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At the optic chiasm axons make a key binary decision either to cross the chiasmal midline to innervate the contralateral optic tract or to remain uncrossed and innervate the ipsilateral optic tract. In rodents, midline interactions between axons from the two eyes are critical for normal chiasm development. When one eye is removed early in development the hemispheric projections from the remaining eye are disrupted, increasing the crossed projection at the expense of the uncrossed. This is similar to the abnormal decussation pattern seen in albinos. The decussation pattern in marsupials, however, is markedly different. Early eye removal in the marsupial has no impact on projections from the remaining eye. These differences are related to the location of the uncrossed projection through the chiasm. In rodents, axons that will form the uncrossed projection approach the chiasmal midline, while in marsupials they remain segregated laterally through the chiasm. Histological analysis of the optic chiasm in man provides anatomical evidence to suggest that, unlike in rodents, uncrossed axons are confined laterally from the optic nerve through to the optic tract and do not mix in each hemi-chiasm. This is a pattern similar to that found in marsupials. Electrophysiological evidence in human anophthalmics shows that the failure of one eye to develop in man has no impact on the hemispheric projections from the remaining eye. This strongly suggests that the mechanisms regulating chiasmal development in man differ from those in rodents, but may be similar to marsupials. This implies that optic chiasm formation in rodents and ferrets is not common to placental mammals in general.

Chiasm formation in man is fundamentally different from that in the mouse