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Journal of Neurogenetics Jun 2016The most striking structure in the nervous system is the complex yet stereotyped morphology of the neuronal dendritic tree. Dendritic morphologies and the connections... (Review)
Review
The most striking structure in the nervous system is the complex yet stereotyped morphology of the neuronal dendritic tree. Dendritic morphologies and the connections they make govern information flow and integration in the brain. The fundamental mechanisms that regulate dendritic outgrowth and branching are subjects of extensive study. In this review, we summarize recent advances in the molecular and cellular mechanisms for routing dendrites in layers and columns, prevalent organizational structures in the brain. We highlight how dendritic patterning influences the formation of synaptic circuits.
Topics: Animals; Body Patterning; Brain; Connectome; Dendrites; Humans
PubMed: 27315108
DOI: 10.3109/01677063.2016.1173038 -
Neuron Oct 2003Dendrite development is an important and unsolved problem in neuroscience. The nervous system is composed of a vast number of neurons with strikingly different... (Review)
Review
Dendrite development is an important and unsolved problem in neuroscience. The nervous system is composed of a vast number of neurons with strikingly different morphology. Neurons are highly polarized cells with distinct subcellular compartments, including one or multiple dendritic processes arising from the cell body, and a single, extended axon. Communications between neurons involve synapses formed between axons of the presynaptic neurons and dendrites of the postsynaptic neurons. Extensive studies over the past decade have identified many molecules underlying axonal outgrowth and pathfinding. In contrast, the control of dendrite development is still much less well understood. However, recent progress has begun to shed light on the molecular mechanisms that orchestrate dendrite growth, arborization, and guidance.
Topics: Animals; Cell Differentiation; Dendrites; Humans; Nerve Net; Neurons
PubMed: 14556706
DOI: 10.1016/s0896-6273(03)00631-7 -
Scientific Reports Apr 2023With Hebbian learning 'who fires together wires together', well-known problems arise. Hebbian plasticity can cause unstable network dynamics and overwrite stored...
With Hebbian learning 'who fires together wires together', well-known problems arise. Hebbian plasticity can cause unstable network dynamics and overwrite stored memories. Because the known homeostatic plasticity mechanisms tend to be too slow to combat unstable dynamics, it has been proposed that plasticity must be highly gated and synaptic strengths limited. While solving the issue of stability, gating and limiting plasticity does not solve the stability-plasticity dilemma. We propose that dendrites enable both stable network dynamics and considerable synaptic changes, as they allow the gating of plasticity in a compartment-specific manner. We investigate how gating plasticity influences network stability in plastic balanced spiking networks of neurons with dendrites. We compare how different ways to gate plasticity, namely via modulating excitability, learning rate, and inhibition increase stability. We investigate how dendritic versus perisomatic gating allows for different amounts of weight changes in stable networks. We suggest that the compartmentalisation of pyramidal cells enables dendritic synaptic changes while maintaining stability. We show that the coupling between dendrite and soma is critical for the plasticity-stability trade-off. Finally, we show that spatially restricted plasticity additionally improves stability.
Topics: Dendrites; Neuronal Plasticity; Learning; Pyramidal Cells; Homeostasis; Action Potentials
PubMed: 37085642
DOI: 10.1038/s41598-023-32410-0 -
The International Journal of... Nov 2013The Abl2/Arg nonreceptor tyrosine kinase is enriched in dendritic spines where it is essential for maintaining dendrite and synapse stability in the postnatal mouse... (Review)
Review
The Abl2/Arg nonreceptor tyrosine kinase is enriched in dendritic spines where it is essential for maintaining dendrite and synapse stability in the postnatal mouse brain. Arg is activated downstream of integrin α3β1 receptors and it regulates the neuronal actin cytoskeleton by directly binding F-actin and via phosphorylation of substrates including p190RhoGAP and cortactin. Neurons in mice lacking Arg or integrin α3β1 develop normally through postnatal day 21 (P21), however by P42 mice exhibit major reductions in dendrite arbor size and complexity, and lose dendritic spines and synapses. As a result, mice with loss of Arg and Arg-dependent signaling pathways have impairments in memory tasks, heightened sensitivity to cocaine, and vulnerability to corticosteroid-induced neuronal remodeling. Therefore, understanding the molecular mechanisms of Arg regulation may lead to therapeutic approaches to treat human psychiatric and neurodegenerative diseases in which neuronal structure is destabilized.
Topics: Animals; Cocaine; Dendrites; Humans; Memory; Protein-Tyrosine Kinases; Signal Transduction; Stress, Psychological; Synapses
PubMed: 23916785
DOI: 10.1016/j.biocel.2013.07.018 -
The Journal of Cell Biology Oct 2018The mechanisms by which the actin cytoskeleton regulates dendritic branching are not fully understood. Nithianandam and Chien (2018....
The mechanisms by which the actin cytoskeleton regulates dendritic branching are not fully understood. Nithianandam and Chien (2018. https://doi.org/10.1083/jcb.201711136) discover actin blobs, new structures that mediate dynamic actin delivery within a growing dendrite arbor and that mark sites of future branch formation.
Topics: Actin Cytoskeleton; Actins; Dendrites
PubMed: 30206148
DOI: 10.1083/jcb.201808095 -
Acta Neuropathologica Feb 2021Intellectual disability (ID) corresponds to several neurodevelopmental disorders of heterogeneous origin in which cognitive deficits are commonly associated with... (Review)
Review
Intellectual disability (ID) corresponds to several neurodevelopmental disorders of heterogeneous origin in which cognitive deficits are commonly associated with abnormalities of dendrites and dendritic spines. These histological changes in the brain serve as a proxy for underlying deficits in neuronal network connectivity, mostly a result of genetic factors. Historically, chromosomal abnormalities have been reported by conventional karyotyping, targeted fluorescence in situ hybridization (FISH), and chromosomal microarray analysis. More recently, cytogenomic mapping, whole-exome sequencing, and bioinformatic mining have led to the identification of novel candidate genes, including genes involved in neuritogenesis, dendrite maintenance, and synaptic plasticity. Greater understanding of the roles of these putative ID genes and their functional interactions might boost investigations into determining the plausible link between cellular and behavioral alterations as well as the mechanisms contributing to the cognitive impairment observed in ID. Genetic data combined with histological abnormalities, clinical presentation, and transgenic animal models provide support for the primacy of dysregulation in dendrite structure and function as the basis for the cognitive deficits observed in ID. In this review, we highlight the importance of dendrite pathophysiology in the etiologies of four prototypical ID syndromes, namely Down Syndrome (DS), Rett Syndrome (RTT), Digeorge Syndrome (DGS) and Fragile X Syndrome (FXS). Clinical characteristics of ID have also been reported in individuals with deletions in the long arm of chromosome 10 (the q26.2/q26.3), a region containing the gene for the collapsin response mediator protein 3 (CRMP3), also known as dihydropyrimidinase-related protein-4 (DRP-4, DPYSL4), which is involved in dendritogenesis. Following a discussion of clinical and genetic findings in these syndromes and their preclinical animal models, we lionize CRMP3/DPYSL4 as a novel candidate gene for ID that may be ripe for therapeutic intervention.
Topics: Animals; Child, Preschool; Chromosome Aberrations; Dendrites; Humans; Intellectual Disability; Nerve Tissue Proteins
PubMed: 33226471
DOI: 10.1007/s00401-020-02244-5 -
PLoS Genetics Nov 2023Sensory neurons enable an organism to perceive external stimuli, which is essential for survival. The sensory capacity of a neuron depends on the elaboration of its...
Sensory neurons enable an organism to perceive external stimuli, which is essential for survival. The sensory capacity of a neuron depends on the elaboration of its dendritic arbor and the localization of sensory ion channels to the dendritic membrane. However, it is not well understood when and how ion channels localize to growing sensory dendrites and whether their delivery is coordinated with growth of the dendritic arbor. We investigated the localization of the DEG/ENaC/ASIC ion channel Pickpocket (Ppk) in the peripheral sensory neurons of developing fruit flies. We used CRISPR-Cas9 genome engineering approaches to tag endogenous Ppk1 and visualize it live, including monitoring Ppk1 membrane localization via a novel secreted split-GFP approach. Fluorescently tagged endogenous Ppk1 localizes to dendrites, as previously reported, and, unexpectedly, to axons and axon terminals. In dendrites, Ppk1 is present throughout actively growing dendrite branches and is stably integrated into the neuronal cell membrane during the expansive growth of the arbor. Although Ppk channels are dispensable for dendrite growth, we found that an over-active channel mutant severely reduces dendrite growth, likely by acting at an internal membrane and not the dendritic membrane. Our data reveal that the molecular motor dynein and recycling endosome GTPase Rab11 are needed for the proper trafficking of Ppk1 to dendrites. Based on our data, we propose that Ppk channel transport is coordinated with dendrite morphogenesis, which ensures proper ion channel density and distribution in sensory dendrites.
Topics: Animals; Drosophila; Dendrites; Sensory Receptor Cells; Axons; Drosophila Proteins; Ion Channels
PubMed: 37943859
DOI: 10.1371/journal.pgen.1011025 -
Cold Spring Harbor Perspectives in... Sep 2010The spatial pattern of branches within axonal or dendritic arbors and the relative arrangement of neighboring arbors with respect to one another impact a neuron's... (Review)
Review
The spatial pattern of branches within axonal or dendritic arbors and the relative arrangement of neighboring arbors with respect to one another impact a neuron's potential connectivity. Although arbors can adopt diverse branching patterns to suit their functions, evenly spread branches that avoid clumping or overlap are a common feature of many axonal and dendritic arbors. The degree of overlap between neighboring arbors innervating a surface is also characteristic within particular neuron types. The arbors of some populations of neurons innervate a target with a comprehensive and nonoverlapping "tiled" arrangement, whereas those of others show substantial territory overlap. This review focuses on cellular and molecular studies that have provided insight into the regulation of spatial arrangements of neurite branches within and between arbors. These studies have revealed principles that govern arbor arrangements in dendrites and axons in both vertebrates and invertebrates. Diverse molecular mechanisms controlling the spatial patterning of sister branches and neighboring arbors have begun to be elucidated.
Topics: Animals; Axons; Dendrites; Humans; Models, Neurological; Nerve Net; Neurons
PubMed: 20573716
DOI: 10.1101/cshperspect.a001750 -
Small GTPases Mar 2018Neurons are highly polarized cells that exhibit one of the more complex morphology and function. Neuronal intracellular trafficking plays a key role in dictating the... (Review)
Review
Neurons are highly polarized cells that exhibit one of the more complex morphology and function. Neuronal intracellular trafficking plays a key role in dictating the directionality and specificity of vesicle formation, transport and fusion, allowing the transmission of information in sophisticate cellular network. Thus, the integrity of protein trafficking and spatial organization is especially important in neuronal cells. RAB proteins, small monomeric GTPases belonging to the RAS superfamily, spatially and temporally orchestrate specific vesicular trafficking steps. In this review we summarise the known roles of RAB GTPases involved in the maintenance of neuronal vesicular trafficking in the central nervous system. In particular, we discriminate the axonal pre-synaptic trafficking and dendritic post-synaptic trafficking, to better underlie how a correct orchestration of vesicle movement is necessary to maintain neuronal polarity and then, to permit an accurate architecture and functionality of synaptic activity.
Topics: Animals; Biological Transport; Dendrites; Humans; Synapses; rab GTP-Binding Proteins
PubMed: 28146371
DOI: 10.1080/21541248.2016.1277001 -
The Journal of Neuroscience : the... Mar 2022Dendrite and axon arbor sizes are critical to neuronal function and vary widely between different neuron types. The relative dendrite and axon sizes of synaptic partners...
Dendrite and axon arbor sizes are critical to neuronal function and vary widely between different neuron types. The relative dendrite and axon sizes of synaptic partners control signal convergence and divergence in neural circuits. The developmental mechanisms that determine cell-type-specific dendrite and axon size and match synaptic partners' arbor territories remain obscure. Here, we discover that retinal horizontal cells express the leucine-rich repeat domain cell adhesion molecule AMIGO1. Horizontal cells provide pathway-specific feedback to photoreceptors-horizontal cell axons to rods and horizontal cell dendrites to cones. AMIGO1 selectively expands the size of horizontal cell axons. When is deleted in all or individual horizontal cells of either sex, their axon arbors shrink. By contrast, horizontal cell dendrites and synapse formation of horizontal cell axons and dendrites are unaffected by AMIGO1 removal. The dendrites of rod bipolar cells, which do not express AMIGO1, shrink in parallel with horizontal cell axons in () mice. This territory matching maintains the function of the rod bipolar pathway, preserving bipolar cell responses and retinal output signals in mice. We previously identified AMIGO2 as a scaling factor that constrains retinal neurite arbors. Our current results identify AMIGO1 as a scaling factor that expands retinal neurite arbors and reveal territory matching as a novel homeostatic mechanism. Territory matching interacts with other homeostatic mechanisms to stabilize the development of the rod bipolar pathway, which mediates vision near the threshold. Neurons send and receive signals through branched axonal and dendritic arbors. The size of these arbors is critical to the function of a neuron. Axons and dendrites grow during development and are stable at maturity. The mechanisms that determine axon and dendrite size are not well understood. Here, we identify a cell surface protein, AMIGO1, that selectively promotes axon growth of horizontal cells, a retinal interneuron. Removal of AMIGO1 reduces the size of horizontal cell axons without affecting the size of their dendrites or the ability of both arbors to form connections. The changes in horizontal cell axons are matched by changes in synaptic partner dendrites to stabilize retinal function. This identifies territory matching as a novel homeostatic plasticity mechanism.
Topics: Animals; Axons; Dendrites; Mice; Retina; Retinal Bipolar Cells; Retinal Cone Photoreceptor Cells
PubMed: 35169021
DOI: 10.1523/JNEUROSCI.1164-21.2022