Disruption of Fast Axonal Transport in Vivo Leads to Alterations in Schwann Cell Gene Expression

Wu, Wendong; Toma, Jean G.; Chan, Honey; Smith, Richard S.; Miller, Freda D.

doi:10.1006/dbio.1994.1159

Cited by 19 publications

(15 citation statements)

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“…8). Based on the length of the peripheral axon in the hindleg of the rat, the only mechanism that could produce such a short latency to onset of the primed state would be rapid axonal transport (Wu et al, 1994;Shubayev and Myers, 2001;Lund et al, 2005;Chidlow et al, 2011). We currently do not know the nature of the signal that is transmitted from the cell body to the peripheral terminal of the nociceptor that is involved in the induction of hyperalgesic priming.…”

Section: Discussionmentioning

confidence: 99%

Distinct Terminal and Cell Body Mechanisms in the Nociceptor Mediate Hyperalgesic Priming

2015

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Hyperalgesic priming, a form of neuroplasticity in nociceptors, is a model of the transition from acute to chronic pain in the rat, which involves signaling from the site of an acute tissue insult in the vicinity of the peripheral terminal of a nociceptor to its cell body that, in turn, induces a signal that travels back to the terminal to mediate a marked prolongation of prostaglandin E 2 -induced hyperalgesia. In the present experiments, we studied the underlying mechanisms in the cell body and compared them to the mechanisms in the nerve terminal. Injection of a cell-permeant cAMP analog, 8-bromo cAMP, into the dorsal root ganglion induced mechanical hyperalgesia and priming with an onset more rapid than when induced at the peripheral terminal. Priming induced by intraganglion 8-bromo cAMP was prevented by an oligodeoxynucleotide antisense to mRNA for a transcription factor, cAMP response element-binding protein (CREB), and by an inhibitor of importin, which is required for activated CREB to get into the nucleus. While peripheral administration of 8-bromo cAMP also produced hyperalgesia, it did not produce priming. Conversely, interventions administered in the vicinity of the peripheral terminal of the nociceptor that induces priming-PKC activator, NGF, and TNF-␣-when injected into the ganglion produce hyperalgesia but not priming. The protein translation inhibitor cordycepin, injected at the peripheral terminal but not into the ganglion, reverses priming induced at either the ganglion or peripheral terminal of the nociceptor. These data implicate different mechanisms in the soma and terminal in the transition to chronic pain.

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Section: Discussionmentioning

confidence: 99%

Distinct Terminal and Cell Body Mechanisms in the Nociceptor Mediate Hyperalgesic Priming

2015

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“…However, myelination proceeds relatively normally even in the complete absence of NFs. Axons do appear to affect a number of Schwann cell functions, including translocation of the peripheral myelin protein 22 into myelin (Pareek et al, 1997) and expression of the myelin protein P o (Wu et al, 1994), the p75 nerve growth factor receptor (Wu et al, 1994), ciliary neurotrophic factor (Lee et al, 1995), β4‐integrin (Feltri et al, 1994), and the transcription factor Krox20 (Murphy et al, 1996). Whether any of these processes is involved in the critical signal that indicates to the Schwann cell the axon's intended diameter is unclear.…”

Section: Discussionmentioning

confidence: 99%

Schwann cells and oligodendrocytes read distinct signals in establishing myelin sheath thickness

Elder

Friedrich

Lazzarini

2001

J of Neuroscience Research

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Schwann cells and oligodendrocytes produce myelin sheaths of widely varying sizes. How these cells determine the size of myelin sheath for a particular axon is incompletely understood. Axonal diameter has long been suspected to be a signal in this process. We have analyzed myelin sheath thickness in L5 lumbar root and spinal cord white matter of a series of mouse mutants with diminished axonal calibers resulting from a deficiency of neurofilaments (NFs). In the PNS, average axonal diameters were reduced by 20-37% in the NF mutants. Remarkably, the average myelin sheath thickness remained unchanged from control values, and regression analysis showed sheaths abnormally thick for a given size of axon. These data show that a genetically induced reduction in axonal caliber does not cause a reduction in myelin sheath thickness in PNS and indicate that Schwann cells read some intrinsic signal on axons that can be uncoupled from axonal diameter. Interestingly, myelin sheaths in the spinal cord of these animals were not abnormally thick, arguing that axonal diameter may contribute directly to the regulation of myelination in the CNS and that oligodendrocytes and Schwann cells use different cues to set myelin sheath thickness.

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“…Axonal destruction precedes the disintegration of the associated myelin in Wallerian degeneration (Nathaniel and Pease, 1963). The destruction of axons is thought to be initiated by a calcium-dependent process following axotomy (reviewed by Brü ck, 1997;Schlaepfer and Bunge, 1973), followed by myelin breakdown in SCs, probably in response to a positive signal from the injured axon (Kidd and Health, 1991) or the absence of the signal normally provided by an intact axon (Oaklander and Spencer, 1988;Wu et al, 1994). The clearance of these injured tissue components is one of the most important events preceding the regenerative process (Beuche and Friede, 1984;Scheidt and Friede, 1987).…”

Section: Introductionmentioning

confidence: 99%

Myelin phagocytosis by macrophages and nonmacrophages during Wallerian degeneration

Hirata

Kawabuchi

2002

Microscopy Res & Technique

175

134

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The literature concerning Schwann cells (SCs) and macrophages in myelin phagocytosis during Wallerian degeneration is reviewed. SCs carry out the first step in the removal of myelin by segmenting myelin and then incorporating the degraded myelin. The recruited macrophages then join in the myelin-phagocytosis event, appearing to make full use of their original phagocyte abilities until the end of myelin clearance. The molecular mechanisms of the two cells underlying myelin phagocytosis are thought to be different; myelin phagocytosis by SCs being lectin-mediated, i.e., opsonin-independent, whereas that of macrophages is mainly opsonin-dependent. It is important to note that SCs and macrophages cooperatively accomplish myelin phagocytosis.

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Disruption of Fast Axonal Transport in Vivo Leads to Alterations in Schwann Cell Gene Expression

Cited by 19 publications

References 0 publications

Distinct Terminal and Cell Body Mechanisms in the Nociceptor Mediate Hyperalgesic Priming

Distinct Terminal and Cell Body Mechanisms in the Nociceptor Mediate Hyperalgesic Priming

Schwann cells and oligodendrocytes read distinct signals in establishing myelin sheath thickness

Myelin phagocytosis by macrophages and nonmacrophages during Wallerian degeneration

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