Effects of electrical stimulation and gonadal steroids on rat facial nerve regenerative properties

Sharma, Nijee; Coughlin, Lisa M.; Porter, Ryan G.; Tanzer, Lisa; Wurster, Robert D.; Marzo, Sam J.; Jones, Kathryn J.; Foecking, Eileen M.

doi:10.3233/rnn-2009-0489

Cited by 26 publications

(25 citation statements)

References 48 publications

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“…This finding is consistent with previous studies that have shown that the estrogens can enhance axon regeneration after peripheral nerve crush and transection injuries (Tanzer and Jones, 1997;Jones et al, 2000;Islamov et al, 2002;McMurray et al, 2003;Murashov et al, 2004;Huppenbauer et al, 2005;Sharma et al, 2009;Sekiguchi et al, 2012). Application of exogenous estradiol enhances the number of axon profiles found in the distal stump (Islamov et al, 2002), the number of motoneurons whose axons begin to regenerate (Murashov et al, 2004), the length of axon profiles (Tanzer and Jones, 1997;Sharma et al, 2009) and as shown in the current study, the number of motoneurons whose axons begin to regenerate. Blocking ER signaling at the site of nerve repair prevented the enhancing effects of systemic exogenous estradiol administration on motoneuron participation.…”

Section: Discussionsupporting

confidence: 93%

“…Several previous studies have found that treatment with a non-aromatizable form of testosterone produces less enhancement of axon elongation than treatment with the aromatizable form of testosterone, suggesting that androgens can work synergistically with estrogen signaling to enhance axon regeneration (Tanzer and Jones, 1997;Sharma et al, 2009).The biosynthetic pathway for androgens and estrogens is found in motoneurons (Coirini et al, 2002;Rakotoarivelo et al, 2004) and glial cells in the spinal cord (Patte-Mensah et al, 2004;Garcia-Ovejero et al, 2005). Testosterone in these cells can be converted to estradiol via the cytochrome P450 enzyme aromatase.…”

Section: Introductionmentioning

confidence: 99%

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Estrogen signaling is necessary for exercise‐mediated enhancement of motoneuron participation in axon regeneration after peripheral nerve injury in mice

Acosta

Copley

Harrell

et al. 2017

Developmental Neurobiology

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Thousands of people each year suffer from peripheral nerve injury. Treatment options are limited, and recovery is often incomplete. Treadmill exercise can enhance nerve regeneration; however, this appears to occur in a sex-dependent manner. Females respond best to short duration, high speed interval training; whereas, males respond best to slower, continuous training. Previous studies have shown a role for testosterone in this process, but the role of estrogen is unknown. To evaluate the role of estrogen signaling in treadmill exercise, we blocked estrogen receptor (ER) signaling during treadmill exercise in males and female wild type mice. The right common fibular (CF) branch of the sciatic nerve was cut and repaired with fibrin glue that contained the ER antagonist ICI 182,780. Estradiol-filled or blank Silastic capsules were implanted subcutaneously at the time of nerve transection. Starting three days post-transection, exercised mice received treadmill training using the paradigm appropriate to their sex 5 days a week for 2 weeks. Fourteen days after the initial nerve transection, motoneurons whose axons had regenerated at least 1.5 mm distal to the original cut sites were labeled with a retrograde tracer. Regeneration was quantified by counting the number of fluorescent labeled motoneurons in the lumbar region of the spinal cord. Both treadmill training and estradiol administration increased the number of motoneurons participating in axon regeneration, but these effects were blocked by ER antagonist treatment. Estrogen signaling is important for the enhancing effects of treadmill exercise on motoneuron participation after peripheral nerve cut.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Estrogen signaling is necessary for exercise‐mediated enhancement of motoneuron participation in axon regeneration after peripheral nerve injury in mice

Acosta

Copley

Harrell

et al. 2017

Developmental Neurobiology

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“…The finding of Jones et al that testosterone administration combined with 30 min of 20-Hz ES just prior to facial nerve crush was more effective than either exogenous testosterone or ES alone in accelerating nerve regeneration and recovery of the blink reflex and vibrissae orientation in castrated male rats (Sharma et al, 2009(Sharma et al, , 2010b was the basis for the investigation of English et al of a possible role of androgens in the effect of exercise in enhancing nerve regeneration after injury. Moreover, the fact that continuous treatment of the injured rat facial nerve with testosterone resulted in more sustained upregulation, although with a slower onset, of neurotrophic factors, including BDNF, with the combination of ES and testosterone providing a more rapid and sustained upregulation of the genes encoding these proteins (Sharma et al, 2010a), provided a further rationale for exploring the role of androgens in the effect of exercise in promoting nerve regeneration.…”

Section: Exercise With and Without Es Promotes Nerve Regenerationmentioning

confidence: 99%

Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise

Gordon

English

2015

Eur J of Neuroscience

245

194

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Enhancing the regeneration of axons is often considered a therapeutic target for improving functional recovery after peripheral nerve injury. In this review, the evidence for the efficacy of electrical stimulation (ES), daily exercise, and their combination in promoting nerve regeneration after peripheral nerve injuries in both animal models and in human patients, is explored. The rationale, effectiveness, and molecular basis of ES and exercise in accelerating axon outgrowth are reviewed. In comparing the effects of ES and exercise in enhancing axon regeneration, increased neural activity, neurotrophins, and androgens are considered common requirements. Similar, gender-specific requirements are found for exercise to enhance axon regeneration in the periphery and for sustaining synaptic inputs onto injured motoneurons. ES promotes nerve regeneration after delayed nerve repair in humans and rats. The effectiveness of exercise is less clear. Although ES, but not exercise, results in a significant misdirection of regenerating motor axons to reinnervate different muscle targets, the loss of neuromuscular specificity encountered has only a very small impact on resulting functional recovery. Both ES and exercise are promising experimental treatments for peripheral nerve injury that seem ready to be translated to clinical use.

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“…Epidural low frequency electric stimulation was applied 30 minutes per day for 4 weeks. The electrical stimulation treatment protocol was similar to that previously reported8,11,19).…”

Section: Methodsmentioning

confidence: 79%

Neuroprotective Effects of Sacral Epidural Neuromodulation Following Spinal Cord Injury : An Experimental Study in Rats

Lee

Hyun

Yoon

et al. 2012

J Korean Neurosurg Soc

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ObjectiveThe purpose of this study is to evaluate neuroprotective effect of sacral neuromodulation in rat spinal cord injury (SCI) model in the histological and functional aspects.MethodsTwenty-one female Sprague Dawley rats were randomly divided into 3 groups : the normal control group (CTL, n=7), the SCI with sham stimulation group (SCI, n=7), and the SCI with electrical stimulation (SCI+ES, n=7). Spinal cord was injured by dropping an impactor from 25 mm height. Sacral nerve electrical stimulation was performed by the following protocol : pulse duration, 0.1 ms; frequency, 20 Hz; stimulation time, 30 minutes; and stimulation duration, 4 weeks. Both locomotor function and histological examination were evaluated as scheduled.ResultsThe number of anterior horn cell was 12.3±5.7 cells/high power field (HPF) in the CTL group, 7.8±4.9 cells/HPF in the SCI group, and 6.9±5.5 cells/HPF in the SCI+ES group, respectively. Both the SCI and the SCI+ES groups showed severe loss of anterior horn cells and myelin fibers compared with the CTL group. Cavitation and demyelinization of the nerve fibers has no significant difference between the SCI group and the SCI+ES group. Cavitation of dorsal column was more evident in only two rats of SCI group than the SCI+ES group. The locomotor function of all rats improved over time but there was no significant difference at any point in time between the SCI and the SCI+ES group.ConclusionIn a rat thoracic spinal cord contusion model, we observed that sacral neuromodulation did not prevent SCI-induced myelin loss and apoptosis.

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Effects of electrical stimulation and gonadal steroids on rat facial nerve regenerative properties

Cited by 26 publications

References 48 publications

Estrogen signaling is necessary for exercise‐mediated enhancement of motoneuron participation in axon regeneration after peripheral nerve injury in mice

Estrogen signaling is necessary for exercise‐mediated enhancement of motoneuron participation in axon regeneration after peripheral nerve injury in mice

Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise

Neuroprotective Effects of Sacral Epidural Neuromodulation Following Spinal Cord Injury : An Experimental Study in Rats

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