Postcritical-period reversal of effects of monocular deprivation on striate cortex cells in the cat

Abstract

1. The possibility that effects of monocular deprivation on cat striate cortex could be reversed after the developmental critical period by removal of the normal eye was investigated. In addition, the time course of any postcriticalperiod reversal was studied. Single-unit recording was conducted in the striate cortex of kittens anesthetized with nitrous oxide.2. Six control kittens were raised with monocular lid suture until they were 4-8 mo old (group MD). In agreement with previous investigators, from 0-10% of the striate cortex cells could be driven by visual stimulation of the deprived eye in these kittens.3. Eleven kittens were raised with monocular lid suture until they were 4-5 mo old, at which time the normal eye was enucleated. In five of these (group MD-DE-immediate), recording was conducted in striate cortex on the day of the enucleation. In these animals, 29-39% of the striate cortex cells could be driven by the deprived eye. In four kittens (group MD-DE-3 mo), the deprived eye remained closed for an additional 3 mo before recording was conducted. In these animals, 17-45% of the striate cortex cells could be driven by the deprived eye. In two kittens (group MD-DE greater than 12 mo), the deprived eye remained closed for 14-15 mo after the normal eye was enucleated. In these kittens, 26-40% of the striate cortex cells could be driven by the deprived eye. Thus, removal of the normal eye after the critical period in monocularly drprived kittens results in a rapid increase in the percent of striate cortex cells that can be driven by visual stimulation of the deprived eye, and there is no further increase in responsiveness over a period of more than a year.4. The receptive-field properties of the cells which responded to the deprived eye following enucleation of the normal eye were usually abnormal; 61% of them had nonspecific receptive fields, 39% of the responsive cells were direction selective, and only 12% were both direction and orientation selective.5. The increase in responsive cells was observed in the striate cortex of both hemispheres. However, the increase was greater in the hemisphere contralateral to the deprived eye. The responsive cells tended to occur in clusters of two to four adjacent cells separated by regions containing nonresponsive cells. These clusters were not related to the horizontal cortical layers; however, they may be related to the ocular dominance columns in striate cortex.6. Several mechanisms were considered for the present findings, including neuronal sprouting, denervation supersensitivity, and release from inhibition. It was suggested that the increased responsiveness to the deprived eye was probably not the result of rapid sprouting in the 4- to 5-mo-old kittens. If this is so, then the results indicate that functional connections from the deprived layers of the DLG to the striate cortex remain following rearing with monocular deprivation...

Effects of monocular visual deprivation on geniculocortical innervation of area 18 in cat

“…Support for this view comes from experiments in which some of the effects of MD were reversed rapidly (DuffL et al, 1976;Kratz et al, 1976;Burchfiel and Dutfy, 198 1;Mower et al, 1984). These data suggest that MD results in an active inhibition of the excitation from the deprived eye.…”

“…J. Friedlander, K. A. C. Martin, and D. Wassenhove-McCarthy, unpublished observations). However, other experimental protocols, including blockade of postsynaptic inhibition (Duffy et al, 1976) enucleation of the nondeprived eye (Kratz et al, 1976) simultaneous binocular activation (Freeman and Ohzawa, 1988) or intracellular recording of synaptic responses to electrical stimulation of the optic nerve (Tsumoto and Suda, 1978) reveal the persistence of excitatory input from the deprived eye. Anatomically, in area 17, MD results in a contraction of the ocular dominance slabs formed by the afferents driven by the deprived eye, while those of the nondeprived eye expand (Hubel et al, 1977;Shatz and Stryker, 1978;Wong-Riley, 1979;LeVay et al, 1980;Kossut et al, 1983;Tumosa et al, 1989).…”

Long- and short-term monocular deprivation in the rhesus monkey: effects on visual fields and optokinetic nystagmus

“…Those that are encountered have abnormal receptive fields and show reduced responsiveness to visual stimuli (Eysel et al, 1979;Hoffmann and Hollander, 1978;Kratz et al, 1978). Similarly, the functional organization (Hoffmann and Cynader, 1977;Hubel et al, 1976;Kratz et al, 1976;Shatz and Stryker, 1978;Singer, 1977;Spear et al, 1980;Wiesel and Hubel, 1965;Wilson and Sherman, 1977) and physiological properties (Baker et al, 1974;Crawford, 1978;Crawford et al, 1975;Wiesel and Hubel, 1963) of cells in the visual cortex are disrupted by brief periods of monocular deprivation.…”

Nasal field loss in kittens reared with convergent squint: neurophysiological and morphological studies of the lateral geniculate nucleus

“…any explanation is speculative. Whether retrograde degeneration, due to binocular competition at geniculo-cortical synapses as proposed by Wiesel & Hubel (1963), ), Guillery & Stelzner (1970), Sherman et al (1972 and Yinon et al (1975), or a tonic inhibitory influence from the visual cortex (Kratz, Spear & Smith, 1976;Duffy, Snodgrass, Burchfiel & Conway, 1976), or inadequate eye movement (Maffei & Bisti, 1976) is responsible for these minor effects remains problematical.…”