Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve

Abstract

Leg lengthening procedure is used increasingly to treat leg length discrepancy and some forms of dwarfism. We investigated adaptation in rat sciatic nerve to the gradual nerve elongation that occurs with leg lengthening. Indirect nerve elongation was produced by leg lengthening by a total of 15, 30, 45, or 70 mm at a rate of 1 m d d a y . One day after leg lengthening completion, transverse semithin sections of sciatic nerve were prepared and examined; a teased-fiber study also was performed. Elongation decreased axon diameter, but not significantly. In teased-fiber preparations, internodal length was increased by 93%, and the longest internode measured 3000 pm after leg lengthening by 70 mm. Slopes of fiber diameter-internodal length regression lines increased with increasing elongation. Paranodal demyelination caused by nerve elongation worsened as elongation increased, stimulating remyelination (i.e., intercalation of a segment). Only 0.8% of axons showed degeneration in the group with 70 mm of elongation. We concluded that adult rat sciatic nerve can adapt itself to leg lengthening procedure with even doubling internodal length.

Modeling mitochondrial dynamics during in vivo axonal elongation

“…The ability of mitochondria to reorganize is crucial in maintaining a uniform density given the factors that lead to gradients in distribution. Namely, axons are viscoelastic structures which can be deformed either by growth cone induced stretching or towed growth of pre-synaptic (Dennerll et al, 1989) or mature neurons (Abe et al, 2004;Pfister et al, 2004), and mitochondria eventually become depolarized and are transported back to the cell body (Miller and Sheetz, 2004).…”

“…As neurons constantly generate tension that minimizes axonal length both before and after synapse formation (Van Essen, 1997), it follows that increases in the length of the axon are the result of forces generated by an increase in body size. Consistent with the view that neurons respond to forced lengthening by increasing the production of new material are studies that have shown that axons are able to maintain viability and increase their caliber when artificially stretched to remarkable lengths (Abe et al, 2004;Pfister et al, 2004Pfister et al, , 2006. For these reasons it would be useful to have a model where influx is allowed to vary over the course of elongation.…”

“…We have concentrated here on mature neurons, yet the idea applies to presynaptic axons as well. Tension has been shown to cause lengthening in both types of neuron, and in those cases the cell bodies have responded by increasing production to restore the axon or nerve to a viable diameter (Abe et al, 2004;Dennerll et al, 1989;Lamoureux et al, 1989;Pfister et al, 2004). For these reasons we hold changes in length as independent and study how production must change to sustain the axon and avoid rupture.…”

Repair of peripheral nerve defect by direct gradual lengthening of the distal nerve stump in rats: Cellular reaction

“…lengthening. Our previous study has shown that changes of deterioration have not been seen in femoral lengthening in rats at 1 mm/day [16].…”

Bioinspired Design of Peripheral Nerve Devices

“…33,34 Intriguingly, the maximum strain at which this straightening occurs is just above 8%, the same threshold at which reversible conduction blocks are initiated. 31,35 Second, nerve lengthening has been reported to irreversibly elongate nodes of Ranvier, 32,33,36,37 which by virtue of their small caliber, are particularly susceptible to mechanical loads. Secondary effects of ischemia to compromised blood flow have also been reported, 30,38 but do not likely induce short-term deficits in electrophysiological or morphological properties.…”