It really gets me how your brain completes what you see. The first picture shows what your brain tells you that you see. But in reality, your retina is covered by blood vessels and you see them all the time. Also, there’s a blind spot on your eye that your brain erases and completes for you by averaging the light conditios around it. And your cornea and lens twist the picture so it is both horizontally and vertically flipped.
So the second picture shows what is really projected on your retina.
The red eye shine seen in alligators arises when light enters the eye and hits a layer of cells called the tapetum lucidum. This membrane is located beneath the photoreceptor cells (rods and cones) in the retina and reflects light back into these cells to increase the amount of light detected, which improves an alligator’s vision in low light conditions.
Several species exhibit this phenomenon, with different colour ‘shines’ observed. Most species with eyeshine are night hunters who must make use of limited light.
Driving a car at 40 mph, you see a child dart into the street. You hit the brakes. Disaster averted.
But how did your eyes detect that movement? It’s a question that has confounded scientists.
Now, studying mice, researchers at Washington University School of Medicine
in St. Louis have an answer: A neural circuit in the retina at the back
of the eye carries signals that enable the eye to detect movement. The
finding could help in efforts to build artificial retinas for people who
have suffered vision loss.
The research is published June 16 in the online journal eLife.
The research team identified specific cell types that form a neural
circuit to carry signals from the eye’s photoreceptors — the rods and
cones that sense light — to the brain’s visual cortex, where those
signals are translated into an image.
“This ability to detect motion is key for animals, allowing them to
detect the presence of predators,” said principal investigator Daniel
Kerschensteiner, MD, an assistant professor of ophthalmology and visual
sciences. “And we know that these same cells are found not only in mice
but in rabbits, cats, primates and likely humans, too. The cells look
similar in every species, and we would assume they function in a similar
manner as well.”
Studying the neural circuit, Tahnbee Kim, a graduate student in
Kerschensteiner’s lab, identified a specific type of cell called an
amacrine cell that’s key to detecting motion. Amacrine cells are thought
to inhibit, or tamp down, the activity of other cells called ganglion
cells. This process ensures that the brain doesn’t receive too much
visual information, which could distort an image.
Using a technique that combines a powerful microscope with a method
that allows researchers to track how often retinal cells fire, the
researchers also showed that when there is motion in the visual field, a
specific subtype of amacrine cell excites ganglion cells, signaling the
brain so it becomes aware that an object is moving.
The discovery that this type of cell transmits object-motion signals
is an important step in understanding how the eye senses motion. It also
provides a high level of detail that will be needed to design
computerized, artificial retinas, which will need to detect motion as
well as sense light.
“There are many elements in the retinal circuitry that we haven’t
figured out yet,” said Kerschensteiner, also an assistant professor of
anatomy and neurobiology. “We know the signals from the rods and cones
are transmitted to the retina — where the amacrine and ganglion cells
are located — and that’s really where the ‘magic’ happens that allows us
to see what we see. Unfortunately, we still have a very limited
understanding of what most of the cells in the inner retina actually
With 576-megapixel resolution, our eyes are incredible cameras, capturing 72-times more high-definition detail than the iPhone 6. To do this, our retinas are packed with many different cell types that help transmit light information to the brain. We know very little, however, about how these cells interconnect, so researchers have turned to mapping and tracing how one cell connects with another…and you can help. A team of scientists at MIT has developed an online game called EyeWire that allows anyone to figure out how cells connect in the retina with real science implications. This image was generated from players correctly tracing connections from one cell to the next, generating a complete connectivity map for these seven cells.
Image by Amy Robinson, Alex Norton, Sebastian Seung, William Silversmith, Jinseop Kim, Kisuk Lee, Aleks Zlasteski, Matt Green, Matthew Balkam, Rachel Prentki, Marissa Sorek, Celia David, Devon Jones, and Doug Bland.
Any science textbook will tell you we can’t see infrared light. Like X-rays and radio waves, infrared light waves are outside the visual spectrum. But an international team of researchers co-led by scientists at Washington University School of Medicine in St. Louis has found that under certain conditions, the retina can sense infrared light after all.
Using cells from the retinas of mice and people, and powerful lasers that emit pulses of infrared light, the researchers found that when laser light pulses rapidly, light-sensing cells in the retina sometimes get a double hit of infrared energy. When that happens, the eye is able to detect light that falls outside the visible spectrum.
“We’re using what we learned in these experiments to try to develop a new tool that would allow physicians to not only examine the eye but also to stimulate specific parts of the retina to determine whether it’s functioning properly,” said senior investigator Vladimir J. Kefalov, PhD, associate professor of ophthalmology and visual sciences at Washington University. “We hope that ultimately this discovery will have some very practical applications.”
The eye can detect light at wavelengths in the visual spectrum. Other wavelengths, such as infrared and ultraviolet, are supposed to be invisible to the human eye, but Washington University scientists have found that under certain conditions, it’s possible for us to see otherwise invisible infrared light. Credit: Sara Dickherber
The eyes differ in their optical properties what results in a blur projected in each retina, despite we see sharp images because the visual system calibrates itself. An international research performed by the
Consejo Superior de Investigaciones Científicas has discovered that when
each eye separately has a different level of blur, our brain uses as
sharp reference the image projected through the less aberrated eye. The
research has been published in Current Biology.
“Our impression about what is sharp is colossal and it is determined
by the sharper image among those which are projected through both
eyes”, explain the CSIC researcher Susana Marcos of the Instituto de
Óptica Daza de Váldes. The research reveals that, despite these blur
differences, the perception of each eye separately about the sharper
image is the same, regardless of the eye we use to make the test and
coincides with the blur image projected through the less aberrated eye.
The nature of these visual calibrations is important in order to
understand the different consequences referred to the refractive errors
between both eyes. “For instance, an available solution to correct the
presbyopia is monovision, in which different refractive corrections are
provided for both eyes. One eye, the dominant eye, is corrected for
distance viewing and the other one is corrected for vision viewing. It
is essential to understand the visual calibration with different levels
of blur to understand the visual processing of the patients, the main
objective is to provide the best possible correction”, conclude the
Glaucoma, the second leading cause of blindness, usually stems from elevated eye pressure, which in turn damages and destroys specialized neurons in the eye known as retinal ganglion cells. To better understand these cellular changes and how they influence the progression and severity of glaucoma, researchers at University of California, San Diego School of Medicine and Shiley Eye Institute turned to a mouse model of the disease. Their study, published Feb. 10 in The Journal of Neuroscience, reveals how some types of retinal ganglion cells alter their structures within seven days of elevated eye pressure, while others do not.
“Understanding the timing and pattern of cellular changes leading to retinal ganglion cell death in glaucoma should facilitate the development of tools to detect and slow or stop those cellular changes, and ultimately preserve vision,” said Andrew D. Huberman, PhD, assistant professor of neurosciences, neurobiology and ophthalmology. Huberman co-authored the study with Rana N. El-Danaf, PhD, a postdoctoral researcher in his lab.
Retinal ganglion cells are specialized neurons that send visual information from the eye’s retina to the brain. Increased pressure within the eye can contribute to retinal ganglion cell damage, leading to glaucoma. Even with pressure-lowering drugs, these cells eventually die, leading to vision loss.
In this study, Huberman and El-Danaf used a mouse model engineered to express a green fluorescent protein in specific retinal ganglion cells subtypes. This tool allowed them to examine four subtypes of retinal ganglion cells. The different cell types differ by the location in the eye to which they send the majority of their dendrites (cellular branches). Within seven days of elevated eye pressure, all retinal ganglion cells that send most or all of their dendrites to a region of the eye known as the OFF sublamina underwent significant rearrangements, such as reductions in number and length of dendritic branches. Retinal ganglion cells with connections in the ON part of the retina did not.
“We are very excited about this discovery,” Huberman said. “One of the major challenges to the detection and treatment of glaucoma is that you have to lose a lot of cells or eye pressure has to go way up before you know you have the disease. These results tell us we should design visual field tests that specifically probe the function of certain retinal cells. In collaboration with the other researcher members of the Glaucoma Research Foundation Catalyst for a Cure, we are doing just that and we are confident these results will positively impact human patients in the near-future.”
Pictured: Example of retinal ganglion cells with dendrites in the retina of a healthy eye.
Seeing – recognising – acting. These three words describe how a sensory input can lead to a targeted movement. However, very little is known about how and where the brain converts external inputs into behavioural responses. Now, scientists at the Max Planck Institute of Neurobiology in Martinsried have been able to shed light on important neural circuitry involved in the prey capture behaviour exhibited by young zebrafish. The findings show that neurons in the retina of the eye already filter out prey objects from other environmental signals. The cells then forward this information to an area of the brain, which, up to now, had no identifiable role. The corresponding swimming movements are then initiated here.
It’s not easy to catch a ball. The ball must first be recognised and tracked by the eyes. At the same time, the body’s own movements must be coordinated in such a way that the hands hang on to the ball at the right time and in the right place. For animals, such coordination of visual inputs and their own movements is critical to their survival: it is only in this way that they can recognise, track and catch prey. For many animals, fundamental prey capture behaviour is therefore innate. Up until now, scientists could not explain how and where the brain recognises and classifies an object and initiates the corresponding movement pattern.
Prey causes the fish brain to light up
As soon as they are hatched, zebrafish larvae can already hunt single-celled organisms such as paramecia. The brain of the tiny fish is able to recognise the single-celled organism as a target, calculate its location and steer its body towards the prey using characteristic tail movements. This innate prey capture behaviour can also be triggered in the laboratory using small, moving dots. Scientists can thus present potential “prey” on a miniature screen and study the subsequent processes in the fish brain – as zebrafish larvae are almost transparent. As a result of genetic modifications, the neurons in the fish brain that are active at a given moment light up in the transparent brain. Processes in the fish brain can therefore be observed using a microscope while the animals recognise and classify their prey and swim towards them.
To understand the neural circuits of the prey capture behaviour, the neurobiologists initially concentrated on the recognition of prey objects. “First of all, we looked at the connections between the retina and the brain,” says Julia Semmelhack, describing her work. Neurons in the zebrafish retina project into 10 areas in the brain known as AF regions; however, very little is known about the role of these regions. The scientists in Martinsried were able to show that the neurons in one of these 10 AF regions always became active when the dots shown fitted the brain’s template of an optimal prey object. Larger or smaller dots had no effect. The AF7 brain region lit up only in the presence of virtual dots that were the “right” size (and in the case of actual paramecia).
A brain region reveals itself
Further investigation showed that the neurons in the retina filter out potential prey objects from the environment. The information is only sent to the AF7 region if a dot is the “right” one. From there, the hunting impulse is then sent to other visual regions and to the areas controlling movement. When the scientists cut the AF7 connections, the fish responded only to a very limited extent to the dots representing the prey.
The AF7 region is therefore essential for classifying visual stimuli as prey and for triggering the associated hunting behaviour. “We have shown how a visual signal from the retina, travelling via the AF7 region, leads to certain behaviour,” says a delighted Herwig Baier, who, together with his department at the Max Planck Institute of Neurobiology, is studying how sensory inputs from the brain are converted into behavioural responses. A major first step has been taken. The neurobiologists now want to find out how the information in the AF7 region is translated into the various swimming movements.
Here a mouse retina is seen en face with these “J” retinal ganglion cells marked by the expression of one fluorescent protein. The millions of other entangled neurons are not marked and thus are invisible in this image. Image obtained with a confocal scanning microscope and pseudocolored.