Nerve Regeneration After Immediate and Delayed Suture

Holmes, William C.; Young, J. Z.

doi:10.1093/oxfordjournals.bmb.a070225

Cited by 71 publications

(105 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Establishment of this supportive microenvironment requires that nerve undergo the morphological changes of Wallerian degeneration (Holmes and Young, 1942;Fawcett and Keynes, 1990;Tonge and Golding, 1993), in which axon segments and myelin distal to a site of trauma degenerate (Holmes and Young, 1942) and are phagocytosed by Schwann cells and macrophages (Perry and Brown, 1992). Coincident with axonal degeneration, normally quiescent Schwann cells dedifferentiate and proliferate, an event critically important for the promotion of axonal regeneration (Hall and Gregson, 1977;Pellegrino et al, 1986;Fawcett and Keynes, 1990;Nadim et al, 1990).…”

Section: Abstract: Neuregulins; Glial Growth Factor; Schwann Cell; Ementioning

confidence: 99%

Expression of Neuregulins and their Putative Receptors, ErbB2 and ErbB3, Is Induced during Wallerian Degeneration

et al. 1997

View full text Add to dashboard Cite

Schwann cell dedifferentiation and proliferation is a prerequisite to axonal regeneration in the injured peripheral nervous system. The neuregulin (NRG) family of growth and differentiation factors may play a particularly important role in this process, because these axon-associated molecules are potent Schwann cell mitogens and differentiation factors in vitro. We have examined Schwann cell DNA synthesis and the expression of NRGs and their receptors, the erbB membrane tyrosine kinases, in rat sciatic nerve, sensory ganglia, and spinal cord 0 -30 d postaxotomy. Analysis of NRG cDNAs from these tissues revealed several novel splice variants and showed that cells endogenous to injured nerve express NRG mRNAs. A selective induction of mRNAs encoding the glial growth factor (GGF) subfamily of NRGs occurs in nerve beginning 3 d postaxotomy and thus coincides with the onset of Schwann cell DNA synthesis. In later stages of Wallerian degeneration, however, Schwann cell mitogenesis markedly decreases, whereas elevated GGF expression persists. Of the four known erbB kinases, Schwann cells express both erbB2 and erbB3 receptors over the entire interval studied. Expression of erbB2 and erbB3 is coordinately induced in response to axotomy, indicating that Schwann cell responses to NRGs may be modulated by changes in receptor density. Neuregulin (including transmembrane precursors) and erbB protein are associated with Schwann cells postaxotomy. Thus, in contrast to the concept of NRGs as axon-associated mitogens, our findings suggest that NRGs produced by Schwann cells themselves may be partially responsible for Schwann cell proliferation during Wallerian degeneration, probably acting via autocrine or paracrine mechanisms.

show abstract

Section: Abstract: Neuregulins; Glial Growth Factor; Schwann Cell; Ementioning

confidence: 99%

Expression of Neuregulins and their Putative Receptors, ErbB2 and ErbB3, Is Induced during Wallerian Degeneration

et al. 1997

View full text Add to dashboard Cite

show abstract

“…The existence of such guidance is suggested by the fact that the branching pattern of a regenerated nerve closely resembles that of the normal nerve (Glees, 1943), and by the observation that the advancing axons are found almost exclusively on the inside surface of empty sheaths, referred to as Schwann tubes (Ramon y Cajal, 1928;Holmes and Young, 1942;Scherer and Easter, 1984;Scherer, 1986). These tubes, which consist of the collagenous endoneurial sheaths and basal laminae of Schwann cells (Thomas, 1964), retain their structure when the distal stump is denervated during Wallerian degeneration (Weddell, 1942).…”

mentioning

confidence: 99%

Guidance of regenerating motor axons in larval and juvenile bullfrogs

Lee

Farel

1988

J. Neurosci.

View full text Add to dashboard Cite

The segmental distribution of regenerating bullfrog motor axons was mapped in advanced tadpoles and juvenile frogs by stimulating selected muscle nerves and recording from the distal ends of the 3 lumbar ventral roots (VRs) that innervate the hindlimb. When motoneurons were axotomized by VR transection, they reestablished their original innervation fields, rarely, if ever, growing beyond the territory normally supplied by their spinal segment. However, when motoneurons were axotomized in the spinal nerves at the level of the hindlimb plexus, some of them regenerated into limb nerves that lay outside the axons' normal segmental boundaries, and many regenerated into the medial femoral cutaneous nerve, a pathway normally limited to sensory axons. These observations suggest that the ultimate destinations of regenerating axons are largely determined by structures the axons encounter as they penetrate the distal nerve stumps. Thus, axons regenerating from a severed VR grow into that root's own distal stump and reinnervate the hindlimb in a manner that is segmentally appropriate; axons transected near the plexus have access to the pathways of sensory, as well as motor, axons in all 3 lumbar segments, and establish innervation fields that are inappropriate for their segment of origin and their motor function.

show abstract

“…Scar formation is a challenge for peripheral nerve surgeon. Traditionally, surgeons attempt to control collagen scar formation by close approximation of corresponding fascicles of the proximal to distal stumps [14,19]. Although excellent coaptation has been achieved in matching proximal and distal nerve stumps and proper guiding axon regeneration toward the original target tissues, full recovery of nerve function does not guarantee in every patients [11].…”

Section: Effect Of Melatonin Treatment On Apoptosis and Neuronal Cellmentioning

confidence: 99%

“…Excessive collagen formation can create a mechanical barrier to axonal regeneration, and the resulting scar formation can hinder axonal regrowth [21,24,31]. A variety of techniques have been proposed to decrease the neuroma formation characterised by accumulation of connective tissue at the lesion site [15,19,31].…”

Section: Effect Of Melatonin Treatment On Apoptosis and Neuronal Cellmentioning

confidence: 99%