Conscious Perception Has Little to Do With Primary Visual Cortex, Research Suggests

0 comments

Posted on 13th March 2012 by Pacific ClearVision Institute in General |Retina

Imaging data suggest that conscious perception has little to do with the primary visual cortex — the region where visual information enters the brain.

From a purely intuitive point of view, it is easy to believe that our ability to actively pay attention to a target is inextricably connected with our capacity to consciously perceive it. However, this proposition remains the subject of extensive debate in the research community, and surprising new findings from a team of scientists in Japan and Europe promise to fuel the debate.

Resolving how these aspects of perception are managed requires a detailed understanding of how the visual centers in our brain process information. A region known as V1 has been investigated as it represents the first portion of the visual cortex to receive and process signals transmitted from the retina.

Many researchers favor a model in which functions pertaining consciousness are widely spread among the whole visual system, including V1. The classical model, which assumes that the neural mechanism of consciousness is integrated into a narrow subset of brain structures, referred to as a homunculus, or ‘little human’, is almost defunct. However, a modern version of this model is under debate. It proposes that the neural mechanism of consciousness is a privileged set of cortical areas, a subpopulation of neurons, or certain neural dynamics (e.g. oscillations); while there are also visual systems that have nothing to do with conscious vision, explains Masataka Watanabe a researcher investigating brain function at the University of Tokyo, Japan.

Watanabe cites studies proposing that visual attention as processed within V1 may be only minimally impacted by conscious perception; but, the experimental data have been contradictory. For example, studies using a technique called functional magnetic resonance imaging (fMRI) to map brain activity have indicated that V1 contributes to both attention and awareness in humans. However, invasive electrophysiological studies in non-human primates yielded different results. “You would find only 10 to 15% of neurons in V1 that are barely modulated by awareness, and 85% or so that are not modulated at all,” says Watanabe. To resolve this ambiguity, he, Kang Cheng from the RIKEN Brain Science Institute, Wako, and their colleagues designed an experiment that examined both processes independently. Surprisingly, their results may lend support the modern homunculus model.

Attentive, but unaware

The results proved striking: for all seven subjects, the shift of attention toward or away from the target had a dramatic effect on brain activity in the region of V1 corresponding to the visual target. However, the ability to consciously perceive the target proved surprisingly unimportant, and shifts in target awareness had no clear or consistent effect on the activity of this subset of neurons. “I was quite surprised that there was zero modulation of awareness in V1,” says Watanabe. “Even in monkey studies where the [animals] showed only 10% of their neurons being modulated, [those researchers] were nevertheless observing modulation.” By comparison, no such awareness effect was observed in the human subjects.

Watanabe and colleagues’ findings indicate that awareness is not a major factor in the earliest stages of visual perception, even though it is clearly a core component of the overall process. Further investigation will be required to determine how consciousness becomes integrated with other visual data. “Scientists are pretty sure that the terminal areas of the visual system, such as the regions that process shape and color or motion, are likely to be heavily modulated by awareness,” says Watanabe. “But where exactly this modulation starts is still an open question.”

Future studies from this research team will seek out the brain structures involved in awareness processing. For now, these data offer surprising support for a still-contested model of visual perception and consciousness. “To tell the truth, three years ago I would not have believed this result,” says Watanabe. “I don’t think the ‘Battle of V1′ is fully settled, but these data could imply that the modern homunculus model may be true.”

How Does Nearsightedness Develop in Children?

0 comments

Posted on 13th March 2012 by Pacific ClearVision Institute in General |Retina

Myopia (nearsightedness) develops in children when the lens stops compensating for continued growth of the eye, according to a study in the March issue of Optometry and Vision Science, official journal of the American Academy of Optometry.

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Using detailed information on eye growth and vision changes in children over time, the new research shows “decoupling” of lens adaptation from eye growth about a year before myopia occurs. Donald O. Mutti, OD, PhD, of The Ohio State University College of Optometry, is lead author of the new study.

Growth Imbalance Leads to Myopia…

The researchers analyzed repeated measurements of vision and eye growth performed over several years in children aged 6 to 14. The study focused on the growth of the two key parts of the eye affecting normal vision: the cornea, the transparent front part that lets light into the eye; and the lens, located behind the cornea, which focuses light rays on the retina at the back of the eye.

Myopia or nearsightedness — difficulty seeing objects at a distance — develops in about 34% of American children as they grow. Vision professionals and scientists typically think of myopia as a problem occurring when the eyeball becomes too long (front to back) for the optical power of the cornea and lens.

However, it has been unclear how this imbalance develops in children who previously had normal vision. To answer this question, Dr. Mutti and colleagues compared changes in eye growth for children who developed myopia at different ages versus those whose vision remained normal.

They found that, in children without myopia, the lens grew thinner and flatter to maintain normal vision as the eye grew. This adaptation maintained a normal balance between the optical power of the lens and the increasing length of the eyeball. From age nine months to nine years, eyeball length increased by an average of three millimeters.

…As Lens Stops Responding to Increasing Eye Length

However, in children who developed myopia, the lens stopped changing in response to eye growth. Nearsightedness developed not just because of increases in the length of the eyeball, but rather because the optical power of the lens no longer changed as the eye grew.

The imbalance occurred rather suddenly: about one year before the children became nearsighted. For at least five years after the development of myopia, the eye kept becoming longer but the lens stopped flattening and thinning.

In contrast to the lens, changes in corneal growth showed little or no relation to the development of myopia. The cornea is responsible for about two-thirds of the optical power of the eye, and the lens for the remaining one-third.

The study provides vision professionals with an important new piece of information on why some children develop myopia. However, what’s still unclear is why the lens suddenly stops adapting to continued growth of the eye. More research will be needed to answer that question — one possibility is that an abnormally thick ciliary muscle within the eye forms a mechanical restriction preventing the stretching that thins and flattens the lens as the eye continues to grow.

The Genetic Basis for Age-Related Macular Degeneration (AMD)

0 comments

Posted on 13th March 2012 by Pacific ClearVision Institute in General |Retina

Age-related macular degeneration (AMD) is one of the leading causes of blindness worldwide, especially in developed countries, and there is currently no known treatment or cure or for the vast majority of AMD patients. New research published in BioMed Central’s open access journal Genome Medicine has identified genes whose expression levels can identify people with AMD, as well as tell apart AMD subtypes.

It is estimated that 6.5% of people over age 40 in the US currently have AMD. There is an inheritable genetic risk factor but risk is also increased for smokers and with exposure to UV light. Genome-wide studies have indicated that genes involved in the innate immune system and fat metabolism are involved in this disease. However none of these prior studies examined gene expression differences between AMD and normal eyes.

In order to address this question, researchers at the University of California Santa Barbara, the University of Utah John Moran Eye Center, and the University of Iowa combined forces and used a human donor eye repository to identify genes up-regulated in AMD. The ability of these genes to recognize AMD was tested on a separate set of samples.

The team discovered over 50 genes that have higher than normal levels in AMD, the top 20 of which were able to ‘predict’ a clinical AMD diagnosis. Genes over-expressed in the RPE-choroid (a tissue complex located beneath the retina) included components of inflammatory responses, while in the retina, the researchers found genes involved in wound healing and the complement cascade, a part of the innate immune system. They found retinal genes with expression levels that matched the disease severity for advanced stages of AMD.

Dr. Monte Radeke, one of the project leaders, explained, “Not only are these genes able to identify people with clinically recognized AMD and distinguish between different advanced types — some of these genes appear to be associated with pre-clinical stages of AMD. This suggests that they may be involved in key processes that drive the disease. Now that we know the identity and function of many of the genes involved in the disease, we can start to look among them to develop new diagnostic methods, and for new targets for the development of treatments for all forms of AMD.”

Zebrafish May Hold Key to Repairing Serious Eye Conditions

0 comments

Posted on 13th March 2012 by Pacific ClearVision Institute in General

University of Michigan Health System research into the mechanisms by which zebrafish are able to regenerate damaged retinas after injury suggests new strategies for one day being able to do the same in humans — potentially allowing doctors to slow or reverse conditions like macular degeneration and glaucoma.

Building on previous studies, Daniel Goldman, Ph.D., a professor at U-M’s Molecular and Behavioral Neuroscience Institute and in the Department of Biological Chemistry, along with postdoctoral fellows Jin Wan and Rajesh Ramachandran, discovered that heparin-binding epidermal-like growth factor (HB-EGF) plays a critical role during retina regeneration. Their findings were recently published in Developmental Cell.

“We found that this factor is sufficient to activate the whole process,” says Goldman.

When a zebrafish’s retina is damaged, HB-EGF is released and sets in motion a series of changes that cause certain cells in the retina known as Muller glia to revert to a stem-cell state from which they can generate new cells and repair the damage. The researchers found that HB-EGF stimulated Muller glia to revert to a stem cell even in fish with uninjured eyes.

The next step, says Goldman, will be to explore if this factor and related pathways can stimulate Muller glia dedifferentiation and stem cell formation in mammals.