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Axonal damage is a common pathological consequence of spinal cord injury. Previous studies have detected axonal injury with silver stains for degeneration or immunohistochemistry for alterations in components such as beta-amyloid precursor protein, neurofilament or ubiquitin. Fluororuby has recently been introduced as a neuronal tracer in studies of spinal cord injury and regeneration. Our study was carried out to determine whether Fluororuby can be used to identify injured axons and monitor the time course of axonal damage. Adult rats underwent needle puncture injury to the white matter in the midline and lateral spinal cord at T11. At the same time, 0.05 microl of Fluororuby was injected into the cord at the same sites. After survival times ranging from 6 h to 3 weeks, spinal cords were cut into longitudinal frozen sections and examined with confocal microscopy. Fluororuby was found to label key features of axonal injury including axonal swelling, retraction balls and disrupted axons. Damaged axons close to the injury site were consistently labeled within 6 h, with indications of swollen and disconnected axons spreading further from the site during the first week. Fewer injured axons were labeled after 1 week survival, but the marker revealed longer distances of degenerating axons both distal and rostral to the injury site. Our findings indicate that Fluororuby is a quick, sensitive, reliable and technically simple fluorescent marker for early stages of acute axonal injury and degeneration.

Prenatal exposure of the developing rat brain to methylazoxymethanol acetate results in the formation of ectopic groups of pyramidal neurons in the subfields CA1 and CA2 of the mature hippocampal formation. These ectopic neurons are situated in regions of increased vascularization and increased activity of cytochrome oxidase, as demonstrated histochemically. Both these findings suggest that there may be an abnormality of distribution or intensity of oxidative metabolic activity in the ectopic pyramidal neurons found in these animals.

The laminar distributions of cytochrome oxidase activity and vascularization of the occipital cortex of animals made micrencephalic by exposure to MAM Ac on E14 or E16 were examined and compared to control animals. Despite severe disruptions of the normal cytoarchitecture in MAM Ac exposed animals, the laminar distributions of vascular profiles, branch points and cytochrome oxidase activity in micrencephalic animals were similar to those in control animals.