What is the LGN all about?

After taking a semester full of different types of Psychology I found myself truly intrigued with the structure and function of the Lateral Geniculate Nucleus. As a result I have decided to submit an overview of this interesting structure of the brain as my final blog entry.

The LGN is a part of the thalamus which receives sensory input directly from the retinas of both eyes. It is therefore the primary processor of visual information in the central nervous system. Structurally the LGN is interesting in that it is composed of 6 layers of neurons in humans and the layers are differentiated based on the eyes from which they receive their visual information. The retinas of both eyes have a system of determining visual perception through a bottom-up system of photoreceptors to ganglion cells, and it is the axons of the ganglion cells that leaves each eye through the Blind Spot and makes up the optic nerve. The optic nerve separates at the optic chiasm so that the axons from the right portion of the retina of one eye corresponds to the axons of the right portion of the retina of the other and the same for the left portions of each retina. These new sets of axons called the optic tracts extend to the LGN and are divided into layers. Now to reiterate the intriguing nature of the layers of this structure, each layer is determined by which retina the visual information originates from (http://thebrain.mcgill.ca/flash/i/i_02/i_02_cr/i_02_cr_vis/i_02_cr_vis.html).

There are two LGN (right and left) so it is important to use terminology that can be applied to both when describing the layers. Layers 1, 4, and 6 receive visual information from the axons of the contralateral retina meaning the opposite retina. Layers 2, 3, and 5 receive visual information from the axons of the ipsilateral retina meaning the retina from the same side of the head. This was discovered by injecting a dye into the retina of one eye and then looking at the slice of brain tissue post-mortem.

 In the picture above (http://webvision.med.utah.edu/imageswv/lgn-projections.jpg) it is clear that the dye was transferred through the synaptic clefts of these neuroconnections and provides the proof to the previous claim. Here layers 1, 4, and 6 are displaying the dye from one eye being injected.

The structure of the LGN is even more dynamic when looking at the individual cells that make up each layer. Further studies of the retina have provided evidence that there are three distinct types of cells that are distributed in the LGN. The first two layers of the LGN are made up of what are known as M-cells (magnocellular cells) that respond vigorously to rapid, abrupt   light intensity within their receptive fields, therefore it is M-cells that signal the presence of rapid movement. The other four layers are made up of P-cells (parvocellular cells) which respond to small intensity differences in light and are the exclusive processors of color information (Perception Text). The third set of cells in the LGN are the K-cells distributed between the layers (koniocellular cells) which are not well understood, but are thought to be involved in color vision. Aside from the dynamics of the individual cells, the layers are all organized so that they match up with one another’s retinotopic maps. This means that each layer has cells organized in accordance with their position on the retina. Through this organization the LGN is able to efficiently process visual information and as stated earlier, serve as the primary area of visual processing in mammals. I am not sure if everyone finds this structure as interesting as I have, but surely some aspect of perception would catch your interest. To those of you who have read these blogs throughout this semester I hope you have found them interesting, and to those of you who are considering which Psychology course to sign up for next semester I highly recommend Perception 214.

Perceiving depth is extremely important for enabling us to interact with our environment and eachother. Therefore, it comes at no great surprise that the means of seeing depth involves mutliple different “cues” that really only create accurate depth perception when they work as an aggregate unit. There are two different classes of cues that can be examined when discussing depth perception; oculomotor cues and visual cues. Oculomotor cues include cues that are kinesthetic in nature, “meaning that the cue itself derives from the act of muscular contraction of either the muscle fibers controlling the focus of the lens or the fibers controlling the positions of the eyes in the head” (Perception, 280). The visual cues are more dynamic and involve how we perceive our position in relation to our environment as well as how the two eyes vary on how they image objects on their retina.

As alluded to, the left and right eye have slightly different images of objects seen in the environment. These slight differences are called disparities. “The perception of relative depth from binocular vision is called stereopsis” (Perception, 282). It is binocular in that it requires the images of both eyes in order to analyze and detect the disparities. Our ability to recognize differences in depth as a result of retinal disparity is an accurate tool for determining “relative distance.” This is the distance between one object and another as opposed to “absolute distance” which is the ability to determine the distance between yourself and a distant object.

A fun experiment to perform that will help you understand disparity involves holding your thumbs up in front of you at different distances. Now close one eye and look at the lateral relation you perceive between your right and left thumbs. Now without moving your thumbs alternate eyes. You should notice that when looking at them from one eye the thumbs appear closer together, and when viewing them from the other eye they appear further apart. The amazing thing is that when you open both eyes you are able to subconsciously put both images together and perceive the accurate relative depth between the two objects.

This may not seem so amazing to you yet, but take from this little experiment the fact that your brain has the amazing ability to effortlessly piece together two separate images (cooperation between the two eyes). Something that you may now appreciate more are the “magic eye” pictures. These are fun pictures that exploit retinal disparity by creating slight shifts in patterns of images that enable you to see a previously ambiguous image. With some practice you can quickly perceive the hidden image. Here is a link to a database full of these images for you to experience for yourself http://www.magiceye.com/3dfun/stwkdisp.shtml .

Stereopsis is only one of the many visual cues to depth perception. The more you learn about each, the more you can appreciate the dynamics of depth perception. Our brains have amazing capabilities that we constantly forget to recognize. I hope that after reading this you will never forget to appreciate the value of retinal disparity and now you understand the general concept of the magic eye effect.

Jean Keats wrote a poem in 1818 that criticized philosophy and modern science as a means for ruining what the world believes in and cherishes. He specifically attacked the discoveries of Newton in that objects do not have “color” they simply reflect light which leads to the perception of “color.” To this Keats wrote,

“Philosophy will clip an Angel’s wings,
Conquer all mysteries by rule and line,
Empty the haunted air, and gnomed mine -
Unweave a rainbow” -Jean Keats

http://www.quoteland.com/author.asp?AUTHOR_ID=781

Whether or not Newton felt that he had made a discovery that would have negative effects is irrelevant. In order to understand where Keats’ hostility arose from, it is important to understand more about “color.” Color is a perception that has three components. The first is hue- the quality that distinguishes blue from green. The second is brightness- related to perceived quantity of light emitted by stimulus. The third is saturation- “paleness” of a perceived stimulus. Together these three components work to create a spectrum of perceived colors. Newton was able to first isolate hues. He did so by passing a beam of white light through a prism and saw that the resulting light on a white backdrop was an array of hues (the rainbow). This was a major discovery and Newton concluded that white light is made up of all the individual “colors” and can be broken down.

 Newton’s discovery however, resulted in a negative backlash from the poetic thinkers. His prism model suggested that white light was made up of many colors which was the opposite of what thinkers such as Goethe believed. To them white light was the most pure and Newton was questioning their beliefs suggesting that white light is “tainted by all the colors.” This argument seems quite ridiculous from a modern standpoint, but at the time of Goethe it was a matter of universal beliefs.

Newton continued his hypothesese regarding components of color perception. He developed color circles that demonstrated the properties earlier discussed (hue, brightness, and saturation) and proposed that objects in the environment reflect light. By reflecting some wavelengths of light and absorbing others humans are able to perceive an “object’s color.” The research that Newton conducted to prove this statement once again was in conflict with traditional beliefs that we live in a colorful world and everything has its own color. Newton proved otherwise. He would agree that an apple is every color except red, meaning that red is the only wavelength that is reflected by the apple’s surface and is therefore what we perceive, yet the colors it absorbs are everything else.

It is this proposal that led Jean Keats to accuse Newton of “unweaving the rainbow.” His poem suggests that discoveries such as Newton’s serve no purpose other than to destroy the beliefs and faith of people. It is true that Newton proposed the world is no beautiful and colorful place, but this does not directly influence our perceptions of the world. Because Newton’s discoveries have proven to be scientifically sound facts and the world is not crumbling down, I must support him and regard the complaints of the poetic philosophers as mere opportunities to complain about something else.

Regardless of my opinion, stop and think for a moment that we live in a colorless world (similar to how it looks at dusk) and the only reason why we see color is because of the light reflected off of objects. How does this influence the way you perceive your environment? Or maybe you can’t even wrap your mind around the idea that this could be so. Did Newton really unweave the rainbow?

In psychology there is an ongoing debate as to whether certain behaviors and other developments are a result of genetics/biology or experience/environment. The debate is known as nature vs. nurture. In this blog however the debate is scaled down to deal with visual development; is vision a result of genetics and biology, experience and our environment, or a bit of both. In order to understand the science behind the claims of both sides of this debate we read an article titled “Neural Limitations on Visual Development in Primates,” by Lynne Kiorpes and J. Anthony Movshon. The research described in this document was a study of macaque monkey’s visual development. Macaque monkeys were chosen because one year in their life is equivalent to about five years in human development which speeds up the research.

The brain structures involved in visual development were observed at different stages in the monkey’s development and were compared to those of adults. This comparison was used to determine whether or not the given visual stage was the area responsible for improved vision. “Newborn primates see poorly”(Kiorpes) which is the same for human babies. What we seek to find out is what causes the connection from poor to improved vision. If visual development is solely based on nature (biology) then the structure responsible for improved vision will be different in a newborn than an adult, if visual development is solely based on nurture (environment/ experience) then the structures will be exactly the same in adults and children.

Kiorpes and Movshon’s research however lead to the conclusion that visual development is a result of both nature and nurture. Yes some structures in the the newborn baby are different than adults (the size of the optics, the receptive fields and responses of visual pathway neurons, and the speed of neurological processes) but these differences do not account for the behavioral changes found in young vision to adult vision.

Each structure studied is quickly removed as the possible site of change because each structure develops before there is a change in behavior. The superior colliculus responses are remarkably adult-like early on and the topographic organization is evident right away. The lateral geniculate nucleus develops six layers even before birth, and within four weeks the structure resembles that of an adult. As the researchers move up into visual cortex areas, V1 and V2 do not provide any evidence to solve this question either. Their structures also develop to become very adult-like within the first eight weeks of life.

Psychologists cannot yet identify the actual site of change that corresponds to change in visual behavior, but they undoubtedly support the idea that to a large extent nature plays a role. Other research involving visual conditioning and impairments has shed light on the second part of the debate, nurture also leads to visual development and changes in visual behavior. One study we discussed in lecture was that kittens who were only presented with horizontal stimuli for the first few months of their life were unable to respond to vertical stimuli or their neural responses were very low. This suggests that our visual development is dependent on what we are exposed to in an early period of our lives. Other nurture studies include those of patients with visual disorders such as amblyopia (lazy eye), strabismus (cross eyes), and Anisometropia (monocular defocus). Through corrective measures such as wearing an eyepatch early on over the stronger eye of someone with amblyopia it is evident that visual development can be assisted by environmental conditions. Without assistence, the above stated conditions alter not only the physiology of the neurons, but also the connections within and between brain structures. Clearly nurture also contributes to visual development.

Well the psychological debate of nature vs. nurture will inevitably continue in all aspects of perception and development, but it is fair to say that the research provided by Kiorpes and Movshon has proven that their are biological changes and environmental factors that contribute to visual development and the extent to which is more influential is yet to be discovered.  

Throughout psychology’s history of study in vision, facial recognition has served as a source of amazement. By using different types of scanning techniques, specifically PET scans, psychologists have been able to link specific regions of the brain to “facial recognition.” The proposed areas include the temporal lobe and the parietal lobe. As discussed in the text, the improved recognition of faces and objects correlates to increased activity in both these regions (Perception, 205). But is facial recognition so simple? Can it be that as humans we are born with specific neurons that respond to the visual stimuli of a person’s face? The answer is no. There are neurons in specific regions of our brain that serve the purpose of “face recognition,” yet they are not inately developed for this purpose, and they can be trained to respond to other stimuli with the same intensity.

In the text it is interesting to note that many studies have been done in order to prove that the adult brain is plastic in that it can be developed depending upon “teaching” a subject or conditioning them to respond to specific stimuli. The first example given was that a man who enjoyed studying moths came acrosse a type of moth that blended in with the bark of trees. After years of examining and identifying these insects his vision in terms of the ability to distinguish the moths from the bark was much better than that of someone who does not routinely do so. Studies have continously proven that many factors lead to improved visual perception (priming, practice, and sleep after practice), but what does this have to do with facial recognition? In fact this is the premise of the argument that facial recognition is not specificly inborn in our brains, but is in fact due to continous exposure.

Facial recognition is a phenomenon whereby there is intense activity of the neurons in the inferior portion of the temporal lobe of a subject who is presented with an image of a human face. While it is tempting to quickly assume that this region or these neurons of the brain are specific to facial recognition, this assumption would be wrong. The neurons of this brain region are responsive to stimuli that the person comes across routinely. One experiment tested this statement by having bird experts, car experts, and control subjects who are not experts in these categories. The first trial scanned the activity of the brain when all three groups were presented with images of cars. Bird experts and the control showed slight activity in the temporal and parietal lobes while car experts showed intense activation of the inferior portion of the temporal lobe. The second trial scanned the activity of the brain when all three groups were presented with images of birds. Car experts and control showed slight activity once again in these brain regions while bird experts showed intense activity in the inferior portion of the temporal lobe. This study therefore proved that the “facial recognition” part of the brain was more accurately a region that was activated when a personally important and routine stimulus was presented to a person.

What can be drawn from this assessment is that faces are in fact objects. In our perception of the visual world we depend on object recognition in order to accurately function with and around the objects in our world. The fact that people have elevated activity in the parietal and temporal lobes of the brain when viewing “faces” serves as evidence that “facial recognition” is essential and routine in normal human interaction. As discussed above, object recognition can be improved with practice, and studies that support this have and continue to serve as proof that to some extent the adult brain is plastic.

Cortical magnification was discovered by neurologist Gordon Holmes (Perception, p 120). His experiments began with looking at patients with visual impairments and then examining the extent of cortical damage, relating the two. He first recognized that “the visual field is represented within the cortex in a very orderly, topographic fashion.” Next he noticed that “visual disturbances always appeared in the visual field contralateral to the damaged hemisphere in the brain.” This means that damage to the right occipital lobe would cause blindness within the left visual field. From his observations he deduced that “the amount of cortical tissue devoted to the central portion of the field far exceeded the amount devoted to the periphery” (Perception, p122). This became known as Cortical Magnification.

Cortical magnification occurs for the central portion of the visual field, the area called the fovea which is what we rely on for our most acute vision.

“For quantitative purposes, the cortical magnification factor is normally expressed in millimeters of cortical surface per degree of visual angle. When expressed in this way, the values of cortical magnification factor vary by a factor of approximately 100 between the foveal and peripheral representation of the primary visual cortex (V1) of primates (Daniel and Whitteridge 1961).

A reduction of the number of neurons for a given area of the visual field implies an increase of the size of the receptive fields of the neurons, since each neuron has to cover a larger part of the visual field. As a consequence, visual performance (e.g. visual acuity) is best in the center and worse in the periphery” (http://en.wikipedia.org/wiki/Cortical_magnification).

The question that has been asked about cortical magnification is whether or not it is a good thing. The answer is not necessarily clear, but in my opinion I feel that cortical magnification is logical and therefore it is a good thing. The fovea of our retina is the area with the most cones and has a one to one cone to ganglion cell composition. This is why it is the area of best visual acuity. Cones are used for seeing in brighter light conditions and perceive color. It is logical therefore that our cortex has a larger representation for the area that we rely on most to perceive the world around us in daytime conditions. As we are not nocternal animals and we do not rely heavily on our ability to see in the dark (utilizing rods in the periphery of our retina) it seems that having less cortex devoted to this just makes sense.

“In primary visual cortex (V1), the scaling of cortical magnification with eccentricity is also known as M scaling (M=magnification). Different cortical areas have different emphases on the representation of the fovea. Areas involved in fine analyses of shape and texture (such as V4) typically show a very high foveal magnification factor, and very little representation of the peripheral visual field. In contrast, other areas show a more gradual decay of magnification factor from fovea to periphery (for example, the dorsomedial area (V6)” (http://en.wikipedia.org/wiki/Cortical_magnification).

There are many different theories about how cortical magnification differs between individuals, but I feel that regardless of the extent of cortical magnification among individuals cortical magnifcation serves a logical and beneficial purpose. Leave a comment and let me know what you think!

In the past week of class we discussed the receptive fields of Ganglion Cells. These are the only neurons in the eye whose axons leave the eye and project directly to the brain! Don’t be confused however, Ganglion cells do not absorb or record light passing into the eye. What actually occurs is that light enters the eye and then passes through the layers of ganglion cells, bipolar cells, horizontal and amacrine cells, then is processed by the photoreceptors. The photoreceptors (rods, and cones) are the only cells that actually absorb and process light in the retina! So then how exactly do ganglion cells receive the information that is sent to the brain and processed as an image? It is actually an extensive process whereby some photoreceptor signals are suppressed and some enhanced to then be sent up to the ganglion cells. The message sent to the ganglion cells by the photoreceptors constitutes the individual receptive field of each ganglion cell.

There are two types of ganglion cell receptive fields, ON-Center OFF-Surround, and OFF-Center ON-Surround. To understand what this means it is necessary to imagine the retinal layers whereby the photoreceptors project up to the ganglion cells. Each ganglion cell is attached to many photoreceptors and each photoreceptor is attached to many ganglion cells. The pattern of attachment creates a circular “field” of photoreceptors sending messages up to a ganglion cell. The field is unique however because there are two types of photoreceptor signals. One that corresponds to an increase in light and one that responds to a decrease in light. This difference creates a “field” within a “field” or the Center and Surround.

Some ganglion cell centers respond to signals of increased light from photoreceptors and these are called ON-Center OFF-Surround. Some ganglion cell centers respond to signals of decreased light from photoreceptors and these are called OFF-Center ON-Surround. Therefore it can now be understood that the receptive fields of ganglion cells are of two categories that work together to accurately determine changes in light and register edges, gradients, and textures of objects in our surroundings. Once again it is important to understand that the ganglion cells themselves do not absorb light and that their receptive fields correspond to signals sent throught the retinal layers from the rods and cones. When I first came across this information in lecture it took me a while to understand, so I hope that anyone who chooses to read this blog will find some assistance from what I have written.

Over spring break I decided to test an aspect of the gustatory system that we discussed in lecture. In class we learned that chili peppers contain a chemical compound called capsaicin. This chemical causes a burning sensation on tissue and is responsible for the burning sensation in someone’s mouth and throat when they eat spicy foods that contain hot peppers. The experiment that I performed at a restuarant went beyond the mere sensation of “heat” and tested the fact that if tissue is exposed to large quantities of capsaicin then the “heat” receptors will be reduced and the painful sensation will no longer be perceived.

At first I thought of the experiment when I ordered “loaded fries” as an appetizer and the menu had a chili pepper option. Naturally I was thinking of the information I learned in Perception and decided to order the chili peppers. I took a bite of one to impress my girlfriend, and my mouth was on fire, but instead of taking a drink of water I decided to keep eating more peppers because in lecture we learned the pain goes away! It definately took longer than I would have liked, but after a while and a few peppers I could no longer taste the “heat.” As far as the claim of lost capsaicin receptors I would have to say my experiment supports this, but we did not discuss in lecture the other effects of eating so many peppers. My eyes were watering, my nose was running, and the rest of my meal really did not have much flavor!

Capsaicin is a useful chemical in the sense that it is used to reduce painful sensations.

“Capsaicin is currently used in topical ointments to relieve the pain of peripheral neuropathy such as post-herpetic neuralgia caused by shingles. It may be used in concentrations of between 0.025% and 0.075%. It may be used as a cream for the temporary relief of minor aches and pains of muscles and joints associated with arthritis, simple backache, strains and sprains. The treatment typically involves the application of a topical anesthetic until the area is numb. Then the capsaicin is applied by a therapist wearing rubber gloves and a face mask. The capsaicin remains on the skin until the patient starts to feel the “heat”, at which point it is promptly removed. Capsaicin is also available in large adhesive bandages that can be applied to the back (http://en.wikipedia.org/wiki/Capsaicin).”

“The result appears to be that the chemical mimics a burning sensation, the nerves are overwhelmed by the influx, and are unable to report pain for an extended period of time. With chronic exposure to capsaicin, neurons are depleted of neurotransmitters and it leads to reduction in sensation of pain and blockade of neurogenic inflammation. If capsaicin is removed, the neurons recover (http://en.wikipedia.org/wiki/Capsaicin).”

Needless to say, the next day my mouth had recovered and I decided that this was one experiment that I would not have to replicate any time soon!

This past week we were introduced to two different auditory aphasias; Broca’s Aphasia, and Wernicke’s Aphasia. I am very interested in what psychology has discerned from these impairments and therefore have decided to expand on the material we discussed in class. To begin with let’s look at the differences between these two aphasias.

Broca’s Aphasia also known as “Expressive aphasia or agrammatical aphasia, is caused by damage to or developmental issues in anterior regions of the brain, including (but not limited to) the left inferior frontal region known as Broca’s area” (http://en.wikipedia.org/wiki/Broca%27s_aphasia). Broca’s area is one of the main language areas in the cerebral cortex because it controls the motor aspects of speech. Therefore, people with Broca’s aphasia can usually understand what words mean, but they have trouble performing the motor or output aspects of speech (http://www.sci.uidaho.edu/med532/Broca.htm).  In the example presented in class from a web-clip, a man was asked about his leg which had been bothering him. The man (suffering from Broca’s aphasia) could not formulate any type of sentence to respond to the question. He instead responded, “leg…..no good……….rest……….home……….doctor.” This is a perfect way to understand the importance of this area of the cerebral cortex. It demonstrates that the region is only responsible for the production of “grammatical structure,” it is not responsible for the interpretation of “grammatical structure.” The man understood the questions being presented to him, the aphasia however impaired his ability to express a meaningful and collected response. It is impressive how psychologists are able to use disorders or brain impairments in order to gain further understanding of how certain regions of the brain contribute to the body’s functions. By simply observing the behavior of patients with this aphasia it is easily discerned that Broca’s area is only responsible for output of language, not the input or encoding.

Wernicke’s aphasia also known as “receptive aphasia, or sensory aphasia, is often (but not always) caused by neurological damage to Wernicke’s area in the brain (Brodman area 22, in the posterior part of the superior temporal gyrus of the dominant hemisphere)” (http://en.wikipedia.org/wiki/Receptive_aphasia). This area of the cortex is responsible for naming objects and comprehending language. People who suffer from Wernicke’s aphasia are able to speak, yet their language context is incorrect and they often speak in what is called “word salad” (a random assortment of words into meaningless speach). The example we were presented in class is from YouTube http://www.youtube.com/watch?v=aVhYN7NTIKU and is very interesting to observe (feel free to use this link!). Once again, psychologists have been able to use observable symptoms to draw conclusions about the division between structures responsible for comprehension of language and those responsible for production. To me the existance of such is simply amazing! If you have any further questions about these two aphasias, leave a comment and I will be glad to look up the answers for you!

Audition (hearing) is the first sensation that humans use in order to locate auditory stimulus in their environment. It is known as a far sense because it allows a person to recognize a stimulus from a far distance and does not require them to be close by. This would be polar to close senses such as touch or smell which require the stimulus to be very close to the perceiver. Audition, as a far sense, is a method for us to sense and avoid danger. For instance if you were to hear the rumbling of a train you would know to step off the tracks before it was too close for you to react. Due to this ability I feel that hearing is a powerful and necessary tool to perceive the world around us.

My favorite aspect of hearing is the ability to locate auditory stimuli. As I already noted the location aspect of hearing allows us to avoid danger whether it be from a moving object such as a car or train, or some type of predator such as a lion or a snake. Aside from the avoidance of danger, exploiting our locator sense allows us to communicate with eachother. When you hear a person’s voice the difference in the air pressure sends an “auditory wave” to your ear. Depending upon the location of the peron who is speaking, the “perceiver” will feel the compression in the ear closer to the source first then the further ear will feel it. This is how we locate the source of sound. Therefore when you have your eyes closed and you hear someone speak you will be able to turn your head and face the person without even using your sight!!!

Ever since I was very little I have enjoyed exploiting the “locator” ability of hearing. My sister and I used to play Marco Polo in the pool which is a game that completely relies on the ability to detect the location of a person based on the sound of their voice and the sound of the water. Hearing is remarkable in that sense. Some people love to exploit their audition sense through listening to music, but I truly love to “locate.” In class Professor Boucher told us an anecdote about a boy who was able to completely rely on his hearing to locate objects because he was blind. His method was very similar to that used by dolphin and bats whereby he would make clicking sounds to echolocate. This technique is based on the fact that when someone produces a sound, the sound will bounce back off of objects and if one trains themself it can even be used to determine the object’s location.

After hearing this anecdote and watching the demonstration in class, I went back to my dorm room and set to work “echolocating.” I started by sitting on my bed and making a “bop” sound with my eyes closed. I did this for a while to create a general sense of the sound that was associated with all the objects the way they were in my room. I then took objects such as pens, calculators, and binders and placed them on my bed and “bopped” again. Honestly, there was no way that I could sense a change in sound feedback. I supposed that this was a result of me never developing my “echolocating” ability before. So I resorted to larger objects such as my printer and subwoofer wich I put on my bed and “bopped” again. This time success!!! I had no idea how to determine the distance the object was from me by the sound alone, but I sensed it was there!

I love how the experiments and anecdotes that we discuss and perform in class are replicable in a personal setting as well. As you can tell from my previous blog and this one, I truly enjoy performing mini-experiments and determining for myself whether or not there are any practical results. To my excitement, the echolocation experiment resulted in the positive and now I may spend the next few months teaching myself to echolocate efficiently (or maybe not, but it would be fun to do!).