photoreceptor cells

Cephalopod eyes are fascinating. Just like us vertebrates they have camera-type eyes, a hollow liquid-filled chamber with an opening, the iris, and a lens through which light enters and is projected onto the photosensitive surface, the retina. Despite their similarities, vertebrate and cephalopod camera-type eyes have different origins and evolved independently. There are some striking differences that highlight this:

Unlike us, the photoreceptor cells of cephalopods point outwards towards the source of the light rather than inwards. This not only means the we have “inverted” retinas, it also means that cephalopods don’t have a blind spot because the nerve fibers that transmit the visual impulses from the retina to the brain collect and exit the eye behind the retina rather than in front of it. The developmental origins of the eye tissues are also different. For instance, in vertebrates the complex layers of the retina develop from nerve tissue, while the lens develops from skin tissue. In cephalopods both tissues develop from progenitor skin cells.

Cephalopods have excellent vision, and use complex visual cues to communicate with each other, camouflage themselves, and send signals to their environment. To do this they use highly adaptible pigment-filled cells in their skin called chromatophores. The capricorn night octopus (Callistoctopus alpheus) in the photo looks blue, but if it would open all its chromatophores it would turn deep red with bright white polka dots.

Photo credit: David Liittschwager, National Geographic.

ELI5: why do you see weird patterns when you close your eyes and apply pressure onto them?

This phenomenon is called phosphene.

When light hits the cells in the eye, these cells send a signal to the brain to give an image of what is seen. These cells are called photoreceptor cells, and their main means of activation is when a photon of light hits them. Another way to activate them is via mechanical stimulation (aka applying pressure to they eyes). When you apply mechanical stimulation, the subsequent activation of the cells will be random (not patterned), and when this signal is transmitted to the brain areas that are responsible for generating an image, you will see weird patterns instead of the normal images that would be generated by photon-induced stimulation.

Explain Like I`m Five: good questions, best answers.

Cranial Nerves

Nerves supplying the body can be divided in to cranial and spinal. Cranial nerves emerge from the brain or brain stem and spinal from the spinal chord. There are 12 pairs of cranial nerves. They are components of the peripheral nervous system, with the exception of the optic nerve, as their axons extend beyond the brain to supply other parts of the body. They are named numerically from region of the nose (rostral) to back of the head (caudal). Here’s a brief overview of all twelve nerves and their basic functions.

I – The Olfactory Nerve. The cells of this nerve arise from the olfactory membrane of the nasal mucosa. The dendrites of the nerve cells project in to the olfactory mucosa. The axons of these cells combine to form the olfactory nerve. They join the brain at the olfactory bulb, located at the end nearest the nose. The fibres are short and lie deep and protected from casual injury. It is often found that loss or interference of sense of smell is due to blockage of the air passage leading to the olfactory mucosa, not due to nerve damage.

II – The Optic Nerve. This nerve connects the retina to the diencephalon of the brain. It is the only cranial nerve considered to be part of the central nervous system. This means the fibres are incapable of regeneration, hence why damage to the optic nerve produces irreversible blindness. Interestingly the eye's blind spot is a result of the absence of photoreceptor cells in the area of the retina where the optic nerve leaves the eye. I find the optic nerves easy to spot when looking at the brain from below as they form the optic chiasm. This is the point at which they cross and forms a clear ‘x’.

III- The Oculomotor Nerve. This nerve controls most of the eye’s movements including the constriction of the pupil and levitation of the eyelid. Damage to the nerve can cause double vision and inability to open the eye. A symptom of damage to this nerve is tilting of the head.

IV – The Trochlear Nerve. This nerve is a small somatic motor nerve and innervates the dorsal oblique muscle of the eye, responsible for allowing the eye to look down and up as well as internal rotations. Damage to the nerve can cause one eye to drift upwards in relation to the undamaged eye, meaning patients tilt their heads down to compensate.

V – The Trigeminal Nerve. This is the largest cranial nerve and is so called as it has three major divisions. It is sensory to the skin and deeper tissue of the face and motor to certain facial muscles, playing a large role in mastication.

VI – The Abducent Nerve. This nerve controls the movement of the lateral rectus muscle of the eye. It also plays a role in eye retraction for protection. Injury produces the inability to deviate the eyeball away from the midline of the body.

VII – The Facial Nerve. This nerve innervates the muscles of facial expression. It also functions in the conveyance of taste sensations from the front two thirds of the tongue. As well as this it can increase saliva flow through certain salivary glands.

VIII – The Vestibulocochlear Nerve. This nerve is named after the vestibular and cochlear components of the inner ear. It transmits information on sound and balance. Damage can lead to deafness, impaired balance and dizziness.

IX – The Glossopharyngeal Nerve. This nerve has any roles including the innervation of certain muscles of the palate of the mouth, certain salivary glands and the sensory mucosa of the root of the tongue, palate and pharynx. Damage can lead to difficulty swallowing as well as the loss of ability to taste bitter and sour things in humans.

X – The Vagus Nerve. This is a very important nerve and one frequently discussed when considering many important systems within the body. It is the longest of all cranial nerves and extends to supply the pancreas, spleen, kidneys, adrenals, and intestine. It has parasympathetic control of the heart and digestive tract as well as certain glands and involuntary muscles.

XI – The Accessory Nerve. This plays a role in neck turning and elevation of the scapula (shoulder). Muscle atrophy of the shoulder region indicates damage to this nerve.

XII – The Hypoglossal Nerve. This nerve’s name relates to the fact that is runs under the tongue, innervating the tongue’s internal and external musculature. It has important roles in speech, food manipulation and swallowing.

There are 200 trillion atoms in 1 human cell. In your eye there are 130 million photoreceptor cells. In your body there are about 100 trillion cells. That means there are approximately 100 times more atoms (200 septillion) in a single human body than there are stars in the entire universe! 

In terms of atoms the body is made up of roughly: 
hydrogen 62.2%
oxygen 24.1%
carbon 12%
nitrogen 1.2%
phosphorus 0.2%
calcium 0.2%

That being said, in terms of mass, we are around 4 parts oxygen, 1 part carbon, and .5 parts hydrogen. This is similar to the composition of a white dwarf star.

In Black & White

The human eye is one of nature’s most complex and sophisticated creations. The really amazing part of what your eye does is the transformation of light into electrical impulses. This is done by the photoreceptor cells in your retina.

There are two kinds of these cells. The rods and the cones. Your cones are responsible for all the colorful and vivid images you see. They are concentrated at the center of the retina, so when you look straight ahead, you see what the cones are showing you. The rods only see black & white. But they are more sensitive to light, and much better at detecting movement.

This gives rise to some interesting phenomena. You’re outside on a beautiful night. And then, out of the corner of your eye, you see a bright star. But when you turn that way, the star is gone. This is because what you saw from the corner of your eye was shown to you by the rods. When you turned, the star moved to the field of the cones, who, of course are not sensitive enough to show you that star. So in a way, now you are not seeing that which is already there. The eye truly sees a lot more than you realize.

So think about the last time you saw something out of the corner of your eye. A blurred image or a moving object. You turned towards it and it was gone. Next time, don’t turn. Your rods are trying to show you something.

When your life is a back-and-forth battlefield of lies and compromises, and your skin is burned with betrayal, bring into light the absolute truths of your existence.

1. Your shadow is not empty space. It is the color that occurs when the sun itself sends millions of light particles, hurtled over 93 million miles your way at quite literally the speed of light, all in order to acknowledge your corporeal existence. It is the hands of the sun, transmuting at your feet in the reflection of the dark side of the moon.

2.The amount of quantum matter in the universe is, and always has been, in a constant state, due to contrasting gravitational forces. This would suggest that matter destroys itself only to be reborn simultaneously in a new form, causing new space, new planets, new possibilities, and most importantly, you. You were born your own masterpiece. Your eyes are made of starlight, and there are oceans under your tongue. Your skin is a patchwork collage of leaves that fell 50 million Autumns ago, and the blood in your veins came from the heart of Vesuvius. When your cheeks sting nettle red in the winter wind, remember that the color flushing into your face was once a lover’s rose bouquet, and when crocodile tears roll from your lashes, think of the almighty Amazon. Do not be afraid from whence you came.

3. If, on days, you cannot see the light in your eyes, then at least consider the following: At the heart of every star, there lies an immense amount of gas and dust particles that are eventually condensed down into different elements through nucleosynthesis. When the star dies, these elements explode outwards and conglomerate to form new planets, new stars, the earth, and you. You are literally made of starstuff. The iron in your blood and bones was fine-tuned by the weight of the universe, and the oxygen that lives in your lungs was once the gentle exhale of Andromeda. Your brain is a perfect composition of cosmic neurons, and your bursting heart is woven with the same molten plasmas and magnetic fields as the sun.

4. Alone, each of your eyes contains 130 million photoreceptor cells. If you were to count the amount of atoms inside those cells, you would end up with a number bigger than there are stars in the Milky Way. As we know, these very atoms were created by stars billions of years ago, light years away, and now exist in your eyes purely to capture the energy released from where they were born.

5. By the time the average reader reaches the end of this sentence, approximately 25,000,000 of their body’s cells will have perished. But you are in the hands of the universe, and it refuses to let you perish. By the time the moon has circled the earth, your body will have made over 300 billion new cells to compensate for the ones you lost.

6. The universe has been crafting you from the beginning of time, giving up parts of itself purely for the sake of your existence and to expand the consciousness of your metaphysical self.

7. The supreme entropy of the universe thrives in your skin and bends at your will to exist. You are the universe, here to witness the universe. You matter (literally).

—  Meghan Faulkner “You Matter”
Making artificial vision look more natural

In laboratory tests, researchers have used electrical stimulation of retinal cells to produce the same patterns of activity that occur when the retina sees a moving object. Although more work remains, this is a step toward restoring natural, high-fidelity vision to blind people, the researchers say. The work was funded in part by the National Institutes of Health.

(Image caption: Chichilnisky and colleagues used an electrode array to record activity from retinal ganglion cells (yellow and blue) and feed it back to them, reproducing the cells’ responses to visual stimulation. Credit: E.J. Chichilnisky, Stanford.)

Just 20 years ago, bionic vision was more a science fiction cliché than a realistic medical goal. But in the past few years, the first artificial vision technology has come on the market in the United States and Western Europe, allowing people who’ve been blinded by retinitis pigmentosa to regain some of their sight. While remarkable, the technology has its limits. It has enabled people to navigate through a door and even read headline-sized letters, but not to drive, jog down the street, or see a loved one’s face.

A team based at Stanford University in California is working to improve the technology by targeting specific cells in the retina—the neural tissue at the back of the eye that converts light into electrical activity.

“We’ve found that we can reproduce natural patterns of activity in the retina with exquisite precision,” said E.J. Chichilnisky, Ph.D., a professor of neurosurgery at Stanford’s School of Medicine and Hansen Experimental Physics Laboratory. The study was published in Neuron, and was funded in part by NIH’s National Eye Institute (NEI) and National Institute of Biomedical Imaging and Bioengineering (NIBIB).

The retina contains several cell layers. The first layer contains photoreceptor cells, which detect light and convert it into electrical signals. Retinitis pigmentosa and several other blinding diseases are caused by a loss of these cells. The strategy behind many bionic retinas, or retinal prosthetics, is to bypass the need for photoreceptors and stimulate the retinal ganglion cell layer, the last stop in the retina before visual signals are sent to the brain.

Several types of retinal prostheses are under development. The Argus II, which was developed by Second Sight Therapeutics with more than $25 million in support from NEI, is the best known of these devices. In the United States, it was approved for treating retinitis pigmentosa in 2013, and it’s now available at a limited number of medical centers throughout the country. It consists of a camera, mounted on a pair of goggles, which transmits wireless signals to a grid of electrodes implanted on the retina. The electrodes stimulate retinal ganglion cells and give the person a rough sense of what the camera sees, including changes in light and contrast, edges, and rough shapes.

“It’s very exciting for someone who may not have seen anything for 20-30 years. It’s a big deal. On the other hand, it’s a long way from natural vision,” said Dr. Chichilnisky, who was not involved in development of the Argus II.

Current technology does not have enough specificity or precision to reproduce natural vision, he said. Although much of visual processing occurs within the brain, some processing is accomplished by retinal ganglion cells. There are 1 to 1.5 million retinal ganglion cells inside the retina, in at least 20 varieties. Natural vision—including the ability to see details in shape, color, depth and motion—requires activating the right cells at the right time.

The new study shows that patterned electrical stimulation can do just that in isolated retinal tissue. The lead author was Lauren Jepson, Ph.D., who was a postdoctoral fellow in Dr. Chichilnisky’s former lab at the Salk Institute in La Jolla, California. The pair collaborated with researchers at the University of California, San Diego, the Santa Cruz Institute for Particle Physics, and the AGH University of Science and Technology in Krakow, Poland.

They focused their efforts on a type of retinal ganglion cell called parasol cells. These cells are known to be important for detecting movement, and its direction and speed, within a visual scene. When a moving object passes through visual space, the cells are activated in waves across the retina.

The researchers placed patches of retina on a 61-electrode grid. Then they sent out pulses at each of the electrodes and listened for cells to respond, almost like sonar. This enabled them to identify parasol cells, which have distinct responses from other retinal ganglion cells. It also established the amount of stimulation required to activate each of the cells. Next, the researchers recorded the cells’ responses to a simple moving image—a white bar passing over a gray background. Finally, they electrically stimulated the cells in this same pattern, at the required strengths. They were able to reproduce the same waves of parasol cell activity that they observed with the moving image.

“There is a long way to go between these results and making a device that produces meaningful, patterned activity over a large region of the retina in a human patient,” Dr. Chichilnisky said. “But if we can handle the many technical hurdles ahead, we may be able to speak to the nervous system in its own language, and precisely reproduce its normal function.”

Such advances could help make artificial vision more natural, and could be applied to other types of prosthetic devices, too, such as those being studied to help paralyzed individuals regain movement. NEI supports many other projects geared toward retinal prosthetics.

“Retinal prosthetics hold great promise, but this research is a marathon, not a sprint,” said Thomas Greenwell, Ph.D., a program director in retinal neuroscience at NEI. “This important study helps illustrate the challenges of restoring high-quality vision, one group’s progress toward that goal, and the continued need to for the entire field to keep innovating.”

Rhodopsin is a biological pigment in photoreceptor cells of the retina. It is the primary pigment found in rod photoreceptors.

There are about ~10⁷ rhodopsin molecules in each rod. And ~120×10⁶ rods in a typical eye. (And 5–6e6 cones.) When a few hundred “unphotobleached” rhodopsins interact with light, they become “photobleached”, open up, and that changes the shape of the rod cell. If the rod cell gets big enough, it is more likely to send a glutamate signal “down the line”.

Photoreceptors hyperpolarise to light. Therefore, gluatamate is released when there is a decrease in illumination.

Also your body replaces rods over time.

About 45 minutes after photobleaching, all the rhodopsin proteins will have returned to their closed shape.

sometimes it’s nice to stop and say hello to your brain cells. inform your nerves they’re cute. acknowledge how nice you are by allowing the bacteria in your digestive system free rent. look yourself in the eye and tell your photoreceptor cells “grazie.” your body is a curious place. every inch of it is living.

Before you judge others or claim any absolute truth, consider that… You can see less than 1% of the electromagnetic spectrum and hear less than 1% of the acoustic spectrum. As you read this, you are traveling at 220 kilometers per second across the galaxy. 90% of the cells in your body carry their own microbial DNA and are not “you”. The atoms in your body are 99.9999999999999999% empty space and none of them are the ones you were born with, but they all originated in the belly of a star. Human beings have 46 chromosomes, 2 less than the common potato. The existence of the rainbow depends on the conical photoreceptors in your eyes; to animals without cones, the rainbow does not exist. So you don’t just look at a rainbow, you create it. This is pretty amazing, especially considering that all the beautiful colors you see represent less than 1% of the electromagnetic spectrum.
—  Unknown

this is a psa because we haven’t talked about how incredible the mantis shrimp is enough. most humans have three types of light-detecting cells, or photoreceptors, while the mantis shrimp has sixteen. which means it can see in colors that we can’t even possibly fathom. people can only see in their own perspective and the mantis shrimp sees in colors that our brains aren’t even able to process. like we couldn’t even imagine or guess the colors they see because it’s completely above our scope of understanding. just imagine. the mantis shrimp looks beautiful to us but i wonder how incredible they look to each other. and that’s not even talking about how it can see in ultra violent.

but that’s not all. did i mention that the mantis shrimp is one of the most violent animals on earth and the two appendages on the front of its body can accelerate with the same velocity as a gun shot from a twenty two caliber rifle?? they move so quickly the water around them boils. boils. that means that a mantis shrimp can kill prey even if it misses the target because of the force of these bubbles. these bubbles are in the range of several thousand kelvins and admit tiny bursts of light. i know… that sounds like the next super hero movie. basically what i’m saying is the mantis shrimp is the animal version of superman and deserves mad respect

mikanojo  asked:

Have you ever considered the cognitive bias that atheists suffer from, that steadfastly denies any thing said to exist outside of their limited awareness? Is it not the true science, to explore and gain new insight, rather than to jump to conclusions and then perform incredible feats of mental gymnastics to explain away every thing that appears miraculous? A gedankenexperiment for you: Explain the appearance of a blue sky to some one who was born blind.

I totally agree that part of what it is to practice good science is ‘to explore and gain new insight’. However, I disagree that atheism is a cognitive bias or that it is ‘jumping to conclusions to explain away everything miraculous’. First off, atheism, as a word, simply means a lack of belief in a traditionally-constructed deity (i.e. omnipotent and benevolent). Atheists (in general, though there are surely exceptions) aren’t claiming that god cannot exist or that it’s a logical impossibility for a god to exist; rather, atheism is the stance that there’re no compelling reasons to believe that one does. This is the exact opposite of jumping to conclusions. This is adjusting one’s beliefs based on the strength of the evidence. Jumping to a conclusion would be to fill in all of the question marks with periods (e.g. Why are we here? becomes God is why we are here. How did life begin? becomes God created all life. etc.). While scientists are certainly not immune from such hubris, good science involves controlling its effects as much as possible. I highly recommend this video on what it means to be truly open-minded in order to guard oneself from jumping to conclusions.

Science is a tool for exploring the universe (the best that we have, I might add) while atheism is simply a lack of belief in a deity. There are scientists who aren’t atheists and there are atheists who are very unscientific. Science and atheism are so often lumped together because there isn’t any evidence for a god (let alone the Christian god in particular) and good scientists, like I said above, adjust their beliefs to the evidence. So atheism is an easy conclusion to arrive at. On that note, ‘explaining away everything miraculous’ doesn’t require 'incredible feats of mental gymnastics’, it simply requires some good ol’ fashion reason. Lucky for us, David Hume did all the hard work in his essay ’Of Miracles.’ First, he defined a miracle as something that occurs outside the known laws of nature. Then he wondered, How can we know when a miracle occurs? He said that we come to know miracles through the personal testimony of a single person (such as ourselves) or a group of people. Then he asked, When is such an account of a miracle trustworthy? Basically, we should trust the account of a miracle only when it is MORE LIKELY for the laws of nature to have been temporarily suspended than it is for the person to have simply misinterpreted the events, misremembered the events, or deliberately lied. In other words, we should probably never accept the existence of a miracle because we should understand how easily fallible the human mind is. Moreover, if something miraculous occurs in a way where it can be studied repeatedly and empirically (so we no longer have to rely on personal testimony), then our understanding of the laws of nature must adjust to incorporate these 'miracles,’ thus rendering them no longer miraculous. In one fell swoop, Hume was able to discredit miracles. An amazing work of philosophy, really.

Finally, your thought experiment is old news in the philosophy world. A much more intriguing version exists called ’Mary’s Room.’ I recommend reading up on that and then checking out some of the physicalist takedowns. At any rate, the inability for color to be experienced by someone who’s blind since birth (and the difficulties explaining this phenomena to such a person) is utterly irrelevant to the question of god’s existence. And science can explain what’s going on anyway. Color is a result of photons interacting with photoreceptor cells in the eye and then the brain interpreting the data (a process which can easily be explained to a blind person btw). This is an amazing process, yes; miraculous, though? Not by a long shot. If someone, due to a genetic mutation or accident at birth, isn’t properly equipped to experience color in the same way as you and me, then there’s simply a difference in their equipment. If their equipment were altered to allow the above process to function, then voila! they experience color. Again, no miracle needed.

It’s tired and overplayed for religious folk to throw accusations of arrogance at skeptics and vice versa. The reality is that arrogance is abound on both ends and everywhere in between. Accordingly, we owe it to ourselves to do some serious self-reflection and study all the ways in which we can be victim to our own blind-spots and biases. Part of doing that is avoiding practices that stack the deck against us. I’ll leave you with a quote from (who else?) Carl Sagan: “Who is more humble? The scientist who looks at the universe with an open mind and accepts whatever the universe has to teach us, or somebody who says everything in this book must be considered the literal truth and never mind the fallibility of all the human beings involved?”

How the Brain Avoids Blurry Vision

by Lisa Marie Potter, Inside Science

Thank goodness for autostabilization, the digital camera feature that compensates for movement to achieve that crystal-clear, spontaneous selfie. But even more importantly in daily life, our eyes have an ancient form of autostabilization that prevents the world from blurring by. Skinny nerve cells called axons connecting the eye and the brain trigger tiny eye movements that stabilize our field of vision.

For the first time, scientists have identified the molecules that make sure these axons are wired to the exact regions of the brain. The findings could help us understand eye movement disorders and could one day help regenerate damaged nerve cells to restore sight.

Two complementary studies published May 7 in Neuron focused on nerve cells that correct for slow movements in specific directions: One paper focused on the horizontal direction and the other on the vertical direction.

Keep reading

Researchers Use Human Stem Cells to Create Light-Sensitive Retina in a Dish

Using a type of human stem cell, Johns Hopkins researchers say they have created a three-dimensional complement of human retinal tissue in the laboratory, which notably includes functioning photoreceptor cells capable of responding to light, the first step in the process of converting it into visual images.

(Image caption: Rod photoreceptors (in green) within a “mini retina” derived from human iPS cells in the lab. Image courtesy of Johns Hopkins Medicine)

“We have basically created a miniature human retina in a dish that not only has the architectural organization of the retina but also has the ability to sense light,” says study leader M. Valeria Canto-Soler, Ph.D., an assistant professor of ophthalmology at the Johns Hopkins University School of Medicine. She says the work, reported online June 10 in the journal Nature Communications, “advances opportunities for vision-saving research and may ultimately lead to technologies that restore vision in people with retinal diseases.”

Like many processes in the body, vision depends on many different types of cells working in concert, in this case to turn light into something that can be recognized by the brain as an image. Canto-Soler cautions that photoreceptors are only part of the story in the complex eye-brain process of vision, and her lab hasn’t yet recreated all of the functions of the human eye and its links to the visual cortex of the brain. “Is our lab retina capable of producing a visual signal that the brain can interpret into an image? Probably not, but this is a good start,” she says.

The achievement emerged from experiments with human induced pluripotent stem cells (iPS) and could, eventually, enable genetically engineered retinal cell transplants that halt or even reverse a patient’s march toward blindness, the researchers say.

The iPS cells are adult cells that have been genetically reprogrammed to their most primitive state. Under the right circumstances, they can develop into most or all of the 200 cell types in the human body. In this case, the Johns Hopkins team turned them into retinal progenitor cells destined to form light-sensitive retinal tissue that lines the back of the eye.

Using a simple, straightforward technique they developed to foster the growth of the retinal progenitors, Canto-Soler and her team saw retinal cells and then tissue grow in their petri dishes, says Xiufeng Zhong, Ph.D., a postdoctoral researcher in Canto-Soler’s lab. The growth, she says, corresponded in timing and duration to retinal development in a human fetus in the womb. Moreover, the photoreceptors were mature enough to develop outer segments, a structure essential for photoreceptors to function.

Retinal tissue is complex, comprising seven major cell types, including six kinds of neurons, which are all organized into specific cell layers that absorb and process light, “see,” and transmit those visual signals to the brain for interpretation. The lab-grown retinas recreate the three-dimensional architecture of the human retina. “We knew that a 3-D cellular structure was necessary if we wanted to reproduce functional characteristics of the retina,” says Canto-Soler, “but when we began this work, we didn’t think stem cells would be able to build up a retina almost on their own. In our system, somehow the cells knew what to do.”

When the retinal tissue was at a stage equivalent to 28 weeks of development in the womb, with fairly mature photoreceptors, the researchers tested these mini-retinas to see if the photoreceptors could in fact sense and transform light into visual signals.

They did so by placing an electrode into a single photoreceptor cell and then giving a pulse of light to the cell, which reacted in a biochemical pattern similar to the behavior of photoreceptors in people exposed to light.

Specifically, she says, the lab-grown photoreceptors responded to light the way retinal rods do. Human retinas contain two major photoreceptor cell types called rods and cones. The vast majority of photoreceptors in humans are rods, which enable vision in low light. The retinas grown by the Johns Hopkins team were also dominated by rods.

Canto-Soler says that the newly developed system gives them the ability to generate hundreds of mini-retinas at a time directly from a person affected by a particular retinal disease such as retinitis pigmentosa. This provides a unique biological system to study the cause of retinal diseases directly in human tissue, instead of relying on animal models.

The system, she says, also opens an array of possibilities for personalized medicine such as testing drugs to treat these diseases in a patient-specific way. In the long term, the potential is also there to replace diseased or dead retinal tissue with lab-grown material to restore vision.

New function for rods in daylight

Vision – so crucial to human health and well-being – depends on job-sharing by just a few cell types, the rod cells and cone cells, in our retina. Botond Roska and his group have identified a novel function for rod photoreceptor cells in the retina in daylight. Driven by cones and mediated by horizontal cells, rods help to increase contrast information at times when they are not directly sensing light. The retina thus repurposes its cells in different light conditions to increase the amount of visual information about the environment.

(Caption: Horizontal cells in the retina)

Task sharing in the retina seemed clear: Two different kinds of photoreceptor cells take on two different visual tasks. Rods allow us to see at night, cones operate during the day and enable color vision. However, the question as to why there are about 20 times more rods than cones in a human retina, when daytime vision is much more relevant for us, has usually led to a shrug of shoulders. It seemed a waste of resources.

Botond Roska and his group at the Friedrich Miescher Institute for Biomedical Research, could now show in a study published recently in Nature Neuroscience that the rods in mouse take on an important function during daytime vision as well.

The scientists showed that in bright light, the rods mediate a so called surround inhibition. Surround inhibition is an important feature in the retina because it allows not only to transmit information about whether a photoreceptor is exposed to light, but also about contrast. While the cone cells hyperpolarize in bright light and thus send a visual signal to the inner retina, the rods depolarize, inversely matching the activity pattern of the cone cells. The response in the rods is driven by cone cells and mediated through horizontal cells. These horizontal cells connect rods and cones through their dendrites and long axons, and at the same time form a mesh of connections among each other. The hyperpolarization of one cone thus leads to the depolarization of many surrounding rods.

During bright light conditions, the cells of the inner retina receive therefore information through two pathways: First through the well-established cone pathway, and second through this newly identified rod pathway. “We think that the surround information relayed to the inner retina through the rod pathway has different functional properties than the information obtained through the cone pathway,” comments Roska. “In any case it is fascinating to see how the retina repurposes the rod cells during bright light conditions to increase contrast information, at times when they are not directly sensing light.”

After all, these large numbers of rods don’t seem to be present in the retina in vain.