Can lacking a particular receptor help mice's facial nerves survive injury and recover?

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When motor neuron axons in peripheral nerves are injured, expression of the p75 low-affinity neurotrophin receptor increases in their cell bodies and axons. It also increases in Schwann cells undergoing Wallerian degeneration in the distal excised nerve segment.

To investigate p75's role after nerve injury, researchers conducted an experimental mouse study comparing motor neuron survival and regeneration in mice lacking p75, designated p75 (-/-), with mice expressing it, designated p75 (+/+). The injury methods included facial nerve crush and nerve cutting, or axotomy, in adults, as well as axotomy on postnatal day 1.

In adult p75 (-/-) mice, functional recovery of whisker movement after facial nerve crush occurred slightly earlier than in p75 (+/+) mice. Some functional recovery during the 25-day interval after nerve cutting also occurred more frequently in p75 (-/-) mice. However, p75 (-/-) mice had slightly fewer motor neuron profiles and correspondingly fewer axons in the facial nerve.

At 25 days after axotomy, survival of motor neuron profiles was significantly better in adult p75 (-/-) mice: a mean of 85% ± 3% standard error of the mean (n = 11), compared with 67 ± 5% in p75 (+/+) CD-1 mice (n = 11) and 68.0 ± 4% in p75 (+/+) balb/c mice (n = 6). Significantly more regenerating axons were also present in the distal facial nerve of p75 (-/-) mice.

After axotomy on postnatal day 1, p75 (+/+) mice lost almost all motor neuron profiles in the lateral facial nucleus: 1.7 ± 0.3% remained (n = 5). Significantly more survived in p75 (-/-) mice: 17 ± 2.5% (n = 6).

The researchers concluded that p75 expression in motor neurons or Schwann cells after facial nerve injury is not necessary for motor neuron survival or prompt axon regeneration. Instead, p75 may increase motor neurons' risk of dying.