pools supply muscle groups that support posture, inspiration, and expiration. Whether such differences in motor neuron identity and muscle number are associated with segmental distinctions in interneuron diversity has not been resolved. We show that select combinations of nineteen transcription factors that specify lumbar V1 inhibitory interneurons generate subpopulations enriched at limb and thoracic levels. Specification of limb and thoracic V1 interneurons involves the Hox gene Hoxc9 independently of motor neurons. Thus, early Hox patterning of the spinal cord determines the identity of V1 interneurons and motor neurons. These studies reveal a developmental program of V1 interneuron diversity, providing insight into the organization of inhibitory interneurons associated with differential motor output.}, author = {Sweeney, Lora Beatrice Jaeger and Bikoff, Jay B. and Gabitto, Mariano I. and Brenner-Morton, Susan and Baek, Myungin and Yang, Jerry H. and Tabak, Esteban G. and Dasen, Jeremy S. and Kintner, Christopher R. and Jessell, Thomas M.}, issn = {0896-6273}, journal = {Neuron}, number = {2}, pages = {341--355.e3}, publisher = {Elsevier}, title = {{Origin and segmental diversity of spinal inhibitory interneurons}}, doi = {10.1016/j.neuron.2017.12.029}, volume = {97}, year = {2018}, } @article{8016, abstract = {Long-term modifications of neuronal connections are critical for reliable memory storage in the brain. However, their locus of expression—pre- or postsynaptic—is highly variable. Here we introduce a theoretical framework in which long-term plasticity performs an optimization of the postsynaptic response statistics toward a given mean with minimal variance. Consequently, the state of the synapse at the time of plasticity induction determines the ratio of pre- and postsynaptic modifications. Our theory explains the experimentally observed expression loci of the hippocampal and neocortical synaptic potentiation studies we examined. Moreover, the theory predicts presynaptic expression of long-term depression, consistent with experimental observations. At inhibitory synapses, the theory suggests a statistically efficient excitatory-inhibitory balance in which changes in inhibitory postsynaptic response statistics specifically target the mean excitation. Our results provide a unifying theory for understanding the expression mechanisms and functions of long-term synaptic transmission plasticity.}, author = {Costa, Rui Ponte and Padamsey, Zahid and D’Amour, James A. and Emptage, Nigel J. and Froemke, Robert C. and Vogels, Tim P}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {177--189.e7}, publisher = {Elsevier}, title = {{Synaptic transmission optimization predicts expression loci of long-term plasticity}}, doi = {10.1016/j.neuron.2017.09.021}, volume = {96}, year = {2017}, } @article{8020, abstract = {Balance of cortical excitation and inhibition (EI) is thought to be disrupted in several neuropsychiatric conditions, yet it is not clear how it is maintained in the healthy human brain. When EI balance is disturbed during learning and memory in animal models, it can be restabilized via formation of inhibitory replicas of newly formed excitatory connections. Here we assess evidence for such selective inhibitory rebalancing in humans. Using fMRI repetition suppression we measure newly formed cortical associations in the human brain. We show that expression of these associations reduces over time despite persistence in behavior, consistent with inhibitory rebalancing. To test this, we modulated excitation/inhibition balance with transcranial direct current stimulation (tDCS). Using ultra-high-field (7T) MRI and spectroscopy, we show that reducing GABA allows cortical associations to be re-expressed. This suggests that in humans associative memories are stored in balanced excitatory-inhibitory ensembles that lie dormant unless latent inhibitory connections are unmasked.}, author = {Barron, H.C. and Vogels, Tim P and Emir, U.E. and Makin, T.R. and O’Shea, J. and Clare, S. and Jbabdi, S. and Dolan, R.J. and Behrens, T.E.J.}, issn = {0896-6273}, journal = {Neuron}, number = {1}, pages = {191--203}, publisher = {Elsevier}, title = {{Unmasking latent inhibitory connections in human cortex to reveal dormant cortical memories}}, doi = {10.1016/j.neuron.2016.02.031}, volume = {90}, year = {2016}, } @article{8022, abstract = {Populations of neurons in motor cortex engage in complex transient dynamics of large amplitude during the execution of limb movements. Traditional network models with stochastically assigned synapses cannot reproduce this behavior. Here we introduce a class of cortical architectures with strong and random excitatory recurrence that is stabilized by intricate, fine-tuned inhibition, optimized from a control theory perspective. Such networks transiently amplify specific activity states and can be used to reliably execute multidimensional movement patterns. Similar to the experimental observations, these transients must be preceded by a steady-state initialization phase from which the network relaxes back into the background state by way of complex internal dynamics. In our networks, excitation and inhibition are as tightly balanced as recently reported in experiments across several brain areas, suggesting inhibitory control of complex excitatory recurrence as a generic organizational principle in cortex.}, author = {Hennequin, Guillaume and Vogels, Tim P and Gerstner, Wulfram}, issn = {0896-6273}, journal = {Neuron}, number = {6}, pages = {1394--1406}, publisher = {Elsevier}, title = {{Optimal control of transient dynamics in balanced networks supports generation of complex movements}}, doi = {10.1016/j.neuron.2014.04.045}, volume = {82}, year = {2014}, } @article{7785, abstract = {Neural circuit assembly requires selection of specific cell fates, axonal trajectories, and synaptic targets. By analyzing the function of a secreted semaphorin, Sema-2b, in Drosophila olfactory receptor neuron (ORN) development, we identified multiple molecular and cellular mechanisms that link these events. Notch signaling limits Sema-2b expression to ventromedial ORN classes, within which Sema-2b cell-autonomously sensitizes ORN axons to external semaphorins. Central-brain-derived Sema-2a and Sema-2b attract Sema-2b-expressing axons to the ventromedial trajectory. In addition, Sema-2b/PlexB-mediated axon-axon interactions consolidate this trajectory choice and promote ventromedial axon-bundle formation. Selecting the correct developmental trajectory is ultimately essential for proper target choice. These findings demonstrate that Sema-2b couples ORN axon guidance to postsynaptic target neuron dendrite patterning well before the final target selection phase, and exemplify how a single guidance molecule can drive consecutive stages of neural circuit assembly with the help of sophisticated spatial and temporal regulation.}, author = {Joo, William J. and Sweeney, Lora Beatrice Jaeger and Liang, Liang and Luo, Liqun}, issn = {0896-6273}, journal = {Neuron}, number = {4}, pages = {673--686}, publisher = {Elsevier}, title = {{Linking cell fate, trajectory choice, and target selection: Genetic analysis of sema-2b in olfactory axon targeting}}, doi = {10.1016/j.neuron.2013.03.022}, volume = {78}, year = {2013}, } @article{6138, author = {Bretscher, Andrew Jonathan and Kodama-Namba, Eiji and Busch, Karl Emanuel and Murphy, Robin Joseph and Soltesz, Zoltan and Laurent, Patrick and de Bono, Mario}, issn = {0896-6273}, journal = {Neuron}, number = {6}, pages = {1099--1113}, publisher = {Elsevier BV}, title = {{Temperature, oxygen, and salt-sensing neurons in C. elegans are carbon dioxide sensors that control avoidance behavior}}, doi = {10.1016/j.neuron.2011.02.023}, volume = {69}, year = {2011}, } @article{7701, abstract = {During assembly of the Drosophila olfactory circuit, projection neuron (PN) dendrites prepattern the developing antennal lobe before the arrival of axons from their presynaptic partners, the adult olfactory receptor neurons (ORNs). We previously found that levels of transmembrane Semaphorin-1a, which acts as a receptor, instruct PN dendrite targeting along the dorsolateral-ventromedial axis. Here we show that two secreted semaphorins, Sema-2a and Sema-2b, provide spatial cues for PN dendrite targeting. Sema-2a and Sema-2b proteins are distributed in gradients opposing the Sema-1a protein gradient, and Sema-1a binds to Sema-2a-expressing cells. In Sema-2a and Sema-2b double mutants, PN dendrites that normally target dorsolaterally in the antennal lobe mistarget ventromedially, phenocopying cell-autonomous Sema-1a removal from these PNs. Cell ablation, cell-specific knockdown, and rescue experiments indicate that secreted semaphorins from degenerating larval ORN axons direct dendrite targeting. Thus, a degenerating brain structure instructs the wiring of a developing circuit through the repulsive action of secreted semaphorins.}, author = {Sweeney, Lora Beatrice Jaeger and Chou, Ya-Hui and Wu, Zhuhao and Joo, William and Komiyama, Takaki and Potter, Christopher J. and Kolodkin, Alex L. and Garcia, K. Christopher and Luo, Liqun}, issn = {0896-6273}, journal = {Neuron}, number = {5}, pages = {734--747}, publisher = {Elsevier}, title = {{Secreted semaphorins from degenerating larval ORN axons direct adult projection neuron dendrite targeting}}, doi = {10.1016/j.neuron.2011.09.026}, volume = {72}, year = {2011}, }