Animal Studies of Abnormal BV Development

Studies have been limited. Well, not that limited but you can't just patch a babies eye, ruin its BV and then kill it to assess how the visual cortex has developed. It's not allowed. You can do it on cats and macaque monkeys though! That's probably still against many people's wishes but ho hum. Hubel and Wiesel did the most famous early work. Here's what they found w/cats

• VC of neonatal kitten possesses at least the skeleton of organisation present in adults. Orientation columns are present even before the eyes are opened but they subsequently become modified by experience.
• Disruption of binocular input via unilateral eye closure, alternating eye occlusion or artificial strabismus completely disrupts cortical binocular interaction
• Complete binocular deprivation actually has less effect than two monocular ones. It doesn't abolish visual responsiveness with the finality that monocular dep does.
• The physiological effects of abnormal visual experience are mostly confined to the cortex and aren't expressed to any great degree in the LGN. Changes in the LGN are probably due to suppression of the bad eye which in turn alters the neural connections between cortex and LGN.
• The effects of abnormal vis.exp. are only obtained during the moggy's critical period early in its life
• Short periods of occlusion produce severe changes, longer irreversible. When the cat reaches visual maturity, boom! Permanent changes!

The visual system is more plastic and stays more plastic at higher levels of processing. The retina is pretty much hard-wired but the output layers of the primary visual cortex are relatively very plastic indeed! Hubel and Wiesel also saw (when they used monkeys) that the critical period in the visual cortex for the magnocellular system ends earlier than that of the parvocellular system. When reverse suture was done at 3 weeks of age the open eye can reverse the effects of the initial deprivation for the parvocellular system but not the magnocellular system.

Critical period for monocular deprivation in cats starts at 3 weeks, monkeys soon after birth, peaks at one month and ends in one year. It's 0-3 years in humans. The critical period for ocular dominance changes starts soon after the eyes open and continues until some time near puberty.

The peak of the critical period for ocular dominance occurs when ocular dominance columns in V4 (which receives equal input from the right and left eye) are segregating and cells sensitive to disparity are being formed. These crucial peaks:

• Cats 4-6 weeks
• Monkey one month
• Humans 3-5 months

As you may have guessed functions requiring higher levels of processing have later sensitive periods. Interestingly some functions remain plastic until a far later stage in life. If some random human loses its good eye the amblyopic eye can show a marked improvement in VA.

Summary

• Mammals compensate for optical deficits occuring at a young age by anatomical and physiological changes @ the visual cortex. There's very little compensation at the retina and LGN.
• Animal studies have shown the plasticity of the immature visual system and the importance of a sharply focussed image in both eyes to normal binocular visual development.
• Early diagnosis/treatment of infants at risk of amblyopia is important!