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1.
  • Allan, D.W., et al. (författare)
  • Regulators acting in combinatorial codes also act independently in single differentiating neurons
  • 2005
  • Ingår i: Neuron. - 0896-6273 .- 1097-4199. ; 45:5, s. 689-700
  • Tidskriftsartikel (refereegranskat)abstract
    • In the Drosophila ventral nerve cord, a small number of neurons express the LIM-homeodomain gene apterous (ap). These ap neurons can be subdivided based upon axon pathfinding and their expression of neuropeptidergic markers. ap, the zinc finger gene squeeze, the bHLH gene dimmed, and the BMP pathway are all required for proper specification of these cells. Here, using several ap neuron terminal differentiation markers, we have resolved how each of these factors contributes to ap neuron diversity. We find that these factors interact genetically and biochemically in subtype-specific combinatorial codes to determine certain defining aspects of ap neuron subtype identity. However, we also find that ap, dimmed, and squeeze additionally act independently of one another to specify certain other defining aspects of ap neuron subtype identity. Therefore, within single neurons, we show that single regulators acting in numerous molecular contexts differentially specify multiple subtype-specific traits. Copyright ©2005 by Elsevier Inc.
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  • Arthur-Farraj, Peter J., et al. (författare)
  • c-Jun Reprograms Schwann Cells of Injured Nerves to Generate a Repair Cell Essential for Regeneration
  • 2012
  • Ingår i: Neuron. - 0896-6273 .- 1097-4199. ; 75:4, s. 633-647
  • Tidskriftsartikel (refereegranskat)abstract
    • The radical response of peripheral nerves to injury (Wallerian degeneration) is the cornerstone of nerve repair. We show that activation of the transcription factor c-Jun in Schwann cells is a global regulator of Wallerian degeneration. c-Jun governs major aspects of the injury response, determines the expression of trophic factors, adhesion molecules, the formation of regeneration tracks and myelin clearance and controls the distinctive regenerative potential of peripheral nerves. A key function of c-Jun is the activation of a repair program in Schwann cells and the creation of a cell specialized to support regeneration. We show that absence of c-Jun results in the formation of a dysfunctional repair cell, striking failure of functional recovery, and neuronal death. We conclude that a single glial transcription factor is essential for restoration of damaged nerves, acting to control the transdifferentiation of myelin and Remak Schwann cells to dedicated repair cells in damaged tissue.
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  • Barbier, Estelle, et al. (författare)
  • mTORC and ProSAPiP1: How Alcohol Changes Synapses of Reward Circuitry
  • 2017
  • Ingår i: Neuron. - : CELL PRESS. - 0896-6273 .- 1097-4199. ; 96:1
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • Alcohol addiction is characterized by broad and persistent changes in brain function, but the underlying neural adaptations remain largely unknown. In this issue of Neuron, Laguesse et al. (2017) describe a neural mechanism through which long-term alcohol exposure induces structural and synaptic adaptations that promote excessive alcohol use.
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  • Barg, Sebastian, et al. (författare)
  • Delay between fusion pore opening and peptide release from large dense-core vesicles in neuroendocrine cells.
  • 2002
  • Ingår i: Neuron. - : Cell Press. - 0896-6273 .- 1097-4199. ; 33:2, s. 287-299
  • Tidskriftsartikel (refereegranskat)abstract
    • Peptidergic neurotransmission is slow compared to that mediated by classical neurotransmitters. We have studied exocytotic membrane fusion and cargo release by simultaneous capacitance measurements and confocal imaging of single secretory vesicles in neuroendocrine cells. Depletion of the readily releasable pool (RRP) correlated with exocytosis of 10%-20% of the docked vesicles. Some remaining vesicles became releasable after recovery of RRP. Expansion of the fusion pore, seen as an increase in luminal pH, occurred after approximately 0.3 s, and peptide release was delayed by another 1-10 s. We conclude that (1) RRP refilling involves chemical modification of vesicles already in place, (2) the release of large neuropeptides via the fusion pore is negligible and only proceeds after complete fusion, and (3) sluggish peptidergic transmission reflects the time course of vesicle emptying.
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