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371 - 380 of 19679 results
  • Abstract
    Dendrite versus axon regeneration in central nervous system repair: which way to grow?
    Despite intensive research, successful regeneration and subsequent functional recovery of the injured or diseased mammalian central nervous system (CNS) can still not be evoked. One essential component of the neuronal circuitry might have been overlooke...
    Nov 15, 2016
  • Abstract
    Radial glial activation by Kv3 deletion in suppressing inflammatory demyelinaton and axon degeneration
    The development of neuroprotective and repair strategies for treating progressive multiple sclerosis (MS) requires new insights in axonal injury and recovery. 4-aminopyridine (4-AP), a blocker of voltage-gated K+ (Kv) channels, is used in symptomatic tr...
    Nov 15, 2016
  • Abstract
    Axon initial segment changes in a potential new mouse model of Multiple Sclerosis
    Multiple Sclerosis (MS) is a demyelinating disorder of the CNS for which secondary gray matter (GM) damage, including lesions and progressive neurodegeneration, is reemerging as an integral component of the pathophysiology. To investigate this secondary...
    Nov 15, 2016
  • Abstract
    EphB2 released via extracellular vesicles, a contact-independent signaling mechanism in axon guidance
    Eph receptors comprise the largest subfamily of receptor tyrosine kinases and together with their membrane-tethered ligands, the ephrins, they function in many different physiological processes including stem and progenitor cell migration, axon guidance...
    Nov 14, 2016
  • Abstract
    The kruppel like factor gene target dusp 14 regulates axon growth and regeneration
    Central nervous system (CNS) neurons in adult mammals are unable to regenerate their axons after injury. Retinal ganglion cells' (RGCs') intrinsic ability to regenerate and extend their axons is limited after birth. Krüppel-like transcription factor (KL...
    Nov 14, 2016
  • Abstract
    Overexpression of KLF6 in corticospinal tract neurons promotes axon growth after spinal injury
    Axonal regeneration in the central nervous system is limited in part by a developmental decline in the intrinsic regenerative capacity of central nervous system (CNS) neurons. Changes in gene expression are likely involved, and thus transcription factor...
    Nov 14, 2016
  • Abstract
    Identification of an activity-induced, calcium-dependent glutamine transporter in hippocampal axon terminals
    Excessive presynaptic glutamatergic transmission is thought to be involved in various human disorders including epilepsy. Seizure activity or intense glutamatergic transmission requires import of glutamine into axon terminals from glia to maintain vesic...
    Nov 13, 2016
  • Abstract
    Synaptic phospholipid signaling modulates axon outgrowth via glutamate dependent Ca2+-mediated molecular pathways
    Altered synaptic bioactive lipid signaling has been shown to augment neuronal excitation in the hippocampus of adult animals by activation of presynaptic LPA2-receptors leading to increased presynaptic glutamate release. Here we show that this results i...
    Nov 13, 2016
  • Abstract
    Study of genes critical for retinal axon navigational error associated with ocular albinism
    Mutations in the Ocular Albinism 1 (OA1) gene are responsible for the disease, ocular albinism, characterized by abnormal melanosome biogenesis and navigation error of the retinal ganglion cell (RGC) axons to the brain. How the reduced pigmentation of t...
    Nov 13, 2016
  • Etv5 Is Required for Peripheral Nerve Function and the Injury Response | eNeuro
    The development of Schwann cells, which myelinate axons in the peripheral nervous system, is critically dependent on MEK/ERK signaling. While Ets-domain transcription factors ( Etv1 , Etv4 , Etv5 ) are downstream effectors of this pathway, only Etv1 has been specifically linked to Schwann cell development. Here, we examined the functions of Etv5 , which is expressed in Schwann cell precursors, neural crest cells and satellite glia, at embryonic stages and at low levels in mature Schwann cells. In hypomorphic Etv5tm1Kmm homozygous mutant mice, no overt defects in Schwann cell differentiation were observed at embryonic stages. To study the function of Etv5 in juvenile (postnatal days 21–30) and mature adult (6 month) mice, we generated Etv5 conditional knock-outs (cKOs) using a Sox10-Cre driver. In juvenile male Etv5 -cKO mice, Schwann cell numbers increased normally after a peripheral nerve crush injury, a response that was attenuated by 6 months. Transmission electron microscopy of the naive sciatic nerve ...
    Jul 1, 2025 Lauren Belfiore
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