Just Dont Do it: Loud Noise Causes Irreversible Hearing Loss

Experiencing Acoustic Trauma (a very loud noise presented abruptly or over a long period of time) can-and usually does-result in permanent hearing loss. Yes, we’ve all been told this for years, and it doesn’t stop us from going to that rock concert, standing directly infront of the speakers, and loving it, but, what if I told you it actually REALLY was a bad idea. Why? Well, our hair cells-the little sensory epithelial cells that pick up sound information in our ears-die. Earlier this week, I presented on a very interesting article-published in January-that suggests inhibiting a particular developmental mechanism after acoustic trauma actually creates new Hair Cells. I’ll talk about the article next week, but for now, I’m going to tell you how this whole sound process works, and why you reaaally might want to reconsider your standing location.

Hair cells are special

Located in the Cochlea-a spiral structure in our Inner Ear-hair cells sit with supporting cells on top of the Basilar Membrane, and
below the Tectorial membrane, in a region we like to call the organ of Corti. When sound enters the ear, the Basilar Membrane vibrates, causing the hair cells to vibrate up and down with it, which pushes the stereocilia-little hairs on top of the hair cell that can bend back-and-forth- into the Tectorial membrane, thus bending them. The direction of bending either hyperpolarizes or depolarizes the hair cell, thus transducing sound to the afferents.

Now, what I said above is actually only half true. There are actually two types of hair cells, outer hair cells and inner hair cells-arranged as 3 rows of outer and 1 row of inner, and only the inner hairs transduce sound to the auditory nerve. Outer hair cells detecting low-level sound and amplify it so that only inner hair cells that specifically respond to the respective sound frequency
activate.  How is this specificity achieved? Hair cells are MAJORLY organized to respond to specific sound frequency based on their location. That spirally Cochlea structure is actually arranged tonotopically, with the base-the wider end-responding to high frequencies, and the apex-the narrow tip in the center-responding to low frequency sounds. So, when a sound of specific frequency causes the basilar basilar membrane that picks up that frequency-based on the length/width-to vibrate and the outer hair cells to amplify that vibration, allowing only the specific hair cells in that location to pick up the sound.

The important part

When acoustic trauma occurs the overstimulation of the hair cells results in major, and usually fatal problems. Hair cells can experience oxidative cell death causing them to die. Furthermore, with a loud abrupt noise (a gunshot, explosion, firecrackers etc.) the outer hair cells can become structurally deformed causing them and their inner structures to degenerate. For some reason acoustic trauma from a loud abrupt noise (ex. explosion, firecrackers, gunshot) destroy outer hair cells, leaving almost all the inner hair cells
intact. Therefore, although we might be able to hear a sound, our ability to detect differences in the respective frequencies is severely attenuated.

In Mammals, almost all of our cells participate in Cell Turnover-the act of replacing cells with new ones generated from the old ones for optimal functioning, but for unknown reasons, our hair cells don’t. In fish, birds, and amphibians, hair cells actually regenerate after damage, but again, Mammalian hair cells dont. Therefore, I hope you can see just why these hair cells are PIVOTAL and that finding a way to replace them after damage would be quite a great accomplishment.

What is To Come

As I mentioned in the beginning, an article was posted in January suggesting a possible solution to this hair cell problem. In the study, the researchers discovered that inhibiting a specific mechanism that determines the fate of epithelial progenitor cells can actually turn supporting cells into outer hair cells. Next week I’ll explain to you just how they discovered this very interesting mechanism, why it works, and what it really means for long-term hair cell regeneration and regaining the ability to hear after trauma.

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Obamas New Initiative to Map the Brain: Realistic or Idealistic?

A New Goal Emerges

Last month, President Obama announced the start of new project: the BRAIN Initiative to map the Human brain. According to Obama, the BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative aims to “do for the human brain what the Human Genome did for genetics.” To kick it off, Obama has allocated $3 billion towards the entire project of wide-spread neuron mapping, starting with $100 million in the first year, which he plans to split between the NIH (National Institute of Health), DARPA (Defense Advanced Research Project Agency), and NSF (National Science Foundation).

Why Global Mapping?

Why has Obama taken on this initiative to map the entire brain? According to Dr. Collins, director at the NIH (National Institute of Health), “the reality is we cant afford not to;  [we] dont want to stifle innovative thinking.” The scientific answer to this question is that our current available imaging techniques only allow for local mapping of neural circuits and connections—interactions between a few specific neurons in a targeted area, compared to all of the connections throughout the brain  (Saucan, 2008). Although these techniques have allowed us to discover some of the neuronal circuits underlying perception and sensation, our inability to create a global map leaves much room for error in what we think we know. Discovering a global map of these neuronal circuits therefore opens the door to a multitude of potential scientific advances, like the circuitry contributing to our perception and sensation, and—more importantly—the circuitry underlying diseases and disorders, such as PTSD, Schizophrenia, Alzheimers, and Parkinsons Disease.

What then, are the Problems?

Many scientists see this new incentive as potentially groundbreaking, but others see it as too ambitious, nearing unrealistically idealistic and somewhat erroneous in our current economic situation. Either way, the idea is excellent but there appears to be a few hurdles that need be jumped for the initiative to actually work:

1) Steep Taxes inhibit Sucess

According to the Wall Street Journal article by Gregory Sorensen, the BRAIN Initiative is actually hurt by a policy enacted in
Washington on Jan. 1. According the Affordable Care Act of 2010, the medical-technology industry is subject to a $30 billion annual tax on medical devices, making the “generous” $3 billion gift from Obama somewhat ridiculous.

The Reality

Over the past few years, we have definitely seen an increase in obsessive medical testing—in other words, with increased innovation, comes increases in unnecessary, wasteful, and expensive testing. But, taxing these companies at such high prices—although a smart attempt to combatting these issues—is actually decreasing the number of available jobs, and slowing down the rate of innovation.

As of Jan. 1, medical device manufacturers have already paid up to $450 million in taxes. Additionally, the Pacific Research Institute estimates the “health law’s medical-device tax will reduce American medical research and development by $2 billion a year, and the Manhattan Institute says the tax will cost 146,000 American jobs.” So then truly, how can science benefit from this initiative? According the Sorensen, “This tax decelerates and devalues innovation at the very moment when medicine is on the verge of historic breakthroughs. It is foolhardy to believe that the medical-technology community can spark new innovation while the government is overtaxing it.”

2) No Glia Mapping

In an article published in the Scientific American, Douglas Fields-neuroscientist at NIH- elaborates on a major problem with the BRAIN Initiative: the complete ignorance of non-neuronal cells in the brain, specifically Glia.  Glia are supporting cells with a variety of functions, from myelinating a cells axon, to regulating neuron-to-neuron communication. Furthermore, our current understanding of Glia is severely lacking compared to our understanding of neurons.

The Reality

By ignoring the role of Glia and other non-neuronal cells in the BRAIN Initiative, we are literally no better off than we were in our attempts at local mapping. By completely disregarding cells that we do not even fully understand, we cannot obtain a comprehensive understanding of the brains’ connections and their relationship to behaviors and disorders. Thus, we definitely cannot implicate any of the connectivity we do find as key to a particular disease, disorder, sensation, or perception. Similarly to completing only the boarders of a puzzle, we need to map all connectivity components to truly find solutions.

Good or Bad Idea?

These two considerations shine light on the idea that Obamas motives might not have been solely science-based. According to Obama, we are “giving scientists the tools they need to get a dynamic picture of the brain in action; a better idea of how we think, learn and perceive,” but without enough money and cell types, can we truly hope accomplish this feat?

Obama states we “don’t want the next discovery to happen in India or China or Germany; we want it to happen in America; that’s what this initiative is about.” I understand the reasons behind this goal- pushing money and thus jobs into the economy- but “mapping the brain” might not be the most efficient way to achieve this goal. Unless the proposal for the BRAIN initiative is re-clarified and the tax attenuated, it looks like this endeavor might just be too idealistic.

10 Things You Thought You Knew About Neuroscience

After reading an article last month in The Observer on common misperceptions about Neuroscience, I was intrigued to dig a little deeper. I  spent some time researching the many widespread falsities surrounding Sensation and Perception in Neuroscience, and have compiled a lovely little list of what I find to be the 10 most interestingly incorrect beliefs below:

1)   The Assumption: Pheromones are chemicals signals used by a variety of animals for Chemosensation. In rodents, the VNO (Vomeronasal Organ) is the area in the nose that picks up signals from pheromones, and relays the information, through its axons, to higher processing levels in the brain. Pheromones are used by Humans in sexual attraction, repulsion, and aggression.

The Truth: We do not know if Humans use Pheromones. Anatomically, we have not found the receptors for Pheromones that are found in other animals, nor do we have a functional VNO-or any equivalent to it. Physiologically, we cannot find any responses to Pheromones in Human studies. On the other hand, we secrete Androstenone-one of the most common animal Pheromones- from our sweat glands and in our saliva, and when presented with the smell of Adrostenone, subjects have reported an attraction to the odor. Also, Females tend to sync up their menstrual cycles when in close proximity for a period of time, which is hypothesized to be the result of Pheromones. This leaves open the possibility that we do respond to Pheromones, but with a different mechanism, area of activation, and process from other animals. Thus, this question remains unanswered.

2)   The Assumption: Tastes are detected on the tongue by taste buds, which transmit information to through Gustatory Afferents to higher areas in the brain.Different taste modalities-sweet, salty, bitter, umami, or sour-are located in a “tongue map” in different areas of the tongue.

The Truth: Different types of tastes are not segregated in the tongue. There can be slightly increased sensitivities in different locations to different modalities, but this is completely based off of environmental factors (McPheeters, 1990). There is no “specific map.” Originally, the idea of a “tongue map” cam from a mistranslation of a German thesis by Edwin Boring in 1901.

3)    The Assumption: Humans sense and perceive the world around them through only five senses: the sensations of touch, hearing, vision, taste, and smell.

 The Truth: Humans have anywhere from 9-20+ senses. Humans can sense a variety of senses, such as: balance/acceleration (equilibrioception), pain (nociception), body or limb position (proprioception/kinesthetic sense), and relative temperature (thermoception). Other senses can be: time, itching, pressure, hunger, thirst, fullness, the need to  urinate or defecate, and blood carbon dioxide levels.

4)    Assumption: The brain is split into the “Left-Brain,” which is the rational side, and the “Right-Brain,” which is the creative side.

The Truth: Mental abilities are not completely separated into left and right sides. Although some functions, such as speech and language activate can activate one hemisphere more than the other, but there is no clear split between the hemispheres. Evidence  comes from recordings during motor control, memory, and reasoning tasks, in which both hemispheres are activated equally. Additionally, Neuroplasticity-the ability of the brain and neurons to adapt somewhat like “plastic” to changes and injury- occurs if one hemisphere is damaged. The other hemisphere will take on many of the function that would have been carried out by the damaged hemisphere. 

5)    The Assumption: As newborns, we are born with all of the neurons we will ever have.

The Truth: New neurons can generate after birth. Adult avians, Old World Primates, and Humans have all been shown to retain multipotent neural stem cells in the Subventricular Zone of the Lateral Ventricles and Subgranular Zone of the Dentate Gyrus. These new neurons migrate to the Olfactory Bulb and the Dentate Gyrus to enhance existing neural circuits, although the exact function/importance of these neurons is unknown.

6)   The Assumption: We only use 10% of our brains.

The Truth: We use wayyy more than 10% of our brains. Although only a small number of neurons are active at any one time in the brain, the number of neurons ever active-or the number that are active + inactive at any one time exceeds way beyond 10% of the brain.https://www.youtube.com/watch?v=anmYBpWxxag

7)  The Assumption:  Some lucky people have “photographic” or eidetic memory-the ability to remember images as if a picture were taken with a camera.

The Truth: There is no proof for photographic memory. People found to have exceptional memories, usually have accomplished this feat through the use of  mnemonic devices. Recently, there have been reported cases of hyperthymesia, also known as autobiographical memory: the ability to remember every activity/event/meal/interaction on any given day of a persons life completely accurately.  

8)  The Assumption: We achieve balance in walking, running, and our everyday movements by the successful interplay of antagonistic mucles-when a particular muscle relaxes, the paired muscle contracts, allowing for balance.

The Truth: Balance is not due the antagonistic interactions of our muscles, but is primarily a result of Inner Ear Mechanics, specifically, the Vestibular System. Fluid filled chambers inside this system move as we move, and the movement of the fluid sends information to higher processing levels, informing us about balance.

9) The Assumption: We experience the feeling of pleasure because of the neurotransmitter, Dopamine.

The Truth: Dopamine is produced in Dopaminergic Neurons of the Hypothalamus, the Substania Nigra, and the Ventral Tegmental Area. It regulates a variety of functions including: production of breast milk, reward/desire/motivation. Therefore, Dopamine controls the feelings of reward/desire and “seeking,” but not necessarily pleasure.

10)  The Assumption: Low Serotonin levels cause depression.

The Truth:  There is no consistent evidence for low Serotonin levels causing depression. This falsity was promoted by pharmaceutical companies in the 1980’s to sell SSRIs (Selective Serotonin Reuptake Inhibitors), like Prozac. Although correlations between those suffering from depression and low serotonin levels are found, no conclusive evidence is available.

I hope this post helps clarify some of the most believed fallacies about Sensation and Perception in Neuroscience.  If there are any interesting myths or misconceptions I’ve missed, Please let me know and I’ll cover them in a later post!

Pregnancy and Stress: Hormones Causing Mood-Disorders in Children?

It has been known for years that certain environmental factors—such as stress during pregnancy—can influence a baby’s development later on in life. On April 4th at the British Neuroscience Association Festival of Neuroscience in London, researchers presented very interesting findings on a possible mechanism negatively affecting fetuses. According to an article in Science Daily, Professor Megan Holmes, a neuroendocrinologist from the University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science in Scotland (UK), has discovered a possible mechanism whereby a fetus’ exposure to high levels of stress hormones can result in mood disorders later in life.

The Study

Professor Holmes used genetic engineering in Rodents–the process of adding, removing, or manipulating a part of an animals genome via Biotechnology–to remove an enzyme she believed to be vital in correct pre-natal development. Holmes hoped to test how high levels of stress hormones affected both fetuses and puberty-age rodents—another time when drastic changes in development occur.

The Cellular Mechanics 

According to Holmes, increased levels of Glucocorticoids—the steroid hormones that increase a result of stress or abuse– might directly affect the programming of fetal cells, raising the chances of problems later on. The steroid, Cortisol, is believed to be a key factor in the fetal cell programing, for it reduces growth, changes tissues, and has long-term effects on gene expression (Davis, 2010).

The enzyme, 11β-HSD2 (11beta-hydroxysteroid dehydrogenase type 2),  usually found in the placenta and the fetal brain, has been implicated in breaking down Cortisol to inactive form, subsequently preventing it from harming a fetus during growth (Kajantie, 2003). By genetically engineering the mice to not have 11β-HSD2, and exposing them to high levels of stress hormones, Holmes was able to test if too little 11β-HSD2—or, better put, too much active Cortisol—was causing negative changes in programming.

What Holmes Found

The high levels of stress hormones directly reduced fetal growth and led to mood disorders later in life. More-so, the placentas of these 11β-HSD2 knockout mice were smaller, making nutrient transport more difficult in the developing fetus. Holmes therefore suggests that the placental 11β-HSD2 is key in inhibition of later mood disorders, acting as a shield to harmful stress hormones.

Holmes further states  “preliminary new data show that with the loss of the 11ß-HSD2 protective barrier solely in the brain, programming of the developing foetus still occurs, and, therefore, this raises questions about how dominant a role is played by the placental 11ß-HSD2 barrier. This research is currently ongoing and we cannot draw any firm conclusions yet.

The Implications…

You may think this is all great, yet Holmes bring an important issue to question: What implications do these findings have on current treatments? Specifically, for the past 20 years or so, we have treated pregnant mothers expected to prematurely deliver with dosages of synthetic glucocorticoids to stimulate fetal lung development. In trying to enhance the probability of life upon early birth,  we may be causing irreversible mood disorders in children later on. Homes emphasizes “while this glucocorticoid treatment is essential, the dose, number of treatments and the drug used, have to be carefully monitored to ensure that the minimum effective therapy is used, as it may set the stage for effects later in the child’s life.”

What About Adolescence? 

Holmes and her colleagues then decided to look at the affect of stress during early teenage years on mood and emotional behavior. They trained rats to respond to a specific learned task, and then exposed them to stressful environments, postulating that  high levels of glucocorticoids released during times of stress may cause changes in the brains neural networks associated with emotional processing.

The fMRI (Functional Magnetic Resonance Imaging) results successfully  “showed that in stressed ‘teenage’ rats, the part of the brain region involved in emotion and fear (known as amygdala) was activated in an exaggerated fashion when compared to controls.” Therefore, “altered emotional processing occurs in the amygdala in response to stress during this crucial period of development.”

Closing Thoughts…

Holmes emphasizes that “determining the exact molecular and cellular mechanisms that drive fetal programming will help us identify potential therapeutic targets that can be used to reverse the deleterious consequences on mood disorders. In the future, we hope to explore the potential of these targets in studies in humans.” Additionally, she hopes the results will promote awareness that “children exposed to an adverse environment, be it abuse, malnutrition, or bereavement, are at an increased risk of mood disorders” later, and the “children should be carefully monitored and supported to prevent this from happening.”

-Adapted from Science Daily Article

– Abstract title: “Perinatal programming of stress-related behaviour by glucocorticoids”.

– Symposium: “Early life stress and its long-term effects-experimental studies”, at 15.15 hrs BST on Sunday 7 April, Cinema 1.

Sleep Paralysis Causes Next Day Distress

What about the Next Day? 

What if I told you that this fun little experience of Sleep Paralysis actually did affect you. What if your emotions, personality, and general demeanor were completely altered. While reading Science Daily last week, I stumbled upon a very interesting article on Sleep Paralysis. Two researchers, James Cheyne and Gordon Pennycook, released findings from a study in the Clinical Psychological Science Journal, concluding that Sleep Paralysis affects an individuals’ interactions with the world the next day in a negative way.

The Study

By using an online survey and follow-up emails, the two researchers collected information from 293 people  to explore post-episode distress by measuring a range of items. They measured different characteristics relating to the episode itself, such as amount of fear experienced, vividness of experiences, frequency of episodes. They also looked at factors relating to each individual, such as psychological distress sensitivity, supernatural beliefs about the Sleep Paralysis experience, and cognitive style (either fast/intuitive thinking or  slow/reflective/analytic thinking (Evans, 2008)).

The Findings

Concurring with their proposed hypothesis, the researchers found that the characteristics of the episode directly related to the amount of distress the next day. The more fear experienced during the episode, the more distress an individual felt the next day. The distress was further exacerbated in those who felt fear of threats or assault, such as chest pressure, intruders, and near-death experiences. The distress was also worse for people who felt sensations of floating, falling, or out-of-body experiences (Cheyne, 2013)

The researchers also found that an individuals level of psychological distress (anxiety, depression) had had almost no effect on the amount of fear experienced in the episode, although it still resulted in post-episode distress.

Individuals who held supernatural beliefs about the Sleep Paralysis experience reported increased intensity of both fear and threat/assault experiences as well as increased postepisode distress compared to others. Additionally, those with analytic cognitive styles were found to have significantly less supernatural beliefs about the experience. This makes sense, for people with analytical thinking styles would reach out to others for more information and explanations on the experience, dissuading them from supernatural interpretations (Cheyne, 2013).

Surprising to the researchers and myself, those who employ more analytic cognitive styles of thinking experienced noticeably less distress after the Sleep Paralysis episode. Although the above findings directly show this, these results now show the ability of executive control processes in our brains to inhibit, activate, or manage more automatic processes, such as emotional reactivity after the episode. Therefore, analytic people are more likely to override their postepisode feelings of distress.This is further  supported by the findings that individuals the cognitive style had no affect on the  level of fear experienced during a particular episode (Cheyne, 2013).

What Are The Implications?

There are many important implications of this study. According to a post in the Toronto Telegraph, the researchers believe that “the distressing sensory experiences that come with episodes of Sleep Paralysis could exacerbate people’s fear, creating a feedback loop that enhances memories of experiences later”. This is very well supported from the results presented above, for analytic people must inhibit part of the loop preventing the enhancement of the memory later on.

Although a little far-fetched for the current amount of knowledge on Sleep Paralysis, the researchers also emphasize that studying these carryover effects further could “make a significant contribution to the billions of dollars, worldwide, in costs associated with accidents, illnesses, and lost productivity associated with sleep disturbances.”

I believe them- they’ve definitely found interesting correlations, and I applaud them for what they have found- but A LOT more research from other fields-like Neuro- will definitely be needed to truly achieve this goal.

Chest Demons Revealed- The Story Behind Sleep Paralysis

The Scary and The Truth

The Experience

As you lie in your bed and feel your muscles start to slowly relax, you expect your mind-wandering off into dream land-to shortly follow. All of a sudden you realize that you are still awake, but you cannot move. Everything starts to spin and distort, you start getting hot, your chest starts feeling heavy, and you start freaking out. Human nature quickly begins to scream at you to escape; to somehow wake up and just end the nightmare. So you-in your completely conscious state-try with all your might to move just one finger, kick one leg, or just swing one arm over your body, knowing your success would bring you back from the mysterious hell in which you’ve found yourself. Welcome to the world of Sleep Paralysis.

The History

First like to start off by stating, Sleep Paralysis is NOT dangerous. Yes, that horrifying, mind-altering experience explained above is not dangerous, nor is it the result of little Incubus demons sitting on your chest as you sleep-Yes, our ancestors really did believe this. Sleep Paralysis is actually a protective mechanism used by our bodies to pretty much stop us from doing stupid stuff to ourselves while resting. You might wonder, Well, how does someone sleepwalk, then? The answer, my friends, is they have a problem with the exact same system that causes Sleep Paralysis: Where Sleep Paralysis sufferers cannot move their muscles when their minds are still awake, Sleepwalkers cannot stop moving their muscles when their minds are asleep.

Behind Paralysis

Sleep paralysis occurs when Peripheral Atonia comes into the dreamer’s consciousness accidentally. Peripheral Atonia is basically a lack of normal tension or muscle tone, resulting in the perception of paralysis. This mechanism is the primary means of inhibiting movements during REM and non REM sleep. Originally believed to be the result of the neurotransmitter Glycine, more recent work has shown blocking Glycine receptors fails to affect Atonia, leaving the mysterious mechanism of paralysis unknown (Brooks, 2008). Furthermore, many people report the eyes to be the only muscles unaffected during the paralyzed state, leaving one able to view the 180 degrees of the visual spectrum, but unable interact with the world around them.

The Phenomena 

Not everyone experiences sleep paralysis,  it could happen only once or many times in a persons life, and can occur more than once during rest. 60% of the population has experienced Sleep Paralysis at least once, whereas 6% experience it quite frequently. Additionally, there are two types: Hypnagogic Paralysis occurs when one tries to go to sleep, whereas Hypnopompic Paralysis occurs upon waking up. Overall though, the most interesting aspect of the experience  is what you perceive, and apparently it varies quite drastically.

Some people hear voices, sometimes of a threatening or terrifying nature, reminiscent of the auditory hallucinations of schizophrenics. Some of the more common phenomena are heaviness on the chest and feelings of suffocation. Other experiences are weird alterations of 3D depth perception, strange or familiar smells or tastes, feelings of levitation, tactile hallucinations, feelings of heat, or visual hallucinations of shadows, people, or intruders (Peters, 2012).

Personally, I have experienced a variety of phenomena during Sleep Paralysis. I’ve heard a woman shrieking, felt my entire body

begin vibrating, seen a shadow of a woman moving towards me in the dark, and quite enjoyed  John Lennon-a black-and-white poster  on the opposite wall of my bedroom- kneeling at the side of my bed upon waking one morning.

The position of  your body, and the timing of sleep can also affect the chances of experiencing Sleep Paralysis (Cheyne, 2002). Many find paralysis most common when they fall asleep sitting upright, an experience that kept my childhood Car and Airplane rides personally quite frightening, while rather entertaining for everyone else. When failing to stop myself from sleeping, I quite successfully astounded others who believed me to be asleep, by regurgitating entire conversations after forcing myself out of the paralyzed state.

The Emotional Effect

Although I’ve emphasized Sleep Paralysis is not physically dangerous, there are emotional implications. The frightening, terrifying, life-threatening, feelings experienced during the Paralysis not only affect an individual at that moment in time, but also affect a persons mentality and emotions afterwards. In the post to follow, I will explore a recent study on Sleep Paralysis, finding that the distress experienced during the event might actually carry over to the next day, affecting your personal interactions with the world around you.

Color Vision: Physics of the Retina Part 2

The Issue of Clarity versus Color

Although surprising, the primary reason for these differing types of photoreceptors is not to perceive colors, but is to accurately see objects, more specifically spatial acuity. Think of a caveman trying to find an apple surrounded by rocks. Although the differing colors would be considered the telltale sign of which is which, detecting the shape and seeing the object clearly, whether close or far away requires spatial acuity. The physics of the retina (the location and spacing of of different photoreceptors) allows us to see objects clearly, and our ability to see colors came as an result of adhering to these necessary physics.I have condensed and added my own insight to an excellent blog post on Visual Acuity, from the blog WebVision, in order to help me explain this intriguing system.

Why not have more Cones for more color?

Based off of what I explained in Part 1, You might ask: Why not have more Cones types to see more colors? The reason is this magical idea of visual or spatial acuity, and the Physics of our retina.

Snellen letters are used to measure visual acuity in target recognition tasks. Each piece of the letter (stroke width and gap width) subtends 1/5th of the overall height, and the entire letter corresponds to 5 minutes of arc. A person with 20/20 vision should be able to read the letter E at 20 feet (6 meteres), where one of the strokes of the letter subtends one minute of arc at the eye. Visual acuity in Snellen notation is given by the relation: Acuity = D’/D where D’ is the viewing distance, and D is the distance at which each letter subtends 5 minutes of arc. Target resolution, on the other hand, has a threshold defined as the smallest angular size at which subjects can discriminate the spacing between the critical elements of a stimulus patternlike a grating.   Screen Shot 2013-03-11 at 12.12.45 PM

Limitations of the Retina

          Our ability to detect fine details depends on two factors, an optics system that combats aberrations, and the spacing and size of our receptors. The optics of our eyes cause distortions, where an object is imaged on the back of the retina as a distribution or point spread function.Screen Shot 2013-03-11 at 2.40.10 PM

           The optics of the eye combats two necessary aberrations that would inhibit spatial acuity.  First, shorter wavelengths of light refract more than longer ones, meaning that Blue wavelengths would be brought into focus infront of red or green ones in the Retina. The eye corrects for this chromatic aberration by placing Blue cones further out in the periphery of the retina, so they refract to the same nodal point as the Red and Green light wavelengths. As a result, Blue cones have larger receptive fields than Red and Green Cones, creating a sort of blue blur. Second to combat is spherical aberration, which occurs from wavelengths of light at the periphery of the lens refracting more than those going through the center. The eye compensates for this by allowing the pupil muscles to contract and dilate, subsequently increasing and decreasing the size of the lens, in order to block unnecessary peripheral rays that would blur the images of varied distances.

Receptor Spacing and Diffraction

          Raleigh’s criterion is used to calculate the resolution of the eye for stimuli that are degraded by these optics. Two points or lines are resolved (are clear) if the peak of the point spread function lies on the first trough of the other point spread function, or when as=1.22L/d, where L is the wavelength of light, and d is the size of the pupil. This means, that two objects must be separated by the width of their point spread functions in order to be seen as two separate objects, if the width is any less, they are seen as a uniform object.

          The spacing and number of Cone receptors therefore affects the quality of the image perceived. Helmholtz proposed that a grating would be resolved if there is a row of unstimulated cone in between rows of stimulated cones (Peters, 2003). In laymans terms, this means that if each individual receptor were to pick up an individual pixel of visual info, the  spacing between adjacent receptors must be small enough and the number of cones large enough (at least in the foveal area) to not accidentally skip over a pixel, which would cause a blur or distortion of the image (ex. seeing the white separate from the black lines in the grating).  Cone spacing at the fovea is approximately 2.5 um (Curcio, 1990), allowing for a maximum of 60 cycles per degree, directly hindering our visual acuity.

Summing it All Up

         Due to the concave shape of the retina, the properties of refraction and diffraction, and the spacing of receptors throughout the eye, there is no possible way to incorporate more colors into our visual palette without hurting our spatial acuity. Creating a different cone type that was tuned to a larger or shorter wavelength, would require an increase in the spacing between adjacent receptors of similar types, a decrease in the size of the receptors, or a decrease in the number of receptors for each respective wavelength. Decreasing the size of the receptors is not logical, and a decrease in the number or increase in the spacing would both directly affect acuity. With regard to optics of the eye, the lens would have to refract even more than it does already or pupil size would be too small or too large to clearly pick up any image.

         For these reasons, we aere left with only Red, Green and Blue Cones. Because wavelengths for Red and Green only vary by 30nms-compared to Blue wavelengths-we are able to have three types of cones, instead of just two. Therefore, in a sense, our ability to evolve towards only trichromatic color vision is a quite ingenious solution to a rather complex problem: color versus clarity.