Fibre organization of the monkey's optic tract: II. Noncongruent representation of the two half‐retinae

Abstract

The representations of the two half-retinae were examined in the monkey's optic tract. Intravitreal injections of tritiated amino acids were made to reveal the distributions of the crossed and uncrossed populations of optic axons, while localized implants of horseradish peroxidase (HRP) were made into different regions of the optic tract in order to examine the distributions and morphological types of retrogradely labelled cells at corresponding loci in the two half-retinae. Crossed and uncrossed optic axons are intermingled throughout most of the optic tract, but uncrossed axons are very sparse or absent along both the deep and superficial extremes of the tract. Implants of HRP into the deeper regions of the tract demonstrate that the crossed and uncrossed optic axons of the P beta retinal ganglion cells are slightly out of binocular registration, with the uncrossed map being shifted to a slightly superficial location relative to the crossed map. The optic axons for the remaining cell classes, revealed by implants of HRP into the superficial portion of the tract, are much more conspicuously out of binocular registration (in particular, the P alpha optic axons); but in their cases, the uncrossed optic axons are shifted to deeper locations relative to the crossed optic axons. Further evidence that these optic axon classes are markedly out of binocular registration comes from the two optic tracts of a bilaterally destriated monkey, in which most of the P beta optic axons have undergone a transneuronal retrograde degeneration. Following a uni-ocular injection of tritiated amino acids, the distributions of the remaining crossed and uncrossed axonal labelling occupied different positions within the tract rather than being intermingled, with the uncrossed optic axons situated deep to the majority of crossed optic axons. These results demonstrate that the optic chiasm does not combine binocularly corresponding optic axons of similar type. They also demonstrate that noncongruent field defects should be a common consequence of damage to the optic tract in humans. If the fibre order in the mammalian optic tract arises as a consequence of the sequence of axonal addition during development, then differences in the relative times of genesis for nasal and temporal members of any cell class, and/or differences in the relative pathlengths between the eye and two optic tracts, may produce the fibre ordering described herein.