Facial Nerve Recovery in <i>bcl2</i> Overexpression Mice After Crush Injury

Most, Sam P.

doi:10.1001/archfaci.6.2.82

Cited by 26 publications

(17 citation statements)

References 20 publications

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“…Our results are consistent with prior research indicating that Bcl-2 expression is decreased after optic and facial nerve injury [46,47]. The finding that FK treatment increased Bcl-2 expression also coincides with other nerve injury studies suggesting that overexpression of Bcl-2 is neuroprotective and that FK administration upregulates Bcl-2 expression [48][49][50].…”

Section: Discussionsupporting

confidence: 92%

FK506 neuroprotection After cavernous nerve injury is mediated by thioredoxin and glutathione redox systems

Lagoda¹,

Xie²,

Sezen³

et al. 2015

The Journal of Sexual Medicine

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Section: Discussionsupporting

confidence: 92%

FK506 neuroprotection After cavernous nerve injury is mediated by thioredoxin and glutathione redox systems

Lagoda¹,

Xie²,

Sezen³

et al. 2015

The Journal of Sexual Medicine

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“…To evaluate facial nerve paralysis, eye blink and whisker movement of each mouse were scored separately as previously described. 37 Specifically, for each facial area, a score of 0 was given for no detectable movement, 1 for detectable motion, 2 for significant but asymmetric voluntary motion and 3 for symmetric voluntary motion. Facial nerve function was determined by the total scores for eye blink and whisker movement.…”

Section: Clinical Evaluation Of Facial Nerve Paralysismentioning

confidence: 99%

Hepatocyte growth factor incorporated into herpes simplex virus vector accelerates facial nerve regeneration after crush injury

et al. 2011

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Hepatocyte growth factor (HGF) promotes regeneration of the central nervous system, but its effects on the peripheral nervous system remain unclear. This study was conducted to elucidate the effect of HGF on regeneration of the murine facial nerve after crush injury. To do so, a replication-defective herpes simplex virus vector that incorporated HGF was prepared (HSV-HGF). The main trunk of the facial nerve was compressed by mosquito hemostats, and HSV-HGF, control vector or medium was then applied to the compressed nerve. We found that mice in the HGF group required significantly fewer days for complete recovery from nerve compression. Furthermore, the amplitude of the evoked buccinator muscle compound action potential increased following HSV-HGF application. HGF expression in and around the compressed nerve was demonstrated by enzyme-linked immunoassay and immunohistochemistry. In addition, HSV-HGF introduction around the damaged nerve significantly accelerated recovery of function of the facial nerve. These data suggest a possible role of HGF in promoting facial nerve regeneration after nerve damage. Furthermore, this viral delivery method may be applied clinically for many types of severe facial palsy during facial nerve decompression surgery.

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“…Many researchers have used qualitative and semiquantitative methods to examine recovery of the facial nerve after injury 1,10,11 . Our laboratory has recently developed a quantitative system to measure the return of facial nerve function after injury in a rat model 12,13 .…”

Section: Introductionmentioning

confidence: 99%

Nimodipine and Acceleration of Functional Recovery of the Facial Nerve After Crush Injury

Lindsay

Heaton²,

Edwards³

et al. 2010

Arch Facial Plast Surg

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Objective To establish whether nimodipine, a calcium channel blocker, accelerates or otherwise improves functional recovery of whisking after facial nerve crush injury in the rat. Methods Thirty rats underwent exposure of the left main trunk of the facial nerve followed by a standard crush injury, and subsequent quantitative facial movement testing. Animals were randomized into an experimental group (n=15) and a control group (n=15 each). Four days prior to facial nerve manipulation, experimental animals underwent subcutaneous implantation of a nimodipine-secreting pellet. All animals were tested pre-operatively and on post-crush days 2, 8–17, 20, 22, 24, and 31, using a validated, quantitative whisking kinematics apparatus. Whisks were analyzed for amplitude, velocity, and acceleration. Results Animals receiving nimodipine demonstrated significantly better whisking on days 9, 11–13, and 20 compared with control animals (p<.05). Overall, the nimodipine-treated animals showed earlier recovery as compared to the untreated animals. Conclusions We demonstrate that nimodipine improves recovery of whisking after facial nerve crush. This finding corroborates the semi-quantitative findings of others, and provides complete whisking kinematic data on its effects. Given the low side effect profile of nimodipine, there may be clinical implications in its administration in patients experiencing facial nerve injury.

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Facial Nerve Recovery in bcl2 Overexpression Mice After Crush Injury

Abstract: To develop a mouse model for measuring facial nerve injury and recovery and to test the hypothesis that overexpression of the antiapoptotic gene, bcl2, enhances recovery of facial nerve function after peripheral crush injury.

Cited by 26 publications

References 20 publications

FK506 neuroprotection After cavernous nerve injury is mediated by thioredoxin and glutathione redox systems

FK506 neuroprotection After cavernous nerve injury is mediated by thioredoxin and glutathione redox systems

Hepatocyte growth factor incorporated into herpes simplex virus vector accelerates facial nerve regeneration after crush injury

Nimodipine and Acceleration of Functional Recovery of the Facial Nerve After Crush Injury

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