Should We Keep Patients in the Dark?

In 1915, Drs. Long and Evans crossed several Winstar Institute white female rats with a wild gray male rat to derive a general multipurpose model rat for behavioral research.  It is the Long-Evans rat that Elizabeth Quinlan, Ph.D., and her colleagues have been using for some fascinating research into the neuroplasticity of amblyopia.  Dr. Quinlan presented this research to a rapt audience at the Annual Meeting of the College of Optometrists in Vision Development in Ft. Worth, Texas yesterday.  You can read an updated review of her research thoughts here (2018)

The essence of the Quinlan Lab research presented can be summarized briefly as follows:

1) The impact of monocular deprivation on the development of the neurons in V1 is that deprived neurons appear as if their dendritic connections are de-forested, whereas new, unexposed neurons appear to be lacking dendritic connections.  Once synaptic connections are re-established, deprived neurons return to a more normal appearance, more effectively transmitting visual information.

2) Inhibitory input to binocular neurons in V1 of striate cortex from the non-deprived eye is believed to be responsible for brakes or limitations in recovery of functional vision from the deprived eye.

3) Keeping rats in the dark de-afferentiates input to visual cortex from the non-deprived eye.  Dark rearing followed by reverse occlusion resurrects synaptic connections and re-invigorates synaptic activity.

There are two issues here.  One is what we can do in infancy to preserve or extend plasticity.  Another is what we can do in adulthood to remove the brakes on plasticity that seems to reflect arrested development.  As illustrated by Takao Hensch, dark-rearing followed by appropriate stimulation seems to be a way of making the critical period less critical and extending it well into adulthood.

A clinical version of dark-rearing has been in our literature for some time in terms of inverse occlusion for amblyopia, particularly to disrupt eccentric fixation, though this practice has largely been abandoned.

Keeping patients in the dark is impractical, but designing creative ways to preserve visual function may be more attainable.  Binasal occlusion does this to some degree.

Unlike rats who can be sutured and whose environment can be contained, humans cannot be so constrained.  Keeping our eye on Dr. Quinlan’s research will help inform our interventions, and it seems the inverse may be true as well.

Here are some more relevant abstracts and an interesting open access article.

One thought on “Should We Keep Patients in the Dark?

  1. Dr. Press,
    Thanks for the data. Very interesting experiments. I have two thoughts. If the inhibition comes from the “non-deprived eye” (the good eye) wouldn’t direct (patch the good eye) occlusion be indicated? Or is the theory that the non-deprived eye would stop its mischief if the deprived eye were out of the way? Since studies show that 6 hrs a day of occlusion works as well as full time occlusion, how does this fit, since those with 6 hours of patching would spend as much time with the good eye interfering with synaptic connections as not interferring. And yet there is no difference found in the clinical studies. Since active vision therapy 2 hours per day does as much good as full time patching, maybe active therapy is doin more to reverse the interference? Just some thoughts.

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