Secrets of Sight
The number of processes involved in eyesight continues to grow, adding more focus and clarity to the miracle of vision.
Keeping the lens moist: Rays of light are focused by the lens of the eyeball, a precision structure composed of cells. Though transparent, the lens cells are constantly active like other cells, operating molecular machines that go about their work without blocking the view. Science Daily discussed some of the water pores in the lens – active channels in the cell membrane that conduct water and keep other substances out. A special aquaporin, named AQP0, is found only in the mammalian lens.
The lens is primarily made up of unique cells called lens fibers that contain little else besides water and proteins called crystallins. Tight packing of these fibers and of the crystallin proteins within them helps create a uniform medium that allows light to pass through the lens, almost as if it were glass.
AQP0 has a vital role in maintaining the transparency of the lens. Despite the uniformity and simplicity of the design, the lens has these channels that contain moving parts. Those parts, in turn, are activated by another protein called calmodulin that can seal the channel shut: “calmodulin essentially grasps the open channel and forces it to close.” The action is even more nuanced than that, researchers at four American institutions found. With mixed metaphors, they explained:
The AQP0 channel is made up of four identical barrel-shaped units, bundled together side by side. The researchers found that in the presence of calcium, calmodulin binds to one unit and then another, as if grabbing a pair of reins. This makes the channel twist slightly, which causes just a few amino acids within each unit to slide into the channel’s core and block the flow of water.
“Calmodulin essentially throws a molecular switch that moves in and out of the water pore, like the gate valve of a plumbing fixture,” Dr. Hall said.
Mutations in AQP0 or environmental factors can cause the breakdown of this automated cleaning system, leading to cataracts.
Shifty eyes: Your eyes are constantly moving, even when you stare, with tiny jerks called saccades. In the foveola (the center of vision, with the greatest acuity due to its concentration of cones), there are “microsaccades” that continually shift light between the photoreceptors. Current Biology published new work on this, stating that microscopic eye movements compensate for nonhomogeneous vision in the fovea (the larger center that includes the foveola). Like the larger saccades, microsaccades keep the focus on the locus of attention and enable us to study objects with finer detail. The authors explain,
We show that high-acuity judgments are impaired when stimuli are presented just a few arcminutes away from the preferred retinal locus of fixation. Furthermore, we show that this dependence on eccentricity is normally counterbalanced by the occurrence of precisely directed microsaccades, which bring the preferred fixation locus onto the stimulus. Thus, contrary to common assumptions, vision is not uniform within the foveola, but targeted microscopic eye movements compensate for this lack of homogeneity. Our results reveal that microsaccades, like larger saccades, enable examination of the stimulus at a finer level of detail and suggest that a reduced precision in oculomotor control may be responsible for the visual acuity impairments observed in various disorders.
The authors described the foveola as “a tiny region covering approximately half the width of a thumb at arm’s length,” about 1 degree of vision. What are microsaccades good for? The authors discounted the view that they prevent fading or saturation of the cones. Instead, they improve our visual accuracy:
In contrast, our results show that microsaccades are critical for high-acuity judgments, as they serve, at a microscopic scale, the same explorative function as larger saccades, as long hypothesized; both movements reposition the stimulus on the retina to enable its examination at a finer level of detail.
Spatial vision is compromised, they said, in various disorders that interrupt these tiny eye movements.
The learning eye: Science Daily covered another paper in Current Biology about saccades, which occur 4-5 times per second. “Human eye movements for vision are remarkably adaptable,” the headline reads. The brain has the ability to adapt its eye movements, learning to refocus its center of attention if the fovea is obscured. One of the authors said, “We showed that people with normal vision can quickly adjust to a temporary occlusion of their foveal vision by adapting a consistent point in their peripheral vision as their new point of gaze.” Experiments on humans showed they could remember the new training for weeks. The training with gray disks that blocked the fovea provides hope that patients with macular degeneration or cataracts can retrain their center of gaze.
Rods, cones and pRGCs: Light affects other cells in the retina other than the rods and cones. Current Biology investigated a third class of photoreceptors, the melanopsin-expressing photosensitive retinal ganglion cells (pRGCs). These cells respond to light independently, but also take input from the rods and cones. A team of Oxford ophthalmologists found that, in mice, pRGCs have a nonuniform distribution in the retina, contain subtypes with different patterns, and produce spectral tuning of their responses due to gradients in cone opsin expression. They act as “the primary sensory conduit mediating non-image-forming responses to light.” What does this mean to vision? As part of the “melanopsin system,” pRGCs tie into circadian rhythms (the biological clock) and the response of the pupil to the brightness of the light, Neurology.org explains. Here’s how the ophthalmologists concluded their research:
In summary, our results show a previously unreported anatomical and functional specialization of the murine melanopsin system. This study provides the first evidence for a differential distribution of pRGC subtypes and illustrates the importance of classical photoreceptor input in providing spectral tuning of pRGC light responses. These data have clear implications for the complexity of sensory irradiance detection and the study of different non-image-forming responses to light.
Retina map: Want to see what a retina looks like in 3-D? Check out the image on Science Daily about a paper in Nature by researchers who made the first complete neuronal map of a piece of retina, from photoreceptor to visual cortex. 450 grad students helped with the project. Here are some factoids for the water cooler:
Even though the cube of retina was only a tenth of a millimetre on a side, it contained around 1000 neurons and more than half a million contacts between them. “We needed about a month to acquire the data and four years to analyse them” says Helmstaedter. The reason for this long time is the extensive analysis needed to extract the wiring from electron-microscope images of brain tissue. Extremely thin neuronal processes needed to be followed over long distances, without missing any of the multitudes of connections between them. Current computer algorithms are very useful in this process but often not reliable enough. Humans are thus still needed to make the decision whether a neuronal “wire” branches or not. In the current study it took 20,000 hours alone to make those decisions. To analyse an entire mouse brain in this way would require several billion hours of human attention.
—and that’s just drawing the skeleton of connections, not filling in the neuron bodies, which would take 10 to 100 times longer.
New discoveries came from the crowd-sourced project called EyeWire. Out of the 50 to 100 neuron types involved in vision, “We characterize a new type of retinal bipolar interneuron and show that we can subdivide a known type based on connectivity,” the authors said. “Circuit motifs that emerge from our data indicate a functional mechanism for a known cellular response in a ganglion cell that detects localized motion, and predict that another ganglion cell is motion sensitive.” Another article on Science Daily claimed this is the first step in mapping the human brain – that is, if grad students have billions of hours to spare.
Your internal GPS: It doesn’t help to see if you can’t orient yourself. Live Science reported the discovery that humans, like some animals, have grid cells in the hippocampus that provide a kind of GPS. New Scientist described how these cells work in concert with other navigation cells:
We know that animals use three cell types to navigate the world. Direction cells fire only when an animal is facing a particular direction, place cells fire only in a particular location, and grid cells fire at regular intervals as an animal moves around.
To understand how grid cells work, imagine the carpet in front of you has a grid pattern of interlocking triangles. One grid cell will fire whenever you reach the corner of any triangle in that grid. Shift the grid pattern along ever so slightly to another section of the carpet, and another grid cell will be responsible for firing every time you reach the corners of that grid’s triangles – and so on.
The information from these cell types creates a “mental map” to help you understand your location and make sense of movement. The memory linkage helps you remember where you were. Think of how these systems come into play when a skilled tracker looks for his prey in a forest of complex shapes and colors. Those who have a friend or relative that has experienced vertigo know the fear of losing that orientation.
We hope you are fascinated and encouraged by these incredible examples of design. You can’t just take the wide-angle view of vision; the complexity is in the telephoto, microscopic and nanoscopic views. So much is going on in your eye and brain as you read this, it is beyond comprehension. We have only the faintest glimpse of the multitude of precision processes that make our experience of the visual world possible.
Yet evolutionists continue to be blind to this evidence – a willful blindness, not a physical one – attributing all this design to chance. Take a look, for instance, at a stupid article on Medical Xpress that begins, “Your eyes are half a billion years old.” The article gives the mike to “Professor Trevor Lamb” who takes it upon himself to pontificate about “the origin of the vertebrate eye and vision.” Like an episode from Carl Sagan’s Cosmos, (“eyes evolved, and now the cosmos could see”), here comes the typical Darwin fairy tale, glittering generalities and all —
The deep origins of ‘sight’ go back more than 700 million years when the earth was inhabited only by single-celled amoeba-like animals, algae, corals and bacteria. At this time the first light-sensitive chemicals, known as opsins, made their appearance and were used in rudimentary ways by some organisms to sense day from night.
Ancient cells already had signalling cascades that sensed chemicals in their environment, and the advent of opsins allowed them to sense light. “But these animals were tiny, and had no nervous system to process signals from their light sensors,” he explains.
Over the following 200 million years those simple light-sensitive cells and their opsins slowly and progressively became better at detecting light – they became more sensitive, faster, and more reliable – until around 500 million years ago they already closely resembled the cone cells of our present day eyes.
“The first true eyes, consisting of clumps of light-sensing cells, only start to show up in the Cambrian, about 500 million years ago – and represent a huge leap in the evolutionary arms race,” Prof. Lamb says. “Creatures that could see clearly had the jump on those that couldn’t.
La de da de da, on it goes. Complex systems “made their appearance.” They had their “advent.” It was all “slowly and progressively.” This is so 1859. Did you notice how he tiptoed over the Cambrian explosion? Elaborate compound eyes, as found on trilobites, suddenly appear fully formed without precursors. To believe Darwin, you would have to believe in the Popeye Theory of Evolution: eyes just popped into existence, like one evolutionist claimed (5/31/05).
It’s not the research scientists using actual instruments who are saying these things. None of the articles about the details had any use for evolutionary theory. No; it’s the storytelling charlatans who weave the Grand Myth out of glittering generalities, ignoring the specifics of ganglion cells, interneurons, saccades, the foveola, internal GPS. We should hold these papers up to the faces of these storytelling charlatans and demand that they explain all the facts, accounting for every mutation and its supposed selective advantage to get to each step. A trillion million years wouldn’t be enough to accomplish just a fraction of these wonders using unguided processes. The charlatans need to be shamed out of the science departments. Make them get real jobs, inspecting potatoes or something useful.
The rest of us can rejoice at what real scientific inquiry is revealing about the intelligent design of life.