Exp Brain Res (1998) 118:341±351  Springer-Verlag 1998 RESEARCH ARTICLE Yuji Sasaki ´ Han Cheng ´ Earl L. Smith III Yuzo Chino Effects of early discordant binocular vision on the postnatal development of parvocellular neurons in the monkey lateral geniculate nucleus Received: 26 March 1997 / Accepted: 18 July 1997 Y. Sasaki 1 ´ H. Cheng ´ E.L. Smith III ´ Y. Chino ( ) ) College of Optometry, University of Houston, 4901 Calhoun Road, Houston, TX 77204-6052, USA Tel.: +1-713-743-1955, Fax: +1-713-743-2053, e-mail: ychino@uh.edu Present address: 1 Department of Ophthalmology, Tottori University School of Medicine, Yonago, Tottori, Japan Abstract The effects of early discordant binocular vision on the fidelity of signal transfer in parvocellular neurons of the lateral geniculate nucleus (LGN) were investigated in rhesus monkeys reared with ocular misalignment (stra- bismus). Unilateral convergent strabismus (esotropia) was surgically induced in four infant monkeys between 20 and 30 days of age and the animals were reared in a normally lighted environment until they were adults. Extracellular microelectrode recordings were made in individual units of anesthetized and paralyzed subjects. Drifting sinusoidal gratings were used as visual stimuli. Within-unit compar- isons of the LGN action potentials (LGN output) and S potentials (retinal input) were performed to determine the accuracy of signal transfer in the LGN. Contrary to the previous findings in the cat LGN, the signal transfer characteristics of parvocellular units in strabismic mon- keys were normal regardless of stimulus spatial frequen- cy, temporal frequency, or contrast. The differences be- tween cats and monkeys in LGN circuitry and the relative maturity of the central visual pathway at the onset of stra- bismus may have contributed to the apparent species dif- ferences in the functional development of the LGN. Key words Parvocellular neurons ´ Lateral geniculate nucleus ´ Strabismus ´ Signal transfer ´ Monkey Introduction The functional development of the cat lateral geniculate nucleus (LGN) is known to be disrupted by early abnor- mal visual experience (for recent reviews see Garraghty and Sur 1993; Friedlander and Tootle 1990; Movshon and Kiorpes 1990, 1993; but see Shapley and So 1980; Derrington and Hawken 1981; Crewther and Crewther 1988). We have recently demonstrated that these func- tional deficits may arise because LGN relay cells fail to transfer signals from retina to cortex with high precision (Chino et al. 1994a; Cheng et al. 1995b). Specifically, within-unit comparisons of LGN action potentials (LGN output) and S potentials (input) demonstrated that early convergent strabismus leads to substantial reductions in the spatial resolution and contrast sensitivity of X-LGN neurons relative to their direct retinal inputs and causes anomalous delays in the speed of signal transfer within the LGN. These physiological deficits appear to be close- ly associated with abnormal retinal axon-arbor develop- ment in the LGN (Chino et al. 1994a; Garraghty et al. 1994) and with the severe monocular and binocular anom- alies found in the primary visual cortex of strabismic cats (Chino et al. 1983, 1991, 1994b). Contrary to the clear physiological alterations in the cat LGN caused by early abnormal vision, the postnatal development of the primate LGN was reported to be normal despite early monocular form deprivation (Blakemore and Vital-Durand 1986) or optical defocus (Movshon et al. 1987; Levitt et al. 1989). The apparent differences in subcortical development between cats and monkeys may reflect, among many possibilities, species differences in the functional organi- zation of the LGN and/or differences in the relative de- gree of their postnatal maturation (Wilson 1989, 1993; Movshon and Kiorpes 1993). It is also possible, however, that the tranditional population-based comparisons be- tween different neuronal groups that were performed in the previous primate studies were not sensitive enough to detect subtle anomalies in the LGN. Because retinal de- velopment is generally considered to be immutable by vi- sual experience (for reviews see Movshon and Van Sluyters 1981; Mitchell and Timney 1984; Movshon and Kiorpes 1990; Friedlander and Tootle 1990), the optimal method to uncover functional deficits in the primate LGN would be to compare the LGN output directly with its retinal input within the same unit. As demonstrated in cats (Chino et al. 1994a; Cheng et al.