Internodal function in normal and regenerated mammalian axons

TY - JOUR

T1 - Internodal function in normal and regenerated mammalian axons

AU - Moldovan, M

AU - Krarup, C

N1 - Keywords: Adult; Animals; Axons; Humans; Male; Mammals; Membrane Potentials; Motor Neurons; Nerve Fibers, Myelinated; Nerve Regeneration; Neural Conduction; Potassium; Sensory Thresholds; Sodium; Wallerian Degeneration

PY - 2007

Y1 - 2007

N2 - AIM: Following Wallerian degeneration, peripheral myelinated axons have the ability to regenerate and, given a proper pathway, establish functional connections with targets. In spite of this capacity, the clinical outcome of nerve regeneration remains unsatisfactory. Early studies have found that regenerated internodes remain persistently short though this abnormality did not seem to influence recovery in conduction. It remains unclear to which extent abnormalities in axonal function itself may contribute to the poor outcome of nerve regeneration. METHODS: We review experimental evidence indicating that internodes play an active role in axonal function. RESULTS: By investigating internodal contribution to axonal excitability we have found evidence that axonal function may be permanently compromised in regenerated nerves. Furthermore, we illustrate that internodal function is also abnormal in regenerated human nerves. CONCLUSION: The data suggest that persistently shorter regenerated internodes lead to increased Na+/K+-pump activity in response to increased Na+ entry during conduction. This may impair axonal function during prolonged repetitive activity and drain the energy reserves of the axons.

AB - AIM: Following Wallerian degeneration, peripheral myelinated axons have the ability to regenerate and, given a proper pathway, establish functional connections with targets. In spite of this capacity, the clinical outcome of nerve regeneration remains unsatisfactory. Early studies have found that regenerated internodes remain persistently short though this abnormality did not seem to influence recovery in conduction. It remains unclear to which extent abnormalities in axonal function itself may contribute to the poor outcome of nerve regeneration. METHODS: We review experimental evidence indicating that internodes play an active role in axonal function. RESULTS: By investigating internodal contribution to axonal excitability we have found evidence that axonal function may be permanently compromised in regenerated nerves. Furthermore, we illustrate that internodal function is also abnormal in regenerated human nerves. CONCLUSION: The data suggest that persistently shorter regenerated internodes lead to increased Na+/K+-pump activity in response to increased Na+ entry during conduction. This may impair axonal function during prolonged repetitive activity and drain the energy reserves of the axons.

U2 - 10.1111/j.1748-1716.2006.01654.x

DO - 10.1111/j.1748-1716.2006.01654.x

M3 - Journal article

C2 - 17250569

SN - 1748-1708

VL - 189

SP - 191

EP - 200

JO - Acta Physiologica (Print Edition)

JF - Acta Physiologica (Print Edition)

IS - 2

ER -