Long-term exposure of the rabbit eye to silicone oil causes optic nerve atrophy.

A silicone oil endotamponade following vitrectomy has for decades been a standard method in human ophthalmology with a view to restoring a detached retina. However, severe functional deficiencies may remain after treatment. In adult rabbits, the injection of silicone oil into the eye-ball following vitrectomy resulted in a decrease of 89% in the number of myelinated optic nerve fibres after a survival time of 1 year (418,313+/-29,703 versus 45,620+/-23,905). Concomitantly, the cross-sectional area of the optic nerve was also reduced significantly (0.853+/-0.159 mm2 versus 0.355+/-0.107 mm2). The number of non-neuronal elements of the optic nerve remained virtually unchanged immediately behind the eye-ball and in the middle part of the nerve, whereas it increased significantly close to the optic chiasm (3040+/-433 versus 3888+/-403). Thus, destruction of the myelinated optic nerve fibres is likely to be responsible for the functional deficiencies observed after silicone oil implantation.

Chemoanatomical separation of vibrissal trigeminal primary afferents in the rat: a special central representation of supraorbital vibrissae.

A choleratoxin B subunit transganglionic labelling technique and NPY immunohistochemistry were applied in the rat to achieve the chemoanatomical separation of myelinated vibrissal primary afferents, previously considered to be morphologically indistinguishable. Further, a special central representation pattern of supraorbital vibrissae was observed in the trigeminal brainstem nuclear complex: (1) Choleratoxin-labelled supraorbital vibrissal primary afferents terminated densely in their appropriate barrelettes in the trigeminal principal sensory nucleus, in the spinal oral subnucleus, in the caudal part of the spinal interpolar subnucleus, and in lamina IV of the caudal part of the spinal caudal subnucleus. (2) A second population of choleratoxin-labelled vibrissal afferents was also observed, terminating only in lamina III of the caudal subnucleus. (3) After peripheral nerve transection, NPY-immunoreactive supraorbital vibrissal primary afferent fibres appeared in their appropriate barrelettes in the principal sensory nucleus and the caudal part of the interpolar subnucleus, while in the caudal part of the caudal subnucleus NPY-immunoreactive vibrissal primary afferent terminals were found exclusively in the inner part of lamina II, extending over the outer part of lamina III. NPY-immunoreactive supraorbital vibrissal primary afferents were never found in the oral subnucleus. In contrast with the rules of the central representation of the mystacial (infraorbital) vibrissae, the multiple representation of the supraorbital vibrissae in the caudal subnucleus and the dense, barrelette-like terminal arborization of the choleratoxin-labelled supraorbital vibrissal primary afferents in the oral subnucleus apparently indicate an enhanced role of supraorbital vibrissae in reflexes that protect the eyes and the head from damage.

Reinnervation of a single vibrissa after nerve excision in the adult rat.

After a survival time of 180 days following the excision of a 2 mm segment of the vibrissal nerve to the gamma straddler vibrissa in the adult rat, a retrograde fluorescent single-labelling experiment revealed that 46% of the injured vibrissal sensory neurones had regenerated their peripheral processes. Peripheral collateral sprouting was not involved in the reinnervation of the denervated gamma vibrissa, as proved by a retrograde fluorescent double-labelling experiment. The regenerating nerve fibres did not invade the intact neighbouring vibrissae of the gamma vibrissa, and the sensory nerve fibres of the intact vibrissae were not translocated to the denervated gamma vibrissa. Thus, the sensory function of the denervated gamma vibrissa was restored exclusively by the regeneration of the damaged vibrissal nerve.