Organization of the proximal, orbital segment of the infraorbital nerve at multiple intervals after axotomy at birth: A quantitative electron microscopic study in rat

Although much is known of the central consequences of infraorbital nerve (ION) transection at birth, little is known about the effects of this lesion on the organization of the ION itself. To advance our understanding of how deafferentation alters the developing trigeminal neuraxis, 19 newborn rats were subjected to left ION section and perfused 1, 2, 4, 7, 17, or 90 days later. Left IONs were removed in the orbit proximal to the nerve injury site, and axon numbers, types, and fasciculation patterns were assessed with light and electron microscopic methods. Complete axon counts demonstrated that the axotomized ION contained an average (±SD) of 13,945 ± 10,335, 14,112 ± 3,501, 16,531 ± 1,904, 9,045 ± 1,465, 7,018 ± 4,212, and 8,672 ± 1,030 axons at the above‐listed ages, respectively. These values are well below the 33,059 axons in the normal adult ION (Jacquin et al. [1984] Brain Res. 290:131–135) and the 42,219 axons in the newborn ION (Renehan and Rhoades [1984] Brain Res. 322:369–373). The axotomized ION also contained lower than normal percentages of myelinated axons (26.7% ± 6.3% on postnatal day 90 vs. 59.7% ± 6.2% in normal adults). Unmyelinated fibers constituted the vast majority of the remaining fiber types; degenerating fibers never accounted for > 1.6% of all the axons. The number of fascicles making up the axotomized ION overlapped significantly with those found in the normal newborn and adult ION. We conclude that (1) extensive, though variable, axon elimination occurs proximally within one day of the lesion; (2) the 74% reduction in fiber number seen at 90 days is not reliably achieved until postnatal day 7;(3) the higher than normal proportion of unmyelinated axons in the injured ION may underly many of the known effects of neonatal ION injury on the developing whisker‐barrel neuraxis; (4) gross changes in ION fasciculation patterns are not prerequisite to injury‐induced pattern alterations in the developing trigeminal system. © 1993 Wiley‐Liss, Inc.