Effects of monocular deprivation on the morphology of retinogeniculate axon arbors in a primate

Abstract

Previous studies of the monocularly deprived (lid-sutured) primate (Galago crassicaudatus) have shown that magnocellular (M) and parvocellular (P) lateral geniculate nucleus (LGN) cells that receive input from the deprived eye are smaller than counterparts that receive input from the nondeprived eye; deprived koniocellular (K) cells show wide variability in size, but they do not differ from their nondeprived counterparts (Casagrande and Joseph, '80). Although deprivation results in cell-size changes, the physiological properties of deprived LGN cells do not change from normal (that is, P cells have normal X-like properties, M cells have normal Y-like properties, and K cells have normal W-like properties). Because of these findings, we were interested in determining how the morphology of retinogeniculate axon arbors is affected by deprivation. To this end, 104 horseradish-peroxidase-filled retinogeniculate arbors from galagos deprived from birth to maturity were completely reconstructed within the binocular segment of the LGN. These arbors were qualitatively and quantitatively compared with 56 arbors reconstructed from normal galagos as part of another study (Lachica and Casagrande, '88). Our main findings are as follows. Deprived M and P arbors are affected by deprivation in the same general manner: compared with normal arbors, they are altered in shape (rather than being round or columnar, respectively, both groups have terminals that are elongated parallel to laminar borders); they are smaller in area, and they have fewer boutons but innervate the LGN with a greater density of boutons. K arbors are affected by deprivation in the same manner, but less severely. Finally, our results show that nondeprived arbors are also affected by eyelid suture. Specifically, all nondeprived arbor groups are smaller in area than normal and possess more boutons/mm3. We interpret these changes in the morphology of deprived retinogeniculate axons to suggest that abnormal competitive interactions begin by affecting primarily immature LGN cells and their axons and that the retinogeniculate axons presynaptic to these cells experience secondary degenerative effects. Our results also show that similar manipulations of visual experience can result in changes that are not necessarily comparable across species such as cats and primates.