Elsevier

Brain Research

Volume 509, Issue 2, 19 February 1990, Pages 232-236
Brain Research

The effect of a conditioning lesion on sudomotor axon regeneration

https://doi.org/10.1016/0006-8993(90)90547-OGet rights and content

Abstract

The effects of a conditioning lesion on the rate of sudomotor axon regeneration were judged by the recovery of sweat gland (SG) secretion after cholinergic stimulation. Three groups of mice were given a conditioning lesion by crushing the sciatic nerve at mid-thigh 4, 7, and 14 days before a test lesion. A 4th group received a conditioning crush of the tibial nerve at the ankle 7 days before the test lesion. Control mice had a single test lesion. SG reinnervation in control mice began 19 days after the test lesion, and was functionally complete by 41 days. In groups with the conditioning lesion 4, 7 and 14 days before the test operation, the first reactive SGs reappeared at 16, 15, and 16 days respectively after the test lesion, and maximal recovery occurred by 33, 32, and 39 days. In mice with the distal conditioning lesion, reinnervation began at 19 days and was maximal by 36 days. In summary, a nerve conditioning lesion placed from 4 to 14 days prior to and at the same site as a test lesion significantly accelerated the growth rate of the fastest regenerating unmyelinated sudomotor axons and reduced the time until most SGs were reinnervated. A more distally placed test lesion reduced the interval for recovery.

References (30)

Cited by (9)

  • Macrophage biology in the peripheral nervous system after injury

    2019, Progress in Neurobiology
    Citation Excerpt :

    This conditioning lesion effect was shown to occur in both sensory and motor axons (McQuarrie, 1978; McQuarrie et al., 1977). McQuarrie et al. (1978) reported that, in contrast, the rate of regeneration actually decreases in sympathetic axons in the sciatic; however, a later study on sympathetic-cholinergic axons that innervate the sweat gland established that these neurons do show acceleration of regeneration after a conditioning lesion (Navarro and Kennedy, 1990). Though conditioning lesion experiments were initially performed entirely in vivo, the effect of an in vivo conditioning lesion can subsequently be studied in either explant or dissociated cell culture.

  • The neuroimmunology of degeneration and regeneration in the peripheral nervous system

    2015, Neuroscience
    Citation Excerpt :

    Several groups have confirmed marked increases in neurite outgrowth after a CL in explants of DRG and SCG (Edstrom et al., 1996; Shoemaker et al., 2005; Sachs et al., 2007; Niemi et al., 2013), and in dissociated neuron cultures of those ganglia (Hu-Tsai et al., 1994; White et al., 1996; Smith and Skene, 1997; Shoemaker et al., 2005; Sachs et al., 2007; Niemi et al., 2013). Additionally, in vivo regeneration studies established that a CL response occurs in motor, sensory and sympathetic neurons (McQuarrie et al., 1977; McQuarrie, 1978; Navarro and Kennedy, 1990). It is important to note that in DRG neurons, which have both a peripheral and a central branch, a CL is produced only after a lesion of the peripheral branch (e.g. Smith and Skene, 1997; Seijffers et al., 2007).

  • STAT3 integrates cytokine and neurotrophin signals to promote sympathetic axon regeneration

    2013, Molecular and Cellular Neuroscience
    Citation Excerpt :

    These cytokines act via the gp130 receptor (Ip et al., 1992; Taga and Kishimoto, 1997) to promote axon regeneration in the central and peripheral nervous systems (Cafferty et al., 2001; Ekstrom et al., 2000; Homs et al., 2011; Leibinger et al., 2009). In sympathetic neurons cytokines are involved in the “conditioning lesion” response whereby prior injury enhances the subsequent regeneration (Hyatt Sachs et al., 2010; McQuarrie and Grafstein, 1973; Navarro and Kennedy, 1990; Shoemaker et al., 2005). Cytokines are thought to enhance nerve regeneration after injury through stimulating transcription of regeneration associated genes via tyrosine phosphorylation of Signal Transducer and Activator of Transcription 3 (STAT3) (Ben-Yaakov et al., 2012; Habecker et al., 2009; Lee et al., 2004; Liu and Snider, 2001; O'Brien and Nathanson, 2007; Qiu et al., 2005; Smith and Skene, 1997).

  • An In Vitro Model for Conditioning Lesion Effect

    2019, Cellular and Molecular Neurobiology
View all citing articles on Scopus
View full text