Increases in Retrograde Injury Signaling Complex-Related Transcripts in Central Axons following Injury

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Increases in Retrograde Injury Signaling Complex-Related Transcripts in Central Axons following Injury

Axons in the peripheral nervous system respond to injury by activating retrograde injury signaling (RIS) pathways, which promote local axonal protein synthesis (LPS) and neuronal regeneration. RIS is also initiated following injury of neurons in the central nervous system (CNS). However, regulation of the localization of axonal mRNA required for LPS is not well understood. We used a hippocampal...

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Morphological methods were used to examine injury-induced growth of peripheral and central axons of nociceptive mechanosensory neurones in the ventrocaudal (VC) clusters of the pleural ganglia of Aplysia californica. Pedal nerve crush transected all axons in the nerve while leaving the overlying sheath largely intact. Immunohistochemical staining was performed with an antibody to a sensory-neur...

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Axoplasmic Importins Enable Retrograde Injury Signaling in Lesioned Nerve

Axoplasmic proteins containing nuclear localization signals (NLS) signal retrogradely by an unknown mechanism in injured nerve. Here we demonstrate that the importin/karyopherin alpha and beta families underlie this process. We show that importins are found in axons at significant distances from the cell body and that importin beta protein is increased after nerve lesion by local translation of...

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Signaling to transcription networks in the neuronal retrograde injury response.

Retrograde signaling from axon to soma activates intrinsic regeneration mechanisms in lesioned peripheral sensory neurons; however, the links between axonal injury signaling and the cell body response are not well understood. Here, we used phosphoproteomics and microarrays to implicate approximately 900 phosphoproteins in retrograde injury signaling in rat sciatic nerve axons in vivo and approx...

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ژورنال

عنوان ژورنال: Neural Plasticity

سال: 2016

ISSN: 2090-5904,1687-5443

DOI: 10.1155/2016/3572506