Does our brain contain an innate function about closing only one eye?

Does our brain contain an innate function about closing only one eye?

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I wasn't sure where to post this, but biology seemed fitting for me. Sorry if I'm wrong.

I was wondering why, when we close both our eyes and look at light, it is clear we can see the light even though our eyes are closed. We can identify where the light is too.

However, when you look at the light with only one eye closed, suddenly you cannot perceive this anymore and you can only focus on the open eye's vision. It's like our brain is ignoring the closed eye's vision somehow. What is triggering this "ignore vision"? Is it the closing of the eye?

I found this intriguing and wondered how this works and/or if there is any research about it.

I'm only a 17 years old student but i guess this is the answer(its just what i guess, haven't seen it in any books or research):

This is a picture from the book Life. When both eyes are working they send signals to brain. signals from things on the left side are sent to right side of brain and signals from things on the right side are sent to left side of brain(coming from both eyes). as you can see both eyes participate in sending signals to right and left hemisphere.

On the right side of picture you can see visual cortex of right hemisphere , it has signals coming from both left and right and makes the thing we see.

While seeing through only one eye (or when you cut optic nerve from one eye) there is still signals coming to visual cortex from the other eye and that makes image of what you see.(when you close one eye there is still little signal from it if you are facing a bright light source, but signal from the other eye has more effect as its more powerful( try it by closing one of your eyes and put a torch in front of only the closed eye, if the torch is bright enough you can see bright thing there))

when you close both eyes the signals coming from both eyes are almost the same and if you face a bright thing, you almost see it.

i just guess that's the mechanism :)

Innate immunity at the crossroads of healthy brain maturation and neurodevelopmental disorders

The immune and nervous systems have unique developmental trajectories that individually build intricate networks of cells with highly specialized functions. These two systems have extensive mechanistic overlap and frequently coordinate to accomplish the proper growth and maturation of an organism. Brain resident innate immune cells — microglia — have the capacity to sculpt neural circuitry and coordinate copious and diverse neurodevelopmental processes. Moreover, many immune cells and immune-related signalling molecules are found in the developing nervous system and contribute to healthy neurodevelopment. In particular, many components of the innate immune system, including Toll-like receptors, cytokines, inflammasomes and phagocytic signals, are critical contributors to healthy brain development. Accordingly, dysfunction in innate immune signalling pathways has been functionally linked to many neurodevelopmental disorders, including autism and schizophrenia. This review discusses the essential roles of microglia and innate immune signalling in the assembly and maintenance of a properly functioning nervous system.

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The hypothalamus is an important organ in the brain that is only about the size of a pearl. It helps to control several major functions including homeostasis of the body. The hypothalamus also directs the release of the hormone adrenaline in times of stress, fear, excitement, or anger. Additionally, it is an emotional center that causes feelings of anger, sadness, joy and exhilaration.

What the Different Parts of the Brain Do?

The amygdala is a small lobe inside the brain that is part of the limbic system. The Alzheimer&rsquos Disease Research website notes that this area of the brain has many functions including developing, associating and remembering reflexive emotions such as fear and anxiety. In primitive states, this function is an important part of survival and is still used as a protective method by the body.

Positions and Functions of the Four Brain Lobes

The human brain is the most complex organ in the body. Composed of 50 to 100 billion neurons, the human brain remains one of the world's greatest unsolved mysteries. Here we will take a closer look at the four lobes of the brain to discover more about the location and function of each lobe.

Brain Lobes and their Functions

The brain is divided into four sections, known as lobes (as shown in the image). The frontal lobe, occipital lobe, parietal lobe, and temporal lobe have different locations and functions that support the responses and actions of the human body. Let's start by identifying where each lobe is positioned in the brain.

Position of the Lobes

The frontal lobe is the emotional control center of the brain responsible for forming our personality and influencing out decisions. The frontal lobe is located at the front of the central sulcus where it receives information signals from other lobes of the brain.

The parietal lobe processes sensory information for cognitive purposes and helps coordinate spatial relations so we can make sense of the world around us. The parietal lobe resides in the middle section of the brain behind the central sulcus, above the occipital lobe.

The temporal lobe is located on the bottom of the brain below the lateral fissure. This lobe is also the location of the primary auditory cortex, which is important for interpreting the sounds and the language we hear.

The occipital lobe is located at the back portion of the brain behind the parietal and temporal lobes. The occipital lobe is primarily responsible for processing auditory information.

Functions of the Lobes

The frontal lobe has many functions most of which center on regulating social behavior. Here are some of the important functions of the frontal lobe:

  • Cognition, problem solving and reasoning
  • Motor skill development
  • Parts of speech
  • Impulse control
  • Spontaneity
  • Regulating emotions
  • Regulating sexual urges
  • Planning

It is more common to injure the frontal lobe than the other lobes of the brain because the lobe is located at the front of the skull. The effects of damage to the frontal lobe often result in personality changes, difficulty controlling sexual urges, and other impulsive and risk-taking behaviors.

The parietal lobe has several functions including sensation, perception, and spatial reasoning. This lobe is responsible for processing sensory information from various parts of the body. Here are some of the functions of the parietal lobe:

  • Sensing pain, pressure, and touch
  • Regulating and processing the body's five senses
  • Movement and visual orientation
  • Speech
  • Visual perception and recognition
  • Cognition and information processing

Damage to the parietal lobe can result in problems with spatial reasoning, reading, writing, understanding symbols and language. Right-sided damage to the parietal area can affect a person's ability to dress or groom his or herself. While left-sided damage can result in language disorders and disorders with perception.

The temporal lobe. There are two temporal lobes located on both sides of the brain that are in close proximity to the ears. The primary function of the temporal lobes is to processing auditory sounds. Other functions of the temporal lobe include:

  • Since the hippocampus, or part of the brain responsible for transferring short-term memories into long-term memories, is located in the temporal lobe, the temporal lobe helps to form long-term memories and process new information.
  • The formation of visual and verbal memories.
  • The interpretation of smells and sounds.

The type of impairment that results from damage to the temporal lobe depends on where the damage occurred in the lobe. Temporal lobe damage can lead to difficulty processing auditory sensations and visual perceptions, problems concentrating on visual and/or auditory stimuli, long-term memory problems, changes in personality, and changes in sexual behavior.

The occipital lobe, the smallest of the four lobes of the brain, is located near the posterior region of the cerebral cortex, near the back of the skull. The occipital lobe is the primary visual processing center of the brain. Here are some other functions of the occipital lobe:

Since the skull protects the occipital lobe, injury is less likely to occur. However, severe damage to the occipital lobe can result in a variety of visual problems including the loss of color recognition, visual hallucinations or illusions, problems recognizing objects, and difficulty understanding language.

How Your Brain Works

The basic lower brain consists of the spinal cord, brain stem and diencephalon (the cerebellum and cortex are also present, but will be discussed in later sections). In turn, the brain stem comprises the medulla, pons, midbrain, hypothalamus and thalamus [source: Health Pages].

Within each of these structures are centers of neuronal cell bodies, called nuclei, which are specialized for particular functions (breathing, heart-rate regulation, sleep):

  • Medulla -- The medulla contains nuclei for regulating blood pressure and breathing, as well as nuclei for relaying information from the sense organs that comes in from the cranial nerves. It's also the most ancient part of the brain.
  • Pons -- The pons contains nuclei that relay movement and position information from the cerebellum to the cortex. It also contains nuclei that are involved in breathing, taste and sleep, and physically connects medulla to the midbrain.
  • Midbrain -- The midbrain contains nuclei that link the various sections of the brain involved in motor functions (cerebellum, basal ganglia, cerebral cortex), eye movements and auditory control. One portion, called the substantia nigra, is involved in voluntary movements when it does not function, you have the tremored movements of Parkinson's disease.
  • Thalamus -- The thalamus relays incoming sensory pathways to appropriate areas of the cortex, determines which sensory information actually reaches consciousness and participates in motor-information exchange between the cerebellum, basal ganglia and cortex.
  • Hypothalamus -- The hypothalamus contains nuclei that control hormonal secretions from the pituitary gland. These centers govern sexual reproduction, eating, drinking, growth, and maternal behavior such as lactation (milk-production in mammals). The hypothalamus is also involved in almost all aspects of behavior, including your biological "clock," which is linked to the daily light-dark cycle (circadian rhythms).

The spinal cord can be viewed as a separate entity from the brain, or merely as a downward extension of the brain stem. It contains sensory and motor pathways from the body, as well as ascending and descending pathways from the brain. It has reflex pathways that react independently of the brain, as in the knee-jerk reflex.


Immunology, developmental biology, neuroscience, and regenerative medicine are all converging in an emerging interdisciplinary field of profound significance for biomedicine as well as basic biology. 63 While the brain–immune axis is now beginning to be characterized, 9,17,64 many gaps exist in our understanding of the functional links between the brain, response to infection, and regenerative processes triggered by wound healing. 65 This is especially true for the earliest developmental events that shape the future interactions of these subsystems during health and disease. Here, we exploited the highly tractable Xenopus laevis model to identify unrevealed aspects of the innate immune response that rely on the presence of brain, and we characterized the cell-level and transcriptional machinery that underlies the effects.

We challenged Xenopus embryos with UTI E. coli load of 4.5 × 10 3 cfu/ml this dose is up to five orders of magnitude smaller than some model organisms and human organs tolerate, 66,67,68,69 providing a comfortable dynamic range within which to evaluate susceptibility and tolerance. Crucially, we show that the specific presence of the brain strongly impacts the ability of embryos to survive bacterial challenge (Fig. 1). The early brain is protecting the embryo by inducing cellular and physiological responses (decreasing the infection-induced damage and apoptosis Fig. 2, and promoting macrophage migration Figs 3 and 4) and molecular mechanisms (suppressing transcriptional consequences of the infection Fig. 5) that help to overcome the bacterial threat. Pharmacological and functional assays revealed that absence of brain during infection leads to decreased levels of peripheral DA. Targeting the DA-D1R signaling pathway in brainless animals rescues them from infection-induced death (Fig. 6). These results suggest that brain-derived DA signaling is key in mediating the protective effects of the brain signals in response to infection.

The brain is not necessary for the early development and proliferation of primitive myeloid precursors (Supplementary Fig. S2). However, in response to infection, signals from the brain are required for proper macrophage migration (Fig. 3), revealing that brain-dependent signals regulate the behavior of immune cells. Without infection, at later stages with a more mature immune system, the absence of a brain leads to aberrant and ectopic distribution of macrophages and neutrophils (Fig. 4), which occurs in the context of an ectopic neural network which could be a factor guiding the abnormal distribution of immune cells (Fig. 4m–o). Importantly, removing the brain does not induce the migration of immune cells to the injury site (the head region), which clearly occurs with other parts removed from the body, such as tail amputation (Supplementary Fig. S3n).

The protective effects of the brain do not require spinal cord contiguity, an important fact for the design of immune-enhancing therapies. Survival rate of SC – embryos after infection is similar to Ctrl (Fig. 1i), and mature immune cells in SC – animals have similar numbers and general distribution as the control group (Supplementary Fig. S3a, b). Conversely, the peripheral-nerve phenotype in SC – animals showed the same ectopic growth and sprouting of neural network than in BR – animals (Supplementary Fig. S3o–q). Thus, unlike the peripheral-nerve distribution, immune cell behavior is not controlled via the spinal cord. Likewise, neural crest ablation did not recapitulate effects of brain removal (Supplementary Fig. S1e–g), consistent with the essential role of the brain per se.

Important information was provided by two additional groups: tailless (a control for general surgical damage), and the Simvastatin-treated group (Simv, a control for general tissue stress). Simvastatin causes severe myotoxic effects in humans and zebrafish embryos, 39,40 leading to death from continuous exposure or above μM concentration, indicative of a strong drug-derived stress. In Xenopus embryos, Simv treatment led to severe aberrant muscle phenotypes, without altering the brain morphology (Supplementary Fig. S1h–j). Survival after infection (Fig. 1f) and the immune phenotype (Supplementary Fig. S3) of the Simv group are not significantly different than the Ctrl group, indicating that muscle alterations are not a primary cause of immune defects, and the combination of infection + strong stressor does not reduce survival. Thus, the absence of brain when a bacterial infection is present leads to dysfunctional macrophage behavior and high susceptibility to infection that is not recapitulated by even severe general stressors or tissue damage.

To more fully understand the link between brain and immunity, we assessed the bacterial load at 48 h after infection and the relation between survival and pathogen load, using a metric that combines these two variables in a single number: Host-Pathogen Response Index (HPRI Fig. 1i). Comparing survival percentage across the control infected vs. brainless infected vs. brainless noninfected (Fig. 1f, g) under constant pathogen load confirmed brain-dependent susceptibility, which includes a tolerance component (Fig. 1h, i). In addition to the brain, it is likely that other components of the circuit could be discovered in the future. The cellular and morphological mechanisms behind the higher susceptibility in absence of the brain include increased apoptosis and inflammation induced by infection (Fig. 2), which promote an earlier peak of death and hamper the recovery from infection and normal development to st. 48.

Analysis of the embryos’ robust transcriptional response shed light on the pathways related to brain → body, bacteria → body, and bacteria → brainless body signaling. Infection when brain is present induces the differential expression of immune-related elements such as antigen recognition, leukocyte cell adhesion, lymphoid differentiation, T-cell proliferative response and tolerance, basophil activation, disease resistance, thrombocyte aggregation, and virus morphogenesis. Infection. Similarly, some of the more significantly upregulated genes, include genes encoding proteins (ligand-receptor) for immune cell functioning (Fig. 5, Supplementary Fig. S5), such as the gene encoding colony-stimulating factor 3 (CSF 3, a granulocyte growth factor necessary for the differentiation of bone marrow cells to granulocyte-lineage 70 ), the gene encoding for receptor-interacting serine/threonine-protein kinase 3-like (RIP, a component of the Tumor Necrosis Factor-receptor I (TNF-R1) signaling complex, 71 and RAG complex genes involved in maturation of the antibody repertoire of adaptive immunity. The differential regulation of the TNF-signaling pathway is consistent with recent mammalian data showing that innate immune response in mice to Listeria monocytogenes results in upregulation of TNF in cerebrovascular fluid. 2

The deficient response to infection detected in brainless animals, with low survival rates and defects in immune cell location, was transcriptionally reflected, with an increased activity of the innate immune sub-network by

11–12% (Fig. 5e) compared with animals with a brain. The ineffective upregulation of transcripts may indicate compensatory transcriptional responses in the body from other systems in the absence of a brain when challenged with a pathogen. 72 RNA-seq revealed the most significant immune and neural pathways and transcripts affected by absence of brain such as complement activation, macrophage-focused (adhesion, apoptosis, fusion), neutrophil-focused (activation, chemotaxis, extravasation and recruitment), or overexpression of BAG-4 related genes (or TNF-R1 silencers) and cell adhesion proteins (VCAM-1). Networks functionally related to bacteria are inhibited by 20% and eleven neural pathways are uniquely affected after infection when brain is not present.

The dopaminergic transmission is one of the most affected regulatory networks in presence of infection when the brain is absent, and levels of peripheral DA are decreased in absence of brain. Macrophage migration is one of the targets for the protective role of the brain and an increasing number of recent studies relate dopamine and inflammation and immunity. 57,73,74 Based on our cellular, molecular and pharmacological results, a possible mechanism explaining the protective effects of the brain in presence of bacteria is illustrated in the drawings-models of Fig. 6c, d. In presence of bacteria, the immune response of the embryo is initiated in the early brain (st. 25) and communicated to the periphery by modulating DA-signaling pathways in macrophages (trough D1R antagonism) during the first 48 h post infection (or before st. 35). The DA-activated macrophages migrate and act systemically decreasing apoptosis and infection-induced inflammation. As a consequence, embryo’s tolerance to infection is harnessed and by st. 40, induced-infection death is entirely stabilized. In absence of brain, low levels of peripheral DA cannot activate immune cells and promote them to initiate the migratory response. Consequently, in absence of a macrophage network, brainless embryos become more susceptible to the lethal effects of the bacterial infection, which induces high levels of inflammation and apoptotic events that lead to an earlier and massive peak of death by st. 35.

Brainless animals showed an aberrant overexpression of central- (nigrostriatal dopamine) and peripheral- (peripheral-nerve function) neural networks (Fig. 5d), as well as bacteria-related pathways (Fig. S4e), revealing responses of the host to microbial presence that could explain the differences in the HPRI and, consequently, the lower survival rates detected in brainless animals after infection. Specifically, the TNF-R1 pathway is significantly upregulated in intact embryos (developed with brain) in presence of infection, and it seems to be deregulated when brain is absent. Brainless infected animals overexpress genes related to BAG-4 or silencer of death domains (SODD)—a widely expressed 60-kiloDalton protein that associate with the death domain of TNF-R1, silencing it when overexpression is detected. 75 The accumulation of immune cells in niche in absence of brain (Fig. 3m, n) is also detected in transcriptome changes, with the significant upregulation of the vascular cell adhesion protein 1 (VCAM-1) that mediates the adhesion of immune cells. Cell cycle and chromatin-expression regulators, such as ubiquitination of proteins (mediated by tnip1 or cbl), methylation (via downregulation of euchromatic histone-lysine N-methyltransferase 1L that methylates the lysine-9 position of histone H3 and tags it for transcriptional repression) or uridylation of mRNAs appear significantly and exclusively regulated in brainless animals (with or without infection). In infected animals, absence of brain induces the specific networks for ubiquitization of CSF-1R (macrophage receptor for growth and proliferation). This mechanism, along with high expression of adhesion proteins, could be the responsible for the attenuation in the macrophage proliferation detected in brainless animals.

In conclusion, a unique vertebrate model that develops without a brain enabled morphological, transcriptional and functional evidence for brain-mediated modulation of the immune system reactivity. Specifically, we demonstrate that the absence of brain makes embryos more susceptible to pathogen, lowering tolerance 41,42 and increasing apoptosis and inflammation. The influence of the endogenous brain seems to be mediated by control of cell localization, especially affecting macrophage migration to fight infection. RNA-seq revealed the most significant immune and neural pathways and transcripts affected by absence of brain. Overall, 70% of the response at the cellular network level is different based on the presence/absence of brain. Our functional assays reveal that DA signaling could be key in the bacteria–brain–immune crosstalk, suggesting that modulation of dopamine receptors could be an important strategy for mimicking the protective effects of brain signals on the immune response to infection in biomedical settings.

The brain is an active component of the innate immune response. Future work will focus on decoding the bioelectric and biochemical signals that mediate its effects on distant immune cells and identifying heretofore unrecognized cellular targets of these signals. More broadly, beyond the brain–body–bacteria axis, the understanding of the influence of the brain over cell- and molecular-level processes is an interesting frontier, with numerous potential applications across basic biology and medicine. A full understanding of brain effects on cellular behavior (complementing neuroscientists’ focus on whole animal behaviors) is likely to not only shed light on the evolution of neural and immune systems but also to facilitate the development of intervention strategies in biomedical settings. We speculate that combinations of appropriate bioelectrical and neurotransmitter signals can become a useful tool for addressing infectious and other disease states.

Memory Development

While childhood amnesia makes it impossible to recall most of our autobiographical memories from before we were six, this doesn’t mean that the memories we make before this point are unimportant. Children are still able to form stable memories and they shape the way they interact with and learn about the world. Remembering things is also an important skill that takes time, development, and practice.

The Different Types of Memory

Explicit memory, also called declarative memory, is often broken down into semantic memory (recollection of facts) and episodic memory (recollection of experiences), but it is ultimately the kind of memory that you consciously access. This is the first kind of memory that children start to exhibit in the first three years of child life, and may even be present in newborns.

Short-term memory is memory stored within seconds (approximately 15-30 seconds) of it entering the brain. It does not include information processing that puts these memories to use.

Working memory is a lot like a computer’s RAM. This is because it is memory that is stored in the short term and used to make decisions and operate in the moment. This type of memory is critical to behavior regulation and problem solving. Toddlers have about half the working memory capacity as adults, but it will improve with age and practice.

Long-term memory is memory stored indefinitely.

Autobiographical memory is a type of explicit memory where semantic and episodic memory are combined to create “episodes” from a person’s life in their recollection.

Your baby’s memory starts relatively fuzzy, and it grows slowly over their early childhood. There is some indication that babies show preference for their mother’s voice shortly after birth, and babies as young as six months are able to learn and remember cause and effect relationships.

Knowing what kind of memory capabilities your child possesses can be useful in managing expectations of them as well as knowing how best to teach them. For example, as late as age 7 children still have trouble remembering complex memories that involve overlapping elements such as time and place. This makes it difficult for them to remember things that change based on their context, time, or location.

Your child’s ability to remember things will be important throughout their lives. As they grow, it will allow them to plan, make goals, and use previously held information or experiences to make decisions and create new ideas. This makes it an incredibly important tool in the toolkit of cognitive development.

While you won’t really be able to speed up the process of developing memory, there are some things you can do to support them, as well as memory strategies you can teach them to help improve memory. A few of these strategies are listed below:

  • Ask your child to tell a story – There’s a reason storytelling is such a big part of just about every human culture. Storytelling is a powerful tool of self discovery, communication, and yes, memory. Stories survive in our memory far longer than individual facts, so if you want to help your child remember things better, ask them to tell you a story about things that have happened to them.
  • Repetition – Your child is practicing their limited memory capabilities. Repetition is a simple way for them to strengthen connections in their brain and memorize interesting stories or important information.
  • Associations, connections, and acronyms – As your child becomes more self-aware regarding their own memory and cognition, they will be able to use more complicated memory strategies to make learning easier. One such strategy is using associations, connections, and acronyms to make an idea more memorable. This can include drawing pictures that contain imagery representative of an idea, creating an easy-to-remember acronym, or associating mundane ideas with more exciting ones.

Neuroscience For Kids

The retina is the back part of the eye that contains the cells that respond to light. These specialized cells are called photoreceptors. There are 2 types of photoreceptors in the retina: rods and cones.

The rods are most sensitive to light and dark changes, shape and movement and contain only one type of light-sensitive pigment. Rods are not good for color vision. In a dim room, however, we use mainly our rods, but we are "color blind." Rods are more numerous than cones in the periphery of the retina. Next time you want to see a dim star at night, try to look at it with your peripheral vision and use your ROD VISION to see the dim star. There are about 120 million rods in the human retina.

The cones are not as sensitive to light as the rods. However, cones are most sensitive to one of three different colors (green, red or blue). Signals from the cones are sent to the brain which then translates these messages into the perception of color. Cones, however, work only in bright light. That's why you cannot see color very well in dark places. So, the cones are used for color vision and are better suited for detecting fine details. There are about 6 million cones in the human retina. Some people cannot tell some colors from others - these people are "color blind." Someone who is color blind does not have a particular type of cone in the retina or one type of cone may be weak. In the general population, about 8% of all males are color blind and about 0.5% of all females are color blind.

The fovea, shown here on the left, is the central region of the retina that provides for the most clear vision. In the fovea, there are NO rods. only cones. The cones are also packed closer together here in the fovea than in the rest of the retina. Also, blood vessels and nerve fibers go around the fovea so light has a direct path to the photoreceptors.

Here is an easy way to demonstrate the sensitivity of your foveal vision. Stare at the "g" in the word "light" in middle of the following sentence:

"Your vision is best when light falls on the fovea."

The "g" in "light" will be clear, but words and letters on either side of the "g" will not be clear.

One part of the retina does NOT contain any photoreceptors. This is our "blind spot." Therefore any image that falls on this region will NOT be seen. It is in this region that the optic nerves come together and exit the eye on their way to the brain.

To find your blind spot, look at the image below or draw it on a piece of paper:

Hold the image (or place your head from the computer monitor) about 20 inches away. With your right eye, look at the dot. Slowly bring the image (or move your head) closer while looking at the dot. At a certain distance, the + will disappear from sight. this is when the + falls on the blind spot of your retina. Reverse the process. Close your right eye and look at the + with your left eye. Move the image slowly closer to you and the dot should disappear.

Here is another image that will help you find your blind spot.

For this image, close your right eye. With your left eye, look at the red circle. Slowly move your head closer to the image. At a certain distance, the blue line will not look broken!

Did you know? Why can't you see very well when you first go into a darkened room like a movie theater? When you first enter the movie theater, the cones in your retina are working and the rods are not yet activated. Cones need a lot of light to work properly rods need less light to work, but they need about 7-10 minutes to take over for the cones. After 7-10 minutes in the dark, the rods do work, but you cannot see colors very well because the rods do not provide any color information. The cones, which do provide color information, need more light, but do not work well in the dark. After the movie is over and you leave the theater, everything looks very bright and it is hard to see for a minute or two. This is because the rods become "saturated" and stop working in these bright conditions. It takes a few minutes for the cones to begin to function again, and for normal vision to be restored.

A complete lesson plan on the eye and its connections - teacher and student guides available. Also, try some experiments to test your sense of sight and take a short, interactive quiz about the eye and sight.

New Evidence Points to Personal Brain Signatures

Everyone's brain is different. Until recently neuroscience has tended to gloss this over by averaging results from many brain scans in trying to elicit general truths about how the organ works. But in a major development within the field researchers have begun documenting how brain activity differs between individuals. Such differences had been largely thought of as transient and uninteresting but studies are starting to show that they are innate properties of people's brains, and that knowing them better might ultimately help treat neurological disorders.

The latest study, published April 8 in Science, found that the brain activity of individuals who were just biding their time in a brain scanner contained enough information to predict how their brains would function during a range of ordinary activities. The researchers used these at-rest signatures to predict which regions would light up&mdashwhich groups of brain cells would switch on&mdashduring gambling, reading and other tasks they were asked to perform in the scanner. The technique might be used one day to assess whether certain areas of the brains of people who are paralyzed or in a comatose state are still functional, the authors say.

The study capitalizes on a relatively new method of brain imaging that looks at what is going on when a person essentially does nothing. The technique stems from the mid-1990s work of biomedical engineer Bharat Biswal, now at New Jersey Institute of Technology. Biswal noticed that scans he had taken while participants were resting in a functional magnetic resonance imaging (fMRI) scanner displayed orderly, low-frequency oscillations. He had been looking for ways to remove background noise from fMRI signals but quickly realized these oscillations were not noise. His work paved the way for a new approach known as resting-state fMRI.

This type of scan, it turns out, reveals a lot about a particular brain. It analyzes the commonplace slow fluctuations of neural signaling, which form networks of brain cells that fluctuate in synchrony&mdashand these networks often resemble those the brain engages when it is actively doing something. &ldquoWe've known for awhile that the brain networks we pull out of resting-state data look similar to the maps we get from task-induced activity,&rdquo says neuroscience doctoral student Emily Finn of Yale University. Finn and her colleagues published a study last October showing that brain networks contain enough information to identify individuals with up to 99 percent accuracy. &ldquoThis study takes things a step further,&rdquo Finn says.

The team behind the new study, led by neuroscientists Ido Tavor and Saad Jbabdi of the University of Oxford, used data collected by the Human Connectome Project (HCP)&mdasha National Institutes of Health collaboration that is trying to map the wiring of the human brain and is led by Washington University in Saint Louis, the University of Minnesota and Oxford University. The team obtained data for 98 healthy young adults, including scans taken while the participants performed tasks involving memory, motor functions, decision-making (gambling), language (reading) and others as well as just resting. They analyzed the relationships between participants' resting-state brain activity and the oscillations that emerged while they were engaged in various undertakings. They then tried to predict brain activity profiles for a given participant on each of the tasks, using only the individual&rsquos resting-state scan. The predictions matched the brain activity of that person more closely than any of the other participants' scans. &ldquoWe extract a set of images that highlight brain areas that fluctuate together during this mind-wandering state,&rdquo Jbabdi explains. &ldquoOur study shows that these co-fluctuations contain enough information to predict how the brain behaves when it is actually doing something explicit.&rdquo

These are only first steps. What other information might be contained in the resting-state scans, and how the relationship between resting and active states might change under some circumstances, remain open questions. &ldquoIt will be interesting to see if and how this mapping relates to actual performance on the tasks,&rdquo Finn says. &ldquoAnd how it changes with factors like age or neuropsychiatric illness.&rdquo

Tavor says his group was impelled to do this study by a common problem neuroscientists face. For many studies, researchers need to know exactly which brain areas are chugging along during certain tasks&mdashso (for instance) they can see what happens when they block or enhance that activity. The new technique could allow researchers to predict where these regions are without having to conduct a separate scan for each of the tasks, saving time and money. &ldquoIt's a very practical result,&rdquo Finn says. &ldquoResting-state could eventually serve as a &ldquoone-size-fits-all&rdquo scan from which we can glean a lot of information about someone, without actually having them sit though multiple task sessions in the scanner,&rdquo she adds.

One of the next endeavors in this research is to determine whether these findings hold not just for the healthy participants used in this study but for patients with various illnesses. &ldquoWe're looking at brain tumor patients before surgery,&rdquo Tavor says. Knowing what parts of the brain are responsible for sensitive functions, like language, can be crucial information to a neurosurgeon, and tumors can cause shifts in where functions are performed in the brain. &ldquoIf we can predict this shift, it could affect the surgeon's strategy of where to enter to remove the tumor,&rdquo Tavor explains.

Biswal is also interested in medical implications. &ldquoIn clinical cases, if there's a difference in performance, compared to healthy controls, would the resting-state still predict patients' performance?&rdquo he asks. &ldquoOr has something mechanistic happened that means the prediction won't be as good, and might this tell us something about the underlying mechanism of the disease?&rdquo Using the technique for diagnostic applications might enable researchers to measure disease severity by examining the accuracy of predictions for brain functions known to be affected by a particular disease.

Whatever the eventual outcome, this work adds to a body of evidence suggesting the resting brain is anything but. &ldquoDuring this so-called resting-state, the brain is not really resting,&rdquo Tavor says. &ldquoIt does everything, all the time.&rdquo