Biomedical subjects

Yuzo M Chino

Publications and source records attributed to Yuzo M Chino.

4 recordsLinked to original sources

PubMed2005

Neuroscience: rewiring the adult brain.

Any analysis of plastic reorganization at a neuronal locus needs a veridical measure of changes in the functional output--that is, spiking responses of the neurons in question. In a study of the effect of retinal lesions on adult primary visual cortex (V1), Smirnakis et al. propose that there is no cortical reorganization. Their results are based, however, on BOLD (blood-oxygen-level-dependent) fMRI (functional magnetic resonance imaging), which provides an unreliable gauge of spiking activity. We therefore question their criterion for lack of plasticity, particularly in the light of the large body of earlier work that demonstrates cortical plasticity.

Action Potentials↗

PubMed2005

Rapid plasticity of binocular connections in developing monkey visual cortex (V1).

The basic sets of cortical connections are present at birth in the primate visual system. The maintenance and refinement of these innate connections are highly dependent on normal visual experience, and prolonged exposure to binocularly uncorrelated signals early in life severely disrupts the normal development of binocular functions. However, very little is known about how rapidly these changes in the functional organization of primate visual cortex emerge or what are the sequence and the nature of the abnormal neural events that occur immediately after experiencing binocular decorrelation. In this study, we investigated how brief periods of ocular misalignment (strabismus) at the height of the critical period alter the cortical circuits that support binocular vision. After only 3 days of optically imposed strabismus, there was a striking increase in the prevalence of V1 neurons that exhibited binocular suppression, i.e., binocular responses were weaker than monocular responses. However, the sensitivity of these neurons to interocular spatial phase disparity was not significantly altered. These contrasting results suggest that the first significant change in V1 caused by early binocular decorrelation is binocular suppression, and that this suppression originates at a site(s) beyond where binocular signals are initially combined.

Animals↗

PubMed2005

Directional bias of neurons in V1 and V2 of strabismic monkeys: temporal-to-nasal asymmetry?

PURPOSE: Strabismus that develops shortly after birth is known to cause temporal-to-nasal eye movement asymmetries under monocular viewing. The neural mechanisms underlying this deficit are not well understood. In the current study, the hypothesis that this eye movement anomaly reflects a similar asymmetry in the directional response properties of neurons in the early stages of cortical processing was examined. METHODS: Strabismus was simulated with optical methods in infant monkeys between 4 and 14 weeks of age. When the monkeys were mature, microelectrode recording experiments were conducted in the primary visual cortex (V1) and visual area 2 (V2). After the spatial frequency of sine wave-grating stimuli for each neuron was optimized, each neuron's responsiveness to 24 directions of stimulus movement was measured. The preferred direction and the strength of directional bias were determined by a vector summation method: RESULTS: There was not an overabundance of neurons in V1 or V2 of strabismic monkeys preferring the temporal-to-nasal direction of stimulus movement. However, the average directional bias was significantly reduced in these strabismic monkeys. Interocular suppression was highly prevalent, and this suppression was stronger and more common in neurons dominated by the ipsilateral eye. CONCLUSIONS: The results suggest that the eye movement asymmetries in strabismic subjects do not result from similar asymmetries in the directional properties of V1 or V2 neurons, but rather reflect impoverished cortical signals to the brain stem nuclei that control eye movements.

Animals↗

PubMed2002

Effects of the duration of early strabismus on the binocular responses of neurons in the monkey visual cortex (V1).

PURPOSE: To determine how the duration of early strabismus influences the severity of loss of disparity sensitivity in V1 neurons and the effects of extensive poststrabismus visual experience on the maintenance of functional binocular connections. METHODS: Concomitant strabismus was optically simulated in 10 rhesus monkeys using a prism-rearing procedure. The onset of strabismus was kept constant at 4 weeks of age and the duration was maintained for 2, 4, or 8 weeks. In one group of monkeys (infants), the neurophysiological experiments were conducted immediately after the period of rearing with prisms. In another group (adults), after the termination of the prism-rearing regimen at either 8 or 12 weeks of age, the monkeys were kept in a normal housing environment until maturity and behavioral testing was conducted before the recording experiments to determine the animal's monocular and binocular visual capacities. To assess the effects of the period of early strabismus on binocular interactions in V1, extracellular single-unit recording methods were used in anesthetized and paralyzed monkeys, and dichoptic sine-wave gratings were used as stimuli. RESULTS: In all strabismic monkeys, the sensitivity of V1 units to interocular spatial phase disparity (disparity sensitivity) was significantly reduced, and the prevalence of binocular suppression was higher than that found in age-matched control animals. Although 8 weeks of strabismus resulted in a slightly larger loss of disparity sensitivity, the overall effects of the duration of strabismus were surprisingly small in infant strabismic monkeys. After poststrabismus visual experience, a small but significantly higher degree of disparity sensitivity was noted in V1 if prism-rearing was terminated after 4 weeks of strabismus (i.e., at 8 weeks of age), but not after 8 weeks of strabismus (i.e., at 12 weeks of age). CONCLUSIONS: A brief period (2 weeks) of misalignment after the emergence of stereopsis is sufficient to drastically reduce the functional binocular connections in V1, and longer periods of strabismus result in little additional loss in disparity sensitivity. Clinically, these results suggest that taking corrective measures for infantile esotropes before the known onset age for stereopsis may be important for maintaining better binocular sensory function and better interocular alignment at later stages of development.

Aging↗