The effect of a conditioning lesion on the regeneration of motor axons

McQuarrie, Irvine G.

doi:10.1016/0006-8993(78)91116-2

Cited by 114 publications

(50 citation statements)

References 18 publications

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“…The increased axonal outgrowth from the exercise-conditioned neurons closely resembles the conditioning effect of peripheral axotomy, where distal nerve injury primes neurons for more rapid axonal regeneration after a second injury placed proximal to the ''conditioning'' injury (27)(28)(29). In an analogous fashion, our results show enhanced nerve regeneration in animals that had exercised for 7 days compared with sedentary animals.…”

Section: Discussionsupporting

confidence: 70%

Voluntary exercise increases axonal regeneration from sensory neurons

Molteni

Zheng

Ying

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

167

128

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Recent advances in understanding the role of neurotrophins on activity-dependent plasticity have provided insight into how behavior can affect specific aspects of neuronal biology. We present evidence that voluntary exercise can prime adult dorsal root ganglion neurons for increased axonal regeneration through a neurotrophin-dependent mechanism. Dorsal root ganglion neurons showed an increase in neurite outgrowth when cultured from animals that had undergone 3 or 7 days of exercise compared with sedentary animals. Neurite length over 18 -22 h in culture correlated directly with the distance that animals ran. The exerciseconditioned animals also showed enhanced regrowth of axons after an in vivo nerve crush injury. Sensory ganglia from the 3-and 7-day-exercised animals contained higher brain-derived neurotrophic factor, neurotrophin 3, synapsin I, and GAP43 mRNA levels than those from sedentary animals. Consistent with the rise in brain-derived neurotrophic factor and neurotrophin 3 during exercise, the increased growth potential of the exercise-conditioned animals required activation of the neurotrophin signaling in vivo during the exercise period but did not require new mRNA synthesis in culture.neurotrophin ͉ gene expression ͉ plasticity ͉ neural activity ͉ experience A lterations in neuronal activity can lead to lasting changes in the ability of the nervous system to transduce information (1). Such synaptic plasticity is well documented in the developing nervous system where the levels of neuronal activity can influence the eventual organization of cortical circuits (2). More recent studies (3) indicate that activity-dependent plasticity is retained into adulthood. The morphological basis of lasting forms of activity-dependent synaptic plasticity is manifest as an overall change in the number and͞or area of synaptic contacts (1-3). In the developed organism, both of these processes require remodeling of synaptic structures, either through retraction of existing neuronal processes or by growth of new neuronal processes.Formation of synaptic contacts and growth is a dynamic process that is largely affected through interactions with the environment, such that experience can imprint the nervous system by regulating these events (3). Neurotrophins, originally described for their role on growth and differentiation of neurons, are becoming recognized as regulators of synaptic plasticity (4, 5). The levels of the neurotrophins and͞or their receptors can be altered by neuronal activity, thus providing a potential means to perpetuate changes in synaptic transmission (6, 7). Brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) are important for the regulation of sensorimotor function taking place at the muscle-dorsal root ganglion (DRG)-spinal cord interface (8-10). We previously showed that the expression of BDNF and NT-3 is increased in the spinal cord and skeletal muscle after voluntary exercise and this alters expression of synapsin I mRNA in motor neurons (11-13). Here, we have asked how voluntary exer...

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Section: Discussionsupporting

confidence: 70%

Voluntary exercise increases axonal regeneration from sensory neurons

Molteni

Zheng

Ying

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

167

128

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“…After peripheral nerve injury, sensory function in the denervated skin may gradually recover due to either regeneration of severed axons or extension of axonal sprouts from the nerve endings of the adjacent uninjured nerves (collateral sprouting) [17]. The regenerating axons of the adjacent nerves ®rst reinnervated their own territory and then spread into the denervated cutaneous area, for which the term expansive regenerative reinnervation has been proposed [18].…”

Section: Discussionmentioning

confidence: 99%

An animal model of neuropathic pain employing injury to the sciatic nerve branches

et al. 2000

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The present study was conducted to develop a new animal model of neuropathic pain employing injury to the distal sciatic nerve branches. Under halothane anesthesia, the tibial, sural, and/or common peroneal nerves were injured and neuropathic pain behaviors were compared among different groups of rats. Different types of injury produced different levels of neuropathic pain. Rats with injury to the tibial and sural nerves showed the most vigorous mechanical allodynia, cold allodynia, and spontaneous pain. These neuropathic pain behaviors were not relieved by functional sympathectomy using guanethidine.The results suggested that injury to the tibial and sural nerves, while leaving the common peroneal nerve intact, can be used as a new animal model of neuropathic pain and that this model represents sympathetically independent pain (SIP). The present animal model is very simple to produce injury and can produce profound and reliable pain behaviors. These features enable the new animal model to be a useful tool in elucidating the mechanisms of neuropathic pain, especially SIP. NeuroReport

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“…One group of rats was crushed twice, with an interval of 2 weeks (McQuarrie, et al, 1978;Dekker, 1987). The "conditioning" lesion was placed 10 mm distal to the normal crush site 14 d before the test lesion was performed.…”

Section: Methodsmentioning

confidence: 99%

“…Previously, it was shown that axonal regeneration in the crushed sciatic nerve can be facilitated by either the placement of an earlier "conditioning" lesion (McQuarrie and Grafstein, 1973;McQuarrie et al, 1977;McQuarrie, 1978) or by treatment with neurotrophic agents, such as melanocortins (Strand and Kung, 1980;Gispen et al, 1987). Posttranslational products of pro-opiomelanocortin, such as ACTH and MSH peptides, enhance postlesion repair by increasing the number of outgrowing myelinated and unmyelinated newly formed axons (Bijlsma et al, 1983;Verhaagen et al, 1987).…”

mentioning

confidence: 99%

Expression of growth-associated protein B-50 (GAP43) in dorsal root ganglia and sciatic nerve during regenerative sprouting

et al. 1989

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Recently it has been shown that B-50 is identical to the neuron- specific, growth-associated protein GAP43. The present study reports on the fate of B-50/GAP43 mRNA and B-50/GAP43 protein, determined by radioimmunoassay, in a rat model of peripheral nerve regeneration (sciatic nerve crush) over a period of 37 and 312 d, respectively. Moreover, the effects of repeated subcutaneous injection of the neurotrophic peptide Org.2766 (an ACTH4–9 analog) and of a conditioning lesion on B-50/GAP43 protein levels in the regenerating nerve and dorsal root ganglia (DRG) were investigated. Both treatments enhanced the functional recovery as evidenced by a foot-flick withdrawal test. Immunocytochemical analysis using antineurofilament antibodies revealed a peptide-induced increase in the number of outgrowing sprouts in the sciatic nerve. Both the peptide and the conditioning lesion amplified the crush lesion-induced increase in B-50 protein content in the nerve as determined by radioimmunoassay. B-50 protein levels seem to correlate proportionally with the number of sprouts. In the DRG of the crushed sciatic nerve, the time course of B-50 expression was studied. B-50 mRNA was quantified from Northern blots. A linear increase up to 10 times the basal level of B-50 mRNA was observed 2 d postsurgery, followed by a gradual decline to normal levels at day 37. The first significant rise in B-50 mRNA level became apparent between 8 and 16 hr after placement of the crush lesion. The first significant rise in B-50 protein level occurred 40 hr after the crush lesion, reaching a plateau of 3 times the basal level between day 6 and 20. B-50 protein levels in DRG cell bodies remained elevated up to 60 d after crush, a period much longer than that observed for B-50 mRNA. Thus, during a later phase of peripheral axonal regeneration, the presence of B-50 appears to be prolonged, probably by an increase in half-life and not so much by enhanced transcription. Treatment with Org.2766 did not affect the B- 50/GAP43 levels in DRG cell bodies during the first 6 d following crush. Conditioning lesion resulted in a DRG B-50/GAP43 protein amount at the same level as in rats 14 d after the test lesion. B-50/GAP43 levels in DRG are probably influenced by the rapid axonal transport of the protein, as has been reported by others.

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The effect of a conditioning lesion on the regeneration of motor axons

Cited by 114 publications

References 18 publications

Voluntary exercise increases axonal regeneration from sensory neurons

Voluntary exercise increases axonal regeneration from sensory neurons

An animal model of neuropathic pain employing injury to the sciatic nerve branches

Expression of growth-associated protein B-50 (GAP43) in dorsal root ganglia and sciatic nerve during regenerative sprouting

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