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It looks like my goal of world domination have gotten a few steps closer, if two of the popular press articles I posted in the webliography are any indication.

The two articles form a theme of sorts about control.  One of the articles talks about how scientists hacked into a monkey’s brain to control its movements.  There have been reports in the literature describing procedures by which monkeys can control objects in the real world with their brains.  This is usually achieved by an implant of some sort that can be affected by certain patterns of electrical activity in the surrounding brain tissue that then sends a signal to a device in the real world.  This research seems promising for a variety of things, particularly people with paralysis or prosthetic limbs,   Imagine being able to control the prosthetic not only with the muscles near it, but also with your brain to some extent.

Schematic of brain showing the ventral tegmental area (VTA).

Schematic of the brain showing the ventral tegmental area.

Researchers have figured out an elegant way to influence the decision making process of monkeys.  They implanted electrodes into the ventral tegmental area (VTA) of the brain, which is one of the places (as you will learn more about in the coming weeks) that produces dopamine and is involved in reward circuitry of the brain.  Then, they conducted a simple preference test by showing monkeys two pictures of random objects and had them indicate which one they liked better.  This initial preference test was their control procedure since they were interested in what choices the monkeys made without any interference from the experimenters.  Once this was done, they demonstrated that by sending brief electrical bursts through the electrodes implanted in the monkeys brains the researchers could get the monkeys to reliably switch their preferences for pictures.  Now, this doesn’t mean an evil mustache-twirling mastermind, or the government, or the NSA are going to take over your mind or anything like that, though that possibility is certainly there.  But this does build on some fascinating research from the 1950s that helped to further our understanding of the role the brain plays in motivating our specific choices.  The fact that this can be manipulated artificially is an interesting finding.

Long-term potentiation

A schematic of a regular synapse and one that has undergone stimulation to produce a long-term potentiation (LTP).

In the other interesting article, researchers were able to turn memories off and on.  This was done in genetically engineered rats using light pulses that strengthened or weakened synapses in the hippocampus.  This is another thing you’ll be learning about (in Week 5 I think).  One of the amazing things about our nervous system is that it is dynamic and is constantly changing due to our experiences.  It’s why we can learn new things.  One of the ways memories are formed is through strengthening and weakening of synapses, or long-term potentiation (LTP) and long-term depression (LTD).  This strengthening and weakening can be achieved through everyday use, such as when you memorize information for this class, or become classically or operantly conditioned to perform a response to a specific stimulus.  It can also be artificially induced, using different frequencies of light pulses that stimulate the synapse.  If you can find the right frequency of pulses (high or low) you can make the synapse stronger or weaker.  This is the mechanism by which the researchers in this particular study were able to manipulate memory in the rats. They were able to turn a conditioned fear off and on using light pulses to the hippocampus.

Both of these studies are interesting for a couple of reasons.  First, they tie together a lot of the information you’ve already learned in the course, particularly how synapses and neurotransmitters work, as well as brain structure (VTA and hippocampus) and shows how they all work together to produce complex behavior.  The added layer that makes this particularly fascinating to me is the fact that researchers can control behavior through selective brain stimulation, an idea that is exciting and a little terrifying.  I will admit it does conjure up images of a MatrixThe Matrix-like culture where people’s thoughts and behaviors are controlled by others by directly accessing their brains.  It’s easy to see how something like that could be abused at some future point, though we’re a long way from that.

I can see some tremendous potential for good, here, too.  In particular, imagine what the treatment of extreme phobias, Alzheimer’s disease, PTSD, and other types of problems related to memories would look like if we had the ability to either enhance memories or take some memories away at will.  It’s tempting to shrink from an idea like that, because our memories are what make us who we are, and common sense tells us we might be better off learning to just cope with them.  But imagine memories so awful, so debilitating and disturbing, that it becomes difficult or impossible to cope with them, and they begin to affect every aspect of your life.  I’ve never suffered from PTSD, but I imagine it can be quite horrible, and if conventional treatment doesn’t help then perhaps being able to suppress the memories, at least for a little while so that other coping mechanisms can be acquired and strengthened might offer some people a desperately needed reprieve.  And being able to counter the synapse weakening amyloid beta proteins in the brains of people with Alzheimer’s Disease seems like a promising idea worth investigating.

It’s a little harder to see the benefits of influencing choice.  One can easily envision unscrupulous advertisers using something like this to force people to choose their products, but again, I doubt that would ever happen.  I think the significance of this centers on the issue of motivation.  They were able to manipulate motivation, and got monkeys to choose things they might not otherwise choose.  Though it’s a stretch, this might be something beneficial to people suffering from depression or inactivity of one sort or another.  The idea is interesting, anyway. I wouldn’t mind being able to give my brain a little zap to get me motivated.


Arsenault, J.T., Rima, S., Stemmann, H., Vanduffel, W. (2014). Role of the primate ventral tegmental area in reinforcement and motivation.  Current Biology, 24(12), 1347–1353 DOI:

Nabavi, S., Fox, R., Proulx, C.D., Lin, J.Y., Tsien, R.Y., and Malinow, R. (2014). Engineering a memory with LTD and LTP.  Nature, doi:10.1038/nature13294


As I’ve mentioned many times in class, one of the main jobs of the parietal lobe is to integrate sensory information coming from your body and the external world.  The reason for this is so you can navigate more effectively.  The back half of the brain is generally thought to be involved in processing all the sensory information that feeds into it, then that information is sent to the front half of the brain which is responsible for acting on that information.  One piece of information the parietal lobe sends forward to the front half of the brain is a priority map of the environment (Bisley & Goldberg, 2010).

Essentially, sensory information from your eyes and ears pours into your brain through various sense organs, and from that, after some initial processing in association areas that surround the primary sensory cortices in the bran, this information is integrated into a priority map that gives precedence to those things in the environment to which you need to pay attention.  What is particularly interesting about this map is that it isn’t  driven by features in the environment that are perceptually distinct.  It’s tempting to think that the map is constructed such that bright and noisy and smelly and tasty things stand out, and that is partially the case. This is what we would expect if the mapping were produced through bottom-up processes.

In bottom-up processing, we start with the small details, the little pieces of information that make up the whole.  We begin to put the information together until we have the whole thing.  This is in contrast to top-down processing which says just the opposite, that we start with the larger picture, the bigger concept, and work our way down to the smaller details.  As with many things in psychology there has always been a debate about whether information processing is top-down or bottom-up.  As is also often the case, it is a combination of the two, and the priority map the parietal lobe produces is a very good example of the combination of both types of processing information.

As I mentioned, sensory information from the environment is sent to the cortex, processed in association areas, and then integrated in the parietal lobe and other parts of the brain.  From all that information, which is processed in a bottom-up fashion, the parietal lobe then creates a map of things in the environment that you should be behaviorally interested in and paying attention to.  This is where the top-down processing is added to the mix.  When you are in a familiar environment, there may be several perceptually salient features.  There may be a bright light shining nearby, or intermittent ambient noise coming from the weather or other organisms.  But there may also be an area that you should remember and should consider exploring because it might have something good for you to eat contained within it.  If your attention was guided strictly by the brightest, loudest, smelliest things in the environment, you wouldn’t be able to focus your attention onto areas that might be useful to you.  So we obviously need a mechanism to tune out things that might be perceptually strong, but behaviorally irrelevant.  That’s exactly what a priority map does (Bisley & Goldberg, 2010).

How is this represented in the brain?  That is a good question, because if you recall, in an earlier lecture I mentioned that one of the ways the nervous system encodes for stimulus intensity is through frequency.  A strong stimulus is encoded either by neurons having a lot of action potentials, or by a large number of neurons firing at the same time, or a combination of both of these.  It turns out, that’s exactly how priority is encoded in the parietal lobe.  Those things in the environment that should be paid attention to because they are behaviorally relevant are encoded by greater neural activity on the map than those things that are of less interest.  So while physical intensity is directly encoded at least partially by frequency, the increase in neural activity that corresponds to behaviorally significant things in the environment is an aspect the brain adds to the information once it’s been processed.

As I was reading through material about this, it got me thinking about habituation, and the neural mechanisms that mediate that.  Habituation is a type of non-associative learning in which we stop responding to stimuli that are repetitive and contain no important information.  For example, when I first moved to New York City, I lived right next to the emergency room of Bellevue Hospital.  For the first month or so, I barely was able to sleep due to the constant sound of sirens.  New York is a large city, and emergencies are always happening, so there were a lot of ambulances.  Over time, however, I gradually began tuning the sound of the sirens out, until I no longer heard them.  This was brought home to me when my family called a few months after I had been there, and as we were talking, my father asked me what in the world was going on because he could hear all the sirens.  I actually asked “What sirens?” that’s how well I was able to tune them out at that point.  In the laboratory, habituation can be tested by repeatedly presenting a stimulus, such as a particular flavor or a particular sound, and measuring physiological and behavioral responses to it.

It seems logical that habituation, which is a mechanism by which sensory thresholds are gradually increased and which biases an organism toward novelty, must factor into the priority maps of the environment that the parietal lobe constructs for us.  The same bottom-up and top-down processing is possibly at work with habituation as well, with the actual stimulus from the environment to be habituated to being part of the small details of bottom-up processing.  But then, once we have a better picture of the whole environment, and we know that that stimulus we’ve been hearing or seeing that captures our attention isn’t particularly important, we can tune it out in favor of things to which we should be paying attention.


Bisley, J.W. & Goldberg, M.E. (2010). Attention, intention, and priority in the parietal lobe. Annual Review of Neuroscince, 33, 1-21 doi: 10.1146/annurev-neuro-060909-15283

I joined the faculty at Cedar Crest College in August 2009, so the class of 2013 is, in some ways, also my class as they are the students who were new to Cedar Crest, and spent four years learning all about it alongside me.  I don’t teach classes that freshmen take, so I didn’t actually see many of them until they were sophomores or beyond.  One student who came in that year, Lauren Della, is someone I ended up working on research projects two years in a row with, during her junior and senior years.  One of the great privileges of teaching is to watch students grow as they learn.  Grow in knowledge, grow in confidence, grow in leadership.  And all of those were definitely true of Laurian.


A lovely gift from a wonderful student.

When she graduated this past spring, Laurien gave me a wonderful gift, a ceramic brain with a figure of a man with a cane walking along the parietal lobe.  I love it.  It’s sitting on my desk, though a piece of it fell off (from the inferior temporal lobe) and people coming into my office all had to comment on my broken brain.  It was part of her Art Therapy show, and I love that she integrated brain and behavior so beautifully and creatively.  One of the many things the parietal lobe is responsible for is helping to understand and navigate the space around us, so the figure walking across the surface is especially fitting.


The parietal lobe.

It seems appropriate, then, to make the parietal lobe the theme of this series of blogs.  The parietal lobe is located on top of the brain, slightly toward the back and center.  We began the course by looking at the role the parietal lobe plays in consciousness.  People who suffer from unilateral neglect fail to be aware of information coming in from the opposite side.  So if someone has suffered a stroke that damages their right parietal lobe they will ignore things on their left side.  They will write on half a piece of paper, draw half a house, or eat half a pancake.  It’s not that they are numb or blind on the left side;  their sensory capabilities are not diminished.  They simply are not conscious of things on the left, and act as if any objects to their left simply do not exist.


An individual with unilateral neglect drew the flower on the right.

As I mentioned earlier, the parietal lobe helps us to organize and navigate space, not only in terms of what’s out there, but also how we orient relative to objects in the spatial environment.  Also, the parietal lobe also provides feedback for how our body is oriented in space.  So it’s easy to see why damage to this part of the brain manifests itself in an inability to attend to spatial information to the left side of the body.

Most of the sensory information that comes into the brain goes through the back half first to be processed, then is sent forward to the front half to be acted upon.  In addition to kinesthetic feedback from the muscles and joints, the back portion of the brain, including the parietal lobe, also processes information from some of the other senses, particularly touch and vision.  For many of our senses, information from the sensory organs is topographically mapped onto the brain.  The best example of this is the somatosensory cortex, which is an area in the parietal lobe, just before the central fissure and running down from the center to the side of the brain along the surface.  This is the part of the brain that receives touch information from various places around your body.  The entire surface of your body is mapped onto this area of the brain.  It is a distorted map, because some parts of your body, such as your fingertips, are more sensitive and thus require more space in the brain to process the information coming from them, than other areas, such as your back or your thighs.

somatosensory cortex

The parts of our body are topographically mapped in our brains on the primary motor cortex (in red) and the somatosensory cortex (in green). The somatosensory cortex is located in the parietal lobe, just before the central fissure.

Recently, researchers have discovered that the parietal lobe also plays an important role in numerosity or “number sense” seen in many species. Numerosity doesn’t refer to counting because that involves associating specific quantities with a symbolic representation in the form of a number, which is a pretty advanced cognitive capability.  Instead, what our number sense allows us to do is to estimate quantity in a general way, such as when we’re offered a choice between two slices of pie and know that even though we might want the bigger piece, for the sake of our diets we need to take the smaller piece.  It’s the sense that allows us to make “greater than” or “less than” distinctions.

Harvey, Klein, Petridou, and Dumoulin (2013) recently studied the number sense in humans specifically to determine whether or not there was a similar topographic organization in the brain for numerosity despite the fact that there were no specific sense organs associated with a number sense.  They presented stimuli containing different numbers of dots and measured brain activity with a high-field fMRI.  Different areas of the parietal lobe responded to different numbers of dots in the stimuli.  When the number of dots in the stimulus was small, they found the greatest level of activity in the most forward part of the parietal lobe.  As the number of dots increased, not only did the focus of neural activity move further and further back along the parietal lobe, but the total number of neurons activated by the stimuli decreased.  These findings help to explain  why we tend to be good at estimating small numbers of objects, but become less and less accurate as the total number of objects in the stimuli increases.  The authors suggest that our parietal lobe acts as a sort of internal abacus, which is an ancient calculator that represents numbers spatially (Lewis, 2013).

Though it may not seem so, this is an important sense.  For most species, their day is spent searching for and acquiring resources such as food.  The ability to estimate quantity, or even to judge one potential source of food as better in terms of the amount it can provide over another site helps to make the foraging process more efficient.  The less energy an organism has to expend in order to acquire resources to survive, the better, and even something as simple as being able to quickly judge the richness of a resource compared to another one can make all the difference.


Harvey, B.M., Klein, B.P., Petridou, N., & Dumoulin, S.O. (2013).  Topographic representation of numerosity in the human perietal cortex. Science, 341(6150), 1123-1126 doi: 10.1126/science.1239052

Lewis, T. (2013). Is “Numerosity” Humans’ Sixth Sense? 

Pseudobulbar Affect

So, here we are, at the last blog entry of the semester.  What a long, strange trip it’s been. 

I began this series of blogs with a description of an interesting, yet troubling behavior I saw in my mother while visiting her over the summer.  In addition to the Alzheimer’s Disease, which is progressing, she has a movement disorder, and she laughs all the time.  I used this as a springboard to examine laughter (and by extension positive affect) in this series of entries, so I would like to return to that behavior.

While researching the brain mechanisms that contribute to laughter, and discovering that there was no single area of the brain that controls laughter, I cam across a paragraph in Meyer et al (2007) discussing the source of “pathological laughter.”  This is involuntary, mood-independent laughter that often occurs without any external or internal trigger.  Poeck (1985) and Hartje (2006) (as cited by Meyers et al, 2007) suggest that this behavior is not caused by any true affect or emotional state, but is, instead, the result of disinhibition of the motor pathways that control laughter.  It’s seen in a number of neurological disorders, particularly those that are degenerative.

So, it’s somewhat common to see pathological laughter, sometimes termed “pseudobulbar affect” in Alzheimer’s Disease, and as I correctly surmised before doing any research on the matter, it was likely due to some disinhibition.  The frontal lobes are the main sources of this inhibition.  It’s the area of the brain that keeps the expression of inappropriate behaviors at bay in social situations, even though we may be thinking about it.  For people suffering from a neurologically degenerative disease, such as Alzheimer’s Disease, the destruction of neural tissue in the frontal lobe removes that inhibition and produces this behavior.  Anyone who has ever suffered from a mortifying bout of inappropriate laughter probably understands the issue of disinhibition all too well as they desperately attempt to stifle the giggles emanating from them.  I know I certainly have.

It is possible that on top of the Alzheimer’s Disease, my mother is suffering from some other disorder, such as multiple sclerosis, and her doctors are investigating that possibility as well.  I’m sure I will post here about it if we discover something new.  For now, I’m satisfied that there is a reasonable explanation for the behavior, and as I said in my original post, I am glad it is laughter and not some other type of emotion.  Even though the laughter may not have an underlying cause for my mother, it does evoke positive responses from the people around her, including us.  My sister found it very comforting, for example.

So, as always, this journey into a particular behavior has been enlightening and informative, particularly since I have such a personal connection to it.  Like yawning, laughter is a phylogenetically old, and stereotypical behavior.  Like the expression of all emotion, it is designed to communicate something.  Since evolution is conservative, and tends to find new uses for old things, this behavior eventually became a powerful mechanism for social bonding, and an important part of all social interactions.  Its importance in the brain is, I think, highlighted, ironically, by disorders such as those that cause pseudobulbar affect.  It makes me envision laughter as this effervescent substance inside a brain-shaped cauldron.  Its surface is calm, but the laughter is bubbling beneath, always waiting for the chance to escape.  And, in the end, I think that’s a good thing, because the world probably does need more laughter in it.

As this is the last blog of the semester, I’d like to again take this opportunity to thank my students in PSY229 Introduction to Biological Psychology, who have been blogging along with me as a class assignment.  Many of you approached this assignment with trepidation and hesitancy, yet have given it your best effort, which is greatly appreciated by me.  Critical thinking skills are among the most important things we strive to teach you in a college education, and continued, sustained writing is one way to help develop those skills.  For this assignment, you engaged your critical thinking skills to pick out a series of topics of interest to you.  Then, and even more importantly, you used those skills to sift through the enormous amount of information, good and bad, on the web.  While there were a few missteps with respect to that along the way, I think you all learned from it.  I hope this assignment has empowered you to continue investigating and researching those topics that interest you.

And to keep writing about them, too!


Meyer, M., Baumanne, S., Wildgruber, D., & Alter, K. (2007). How the brain laughs: Comparative evidence from behavioral, electrophysiological and neuroimaging studies in human and monkey. Behavioral Brain Research, 182, 245-260.

This week in class we’re going to be discussing emotion. The interesting thing is, when I prepared this course years ago, most of the resources I used focused on so-called negative emotions, such as fear, and anger and aggression. As we all know, Yoda felt that fear and anger were paths to the dark side of the force.

I used the term “so-called” because I don’t believe fear and anger or aggression, in and of themselves, are negative.  All our emotional responses, including fear and anger, evolved for a reason, and when you think about it, they evolved for very good reasons. Fear protects us from danger. Imagine not feeling afraid of that fire racing through the forest threatening your life, or that saber-toothed tiger bearing down on you. Anger, and perhaps aggression, are emotions of possession; we experience them when we perceive that something that we value has been taken from us. In an evolutionary framework, this is also a good thing. So much about survival and reproduction centers on resources. Access to food, access to suitable mates, both of these are vitally important things that must be protected, defended, and yes, reclaimed when lost, because they improve our reproductive success. A species that just let’s others take all their important resources is one that won’t be around very long.

So, in my opinion, Yoda was wrong about a great many things.  (And I really wanted to put that clip from “Return of the Jedi” here, but I couldn’t find it on YouTube).

It isn’t much of a stretch to understand why these emotions evolved in the first place, and the value they actually have in the grand scheme of things. But this blog series is about laughter, so lets focus on that for a bit. I’ve already talked about the social bonding function that laughter plays, which is why it’s important. We’re also not entirely sure what parts of the brain are involved in laughter, but we are beginning to image brains in such a way that we can tell if a person is generally happy or generally sad.

It seems to me that the dopaminergic system is probably a major player. Laughter is accompanied by (or produced by?) positive affect. I think it’s pretty safe to say that other people are most often the cause of our laughter. So a release of dopamine is our reward for sharing a laugh, or engaging in some kind of socially-mediated laughter, like those found in conversation. Mirror neurons, too, probably play a huge role. Most of the time, if someone smiles or laughs, you laugh along.  How many times have you laughed at something you didn’t quite hear because everyone around you laughed?  I do that all the time, and invariably someone turns to me and says “What did they say?” and I have to sit there and feel like a dork because I don’t actually know.

There’s a trend in psychology now, called positive psychology.  One of the important things it brings to the discipline is that it helps get us away from this obsession with abnormal behavior and dysfunction that has taken over psychology.  I talk often of the importance of understanding everyday behavior in class; it becomes depressing to contextualize all behavior in terms of how it goes wrong or is maladaptive, in my opinion.  I think that’s what takes us to the dark side, rather than certain emotions themselves.  People end up getting so caught up in their bad behavior that they downplay or overlook the good behavior, and that’s a shame.  With the rise of positive psychology comes an increased emphasis on understanding happiness and laughter, in figuring out how our nervous system mediates those emotions.  The potentially life-saving advantages of social bonding, which is in part mediated by happiness and laughter, are no less important than the direct benefits of fear and anger.  Social behavior evolved because it conferred an advantage to the individuals who engaged in it; anything that helps us get along in a social group, including mirroring the positive behavior and affect of others, is probably a good and beneficial thing in a broad context.  This is, after all, a major factor in how children learn what to do and how to be.

One goal I have for myself this summer is to revise my emotion lecture.  I think it’s pretty good, but I want to add a section on happiness and positive affect.  Understanding laughter in the nervous system is not only cutting edge in psychology, it has direct benefits for individuals and for my beloved discipline.  And I’m all for that.

Roller coasters

Roller coasters fill me with dread, until they actually start moving. Source:

I kind of like roller coasters.  I don’t love roller coasters in the way that some people do, and there are certain roller coasters I simply won’t go on, such as wooden roller coasters, mostly because they don’t strap you into those types of coasters with hydraulics.  I want that big harness to lock down kind of painfully over my shoulders, and I even pull them down tighter onto my shoulders than is necessary.  And, every single time, I feel a moment of intense panic, because I have been asking myself, all the way through the line, and even as the workers are giving each other the thumbs up signal that will send us on our way, “What if my harness isn’t really locked?”  Of course, it always is, and the car takes off.  But I like them well enough that I can often work up the nerve to ride on them, even if they make me nervous.  That’s part of the fun, right?

Here is here the odd behavior comes in.  The minute the car leaves the starting area, I start laughing.  And I don’t stop until we get to the end.  And it isn’t just a little chuckle.  Oh no, it’s a loud, braying laugh that shakes my whole body and makes the muscles of my stomach ache.  It’s been so obnoxious that sometimes, as we’re climbing that first big steep hill that starts all these coasters off, people have actually twisted around in their seat to give me dirty looks.

What on earth is going on ?  Why am I behaving this way?

Well, in the 70s, Solomon proposed an explanation for this behavior, which he dubbed the Opponent-Process Theory.  There are several different version of the Opponent-Process Theory, each of which addresses different things, such as color vision (which we are familiar with from the lecture on vision) to motivation. Solomon’s theory dealt specifically with emotional responses, and is outlined briefly in the video below, plus I’ll describe it as well.


 So, what Solomon proposed is that every emotional response is biphasic.  In other words, there’s an initial emotional response, which they call the a process, that is experienced.  This a process is followed by the opposite response, the b process.  As the video shows, a person making their first skydive will feel increasing nervousness as the moment of the jump approaches.  Successful completion of the jump produces a state akin to euphoria, which is the opposite of the initial extreme trepidation.

This is a slide from one of my Learning lectures that shows how the two emotions work (on the left) and what is experienced emotionally (on the right).

This is pretty much exactly what happens to me when I ride roller coasters.  I’m horribly nervous standing in line and actually getting into the harness, almost to the point where I feel like I’m going to faint.  As soon as the car gets going, however, the opposite response kicks in.  For most people, it would be after the ride is over.  For me, the worst part is over as soon as the car takes off and I feel safe knowing I’m not going to get flung from the car due to a faulty harness.  So I start laughing.

Obviously, my nervous system is controlling this behavior, and I have to wonder about the exact sequencing of the emotional responses that are experienced.  I think it’s safe to assume my “fight or flight” response, controlled by the sympathetic nervous system, is activated while I’m standing in line.  I feel all the classic symptoms of extreme nervousness.  Nothing new or interesting there—these rides are supposed to make us feel that way (because the designers knew full well about the b process, I think).  The curiosity here is the opposite response.  Why don’t I just go back to my more neutral emotional state after the ride starts?  Why do I have such an extreme response in the opposite direction?

One thing that’s true about our body is that it generally likes to maintain a regulated state.  You’ve heard the word “homeostasis,” which means “steady state” before.  Our body likes to maintain a balanced state of affairs physiologically, neither too hot nor too cold, neither too full nor too hungry, etc.  The same is true of our behaviors as well, including our emotions.  The whole point of the biphasic emotional response is to get back to equilibrium, and perhaps the only way to manage that is for the body to overshoot in the opposite direction after a particularly strong emotion is felt.  So, we feel extreme fear, and to counter that, we feel extreme happiness.  That’s kind of the good way for things to go because we’re left feeling generally more positive even when we get back down to the relatively neutral state.  The bad part is when the initial feeling is extreme happiness, because that’s countered by extreme sadness for a little bit before we recover.  But all of that is necessary to get us back to that even-keel we like to maintain.

I like to think, when I ride roller coasters, that I am laughing in the face of adversity.  However, the truth is, I’m really just laughing in relief!

Several years ago, a study by Ross, Owren, and Zimmerman (2009) made quite a splash.  Prominent scientists, including Jerry Coyne (who pens the excellent blog “Why Evolution is True”) wrote about it, and the study was even featured on news programs that appeared on the BBC.

The reason this particular study generated such interest is because it had long been hypothesized that laughter, some form of which is seen in most of the great ape species, was the result of evolution.  Many researchers, including Provine (1999) argued that laughter was likely present, probably in the form of some kind of panting behavior, in an ancestor common to all extant humans and great ape species.  It’s an idea that makes a great deal of sense.  We have known for a long time that chimpanzees will make a panting sound when tickled that sounds curiously like laughter.  Darwin even describes this behavior in his book on emotional expression (Darwin, 1872).  Orang utans and gorillas do the same.

So here is what Ross and her colleagues did to show that the behavior of laughter is similar across species of great apes, and it is quite stunning in its simplicity.

They tickled a lot of animals.

I mean, imagine yourself as a research assistant in this lab, and your boss comes and tells you that your job is going to be to tickle a bunch of infant great apes!  That sounds like the best job in the world to me.  Specifically, their job was to tickle 21 infant and juvenile chimps, bonobos, gorillas, and orang utans, and three infant humans.  And while they were tickling them, they recorded the sounds they made and subjected them to an analysis.

So, what did they find?

From Ross, et al (2009). This is the tree they constructed by comparing the laughs of several primate species.

As expected, they found some similarities in the acoustical structure of the laughter produced by the species under investigation. Using those similarities, they placed the species into a tree arrangement, which looks like this:

To construct this image, they analyzed the auditory profiles of the laughter from their test subjects.  Essentially, they found the greatest similarity in the auditory structure of laughter between bonobos and chimpanzees.  This is hardly surprising, since those two species are very, very closely related.  Their laughter was structurally similar to humans.  The other two great ape species, gorillas and orang utans, had laughter that was the least similar to human laughter (though it was still fairly close).

What is extraordinary about this particular chart is that it bears a striking resemblance to this:

This is the taxonomic tree for great apes.  In other words, Ross’s, et al (2009) laughter map matches the tree that is produced by analyzing the DNA of all these species, a genetic family tree, if you will, of the hominids.  It is important to note that none of the non-human species have a vocal apparatus that is capable of producing human-like speech, though there are structural similarities in the throat and larynx.

So, why did laughter (tickle-induced laughter, at any rate) evolve?  Provine (1999) suggests that laughter is all about social bonding.  The young of most mammalian species engage in rough and tumble play, and tickling is often an important part of this play.  The tickling produces mutual laughter, accompanied by the release of neurotransmitters that induce positive affect, and the resulting enhanced social bonding is obvious.  This behavior carries over into adulthood and permeates many social encounters. Informal research from Provine’s (1999) laboratory indicate that people laugh the most often in social encounters, many of which do not necessarily include any humor.

I have said in class that the main function of the mammalian brain is to help us navigate the environment.  Some argue that the main function of the human brain is to solve social problems.  I think they are one and the same–the main things we need to navigate in our increasingly complex environment are social relationships of one kind or another.  Our livelihoods, by and large, revolve around successfully navigating relationships with our families, our friends, our teachers, our bosses, our neighbors, and even strangers we encounter in our everyday lives (I consider driving a highly social behavior, for example, even though it doesn’t appear to be that at first).

The other thing that the Ross, et al (2009) study makes quite clear is that laughter in great apes is a distinct and clear behavior that likely serves some purpose (probably social bonding).  In other words, we are not anthropomorphizing the behavior when we hear it.  It really does seem to be laughter in the way we, as humans, understand it.  Though we can never know exactly what a non-human animals is experiencing, we can correlate the behavior that occurs with the laughter.

I want to close out this blog entry with a personal story.  I did quite a lot of research with my mentor at the Smithsonian’s National Zoological Park, in Washington, D.C.  They have several orang utans there, and my mentor was engaged in a research project with them.  The experiments we were doing, which were to look at the cognitive capabilities of the orangs, used touch screens so the orangs could make their responses.  When we were first starting out the project, we had to do a lot of troubleshooting.  This usually involved wheeling the apparatus up, putting a very obvious picture up, such as a big, red leaf, and trying to figure out ways to get the orangs to reach out through the mesh of their habitat to touch the apparatus.  This wasn’t such a problem with the females, since they have smaller hands and could just reach out.  There were other problems with the females, since the first time we rolled the apparatus up to one, named Bonnie, she reached out and punched the apparatus so hard she broke it.

This isn’t Junior, but I wanted to show you what their big, banana-fingers look like. The original picture appears at

The real problem turned out to be the male, Junior.  Male orang utans have very large hands, and these enormous, banana shaped fingers.  We though if we put the apparatus up close enough, Junior could poke his fingers out and make his responses.  So we started training that.  My advisor would often stand near the apparatus, and occasionally would reach in and try to guide his fingers to the stimulus to touch it.  After a few trials of this, he started moving her fingers around whenever she reached in, rather than letting her move his fingers.  We knew he was perfectly capable of touching the screen on his own, so we couldn’t figure out what he was doing until we let him just move her hand around, and he used her hand to touch the stimulus.

At this point, he sat back on his haunches, and started that odd panting laughter that they do.  It was clear to us that he thought this was hilarious.  Of course, once we realized what he was doing, and the fact that he was laughing over it, it made us laugh, too.  Aside from being a great story, his behavior also raises a tantalizing question about a sense of humor in species other than humans.  We know we have it, though humor is highly subjective, and highly complex in terms of behavior.  It’s incredibly difficult to understand what humor is to another species, though I think we got a very clear glimpse of it in the male orang we worked with.

There was a lot of laughter on that research project–orangs are really a joy to work with.


Darwin, C. (1872). The expression of emotion in man and animals. London: John Murray.

Provine, R. (1999). A Big Mystery: Why Do We Laugh? Retrieved 10/9/2012

Ross, M.D., Owren, M.J., and Zimmermann, E. (2009). Reconstructing the evolution of laughter in great apes and humans.  Current Biology, 19, 1106-1111 doi: 10.1016/j.cub.2009.05.028

“Everybody laughs the same in every language because laughter is a universal connection. ”
Yakov Smirnoff

I went two years without cable, relying on Netflix and Hulu+ for most of what I wanted to watch.  With a presidential election looming, however, I simply couldn’t resist the siren song of endless punditry paraded out in front of me on every cable and broadcast channel for the next couple of weeks.  I knew if I got cable for that purpose, I’d also once again lose hours in front of the television laughing as people pawn their family heirlooms and useless junk, try to survive on a remote tropical island, and speculate about ancient astronauts, UFO conspiracies, and the end of the world.  I think I love watching that stuff almost as much as I love watching straight up documentaries about the origins of the universe or animal behavior, even when (and maybe especially because) it makes me lament the lack of critical thinking skills from some of the people on these shows.

So I gave in and got cable again.

And, true to form, if I am home the television is on.  So, unsurprisingly, I was doing some work one morning last week with the TV on when my attention was caught by the sound of laughter.  I looked up in time to see this commercial:

This may be just a commercial, but it is delightful  I found myself laughing along with it as I watched.  I laughed again when I tracked the video down on YouTube.   Laughter, as we see from this ad, knows virtually no boundaries.  Not age.  Not race.  Not gender.  We are all capable of laughter, from the beginning of our life until the end.  This means it is an integral part of our nervous system, as well as an important behavior.

When do we begin laughing, and how does our laughter change as we grow older?  I’d originally thought to write about development of laughter, but I got sidetracked by the fact that the answer to these questions, and indeed the questions themselves are anything but simple since laughter is such a complicated subject.  For example, Meyer, Baumanne, Wildgruber, and Alter (2007) mention an intriguing point about laughter and why it is of interest to researchers.  They report on a widely held opinion that laughter may be a link between animal vocalizations and human speech, with the focus on the affective component of vocalizations across species.  Because laughter takes advantage of our vocal apparatus, and is presumed to have a social and communicative function, understanding laughter is tied to understanding how it is similar and how it is different from speech.  This was one of the surprises as I was looking into this, and in retrospect I guess it shouldn’t have been.  But I always simply considered that we speak, and that we laugh, and never stopped to realize that we often do both together.  Or that the same structures we use to speak are also used to laugh.  It wasn’t until I was writing up my last blog entry, and reviewing Darwin’s book on emotions that it occurred to me that they are probably very related in the brain.

Interestingly, according to Meyer, et al (2007), there is no “laughing center” in the brain.  While the same might be said of language, there are clear areas associated with language in the brain, most notably Broca’s area and Wernicke’s area.

The insular cortex.  Click the picture to read an interesting blog entry about the insular cortex.

They say that laughter seems to be more distributed in the brain.  Major emotion centers of the brain, particularly structures found in the limbic system (such as the amygdala, the thalamus, and the hypothalamus) become active when we laugh, along with many structures from the frontal lobes to the brainstem that mediate motor behavior (for the physical behavior of laughing).  When participants were exposed to laughter, backwards laughter, and silence, the amygdala only became active to the sound of regular laughter.  They suggest that the amygdala, the insula, and areas of the superior temporal lobe particularly mediate the perception and affective responses to laughter (Meyer, et al).  Incidentally, this blog has made me very curious about the insular cortex, since it seems to play a special role in socially mediated emotions, such as embarrassment, among other things.

So I think it’s kind of fitting that an advertisement became the inspiration for this blog entry.  An ad is nothing if not an attempt to communicate, to evoke some kind of emotion from the person viewing it.  In this case, the makers of the ad want to sell you a car, but they chose to go about it without ever once showing you a picture of said car or using much in the way of language (and in fact, no spoken language at all).  Instead, they use a fundamental human behavior, one that taps quickly into the emotion centers of our brain, such as the amygdala and the insula, to evoke an emotional state in us that they undoubtedly hope you will associate with their product.

Most importantly, however, I like to think that the makers of this particular ad also wanted to remind us how integral laughter is to the human condition.


Meyer, M., Baumanne, S., Wildgruber, D., & Alter, K. (2007). How the brain laughs: Comparative evidence from behavioral, electrophysiological and neuroimaging studies in human and monkey. Behavioral Brain Research, 182, 245-260.

I recently visited my mother, who has been in a nursing home with Alzheimer’s Disease since July 2008. Her health is very good, but she has lost nearly all ability to speak, and mutters incoherently a lot, with a recognizable word here and there. She can’t walk, or care for herself at all.  In many ways, the progression of the disorder has been about as typical as can be expected.

I was struck, however, by a new set of behaviors I saw on this visit that have recently emerged. Though she cannot walk, she moves her legs all the time, crossing and uncrossing them, even in her sleep. Her tongue also moves in and out of her mouth, over and over again, involuntarily. But the most interesting new behavior to me was laughter. She laughs all the time. She just bursts out with a chuckle, or sustained laughter interspersed with a mix of muttering and the occasional word. We would say something to her and she would laugh. My sister would ask her a question and she would chuckle. We would sing to her and she would giggle. We would wheel her outside, and she’d laugh as we moved through the corridors into the elevator.  I don’t know whether these new behaviors are part of the dementia or indicative of something else; her doctors are currently assessing them.

This has piqued an interest in laughter on my part. It bears some similarities to yawning, a topic I recently wrote about in this blog. Like yawning, laughter is a common, highly stereotypical behavior that is phylogenetically older and far more complex than it appears at first blush. Naturally, it is of interest to scientists, particularly evolutionary psychologists and neuroscientists. Not only are we interested in the physiological and perceptual activity that provokes laughter, we are also interested in the evolution of such a behavior.  I thought this was a great opportunity to explore the behavior of laughter.

As is often the case with me, when I become interested in something I try to start at the beginning. Those of you who have taken courses from me know I have a great fondness for the history of the discipline of psychology, and talk about it often. It’s fairly common to find that the ancient Greeks wrote about various phenomenon. Such was the case with yawning, with both Aristotle and Hippocrates writing about it. The same is undoubtedly true of laughter, though my research begins with sources more recent than those from ancient Greece. Darwin (1872) published an entire book on emotional expression, and included a chapter (Chapter VIII) entitled “Joy, High Spirits, Love, Tender Feelings, Devotion.”  What I enjoy so much about these older references is the Victorian-era tendency toward excessive description of behavior, and other natural phenomena. In that chapter Darwin brought together many contemporary sources to provide a detailed description of the facial expressions that accompany laughter and smiling across species (yes, other species besides humans smile and laugh), as well as the musculature involved. He talked extensively about the contraction of the zygomaticus (upper cheeks) muscles which pull the ends of the orbicularis oris (mouth) muscles out and up for smiling and laughing.

Duchenne smile

Duchenne artificially stimulates the muscles of a man with facial paralysis.

Most importantly, Darwin and others (including a pioneer of this work, Duchenne) talk about the role of the eyes in smiling.  Duchenne (1862, as cited by Darwin 1872) found he could produce a smile by applying electrical stimulation to the zygomatic muscles.  However, when photographs of that type of smile were compared to genuine smiles, as Darwin himself ascertained, people readily picked the genuine smiles out from the artifical ones created by the stimulation.  This led many to talk about social smiles, those smiles that never quite reach the muscles of the eyes, which we do not have voluntary control over when expressing emotion (unlike the zygomaticus).  In fact, Duchenne advocated that the muscles of the eyes, which contract when we smile causing the skin around the eyes to crinkle, are only involved when the emotion behind the smile is real.  A recent study, however, suggests that people are capable of producing fake smiles that are indistinguishable from fake or social smiles (Krumhuber & Manstead, 2009), but more often than not when they are looking at dynamic, video stimuli, which probably involves other cues.

My guitar

My guitar, which I don’t play often enough anymore.

Darwin (1872) also talked at length about the sound of laughter, and speculates that it is the expression and communication of joy, such as might occur between a parent and their offspring being reunited.  This fits in well with his hypothesis that the expression of emotion serves a communicative function.  He found the peculiarities of the sound of laughter interesting, and speculated that, since it uses the same physiological mechanisms that produce screaming and crying and other forms of vocal communication, that it needed to sound as different from those as possible.  This idea, which I think he’s right about, always makes me think of musical instruments, which can produce a myriad of auditory combinations from the same, limited set of available sounds.  Imagine a guitar, which has a mere six strings, each with a different pitch attached.  Then think about all the different songs you have ever heard played on a guitar, some slow and sad, some fast and joyful, all produced from those same six strings.

It probably hasn’t been lost on you that I’m sticking mainly with a description of laughter (and smiling).  This is on purpose, and it goes back to Mom.  Do I think Mom’s laughter is the result of her being happy all the time and finding everything funny? I wish that was the case. But, while it would be at least a little comforting to think that her general emotional state is one of happiness, I doubt there is much genuine emotion or awareness behind the laughter. When I look into her eyes while she is laughing, all I see is a kind of benign bewilderment, and I think the world must be a very confusing place for her now.  What is more likely, though I cannot know for certain, is that the cortex in her frontal lobes has degenerated so significantly that their inhibitory effect on some of these behaviors is almost nonexistent. Still, it is curious that she laughs rather than other, more negative expressions.  So I take comfort in that, as well as the fact that she does not appear to be fearful.  While Duchenne did not really study laughter, the first time I saw her involuntarily smiling and laughing made me immediately think of the gentleman with facial paralysis in the research by Duchenne.  Here, however, there is no man administering a mild electrical shock to the muscles of my mother’s face to make them contract.  Instead, something far more terrible has happened inside of her to the parts of her brain that make her who she is.

In future entries, I think I will continue with the laughter topic.  I want to talk about brain structures involved in laughter for the next entry, since we now understand more about that. And I want to delve into the evolution of laughter.  I have also looked a little into the pathology of laughter, because I want to find out more about my mother’s condition, but there is surprisingly little information about dementia and laughter.  I will report on anything I find out about that here, however.  As always, my interests lie less in abnormal behavior and pathology and more in everyday, normal behavior, so that’s what I will likely focus on.  My mother’s involuntary laughter is the impetus for my curiosity, but I realized that I have never once really thought about the behavior of laughter, or taken a moment to really appreciate it as an important and complex behavior.

Maybe this is yet one more gift from my mother.


The title of this blog entry is from The Illiad by Homer, describing the laughter of the gods.


Darwin, C. (1872). The expression of emotion in man and animals. London: John Murray.

Duchenne (de Boulogne), G. B. (1862). Mécanisme de la physionomie humaine ou analyse électro-physiologique de l’expression des passions. Texte: Première partie. Deuxième édition. Paris: Librairie J.-B. Bailliere et Fils.

Krumhuber, E. G. and Manstead, A. S. R. (2009). Can Duchenne smiles be feigned? New evidence on felt and false smiles.  Emotion, 9(6), 807-820.

“’Tis now the very witching time of night, When churchyards yawn and hell itself breathes out Contagion to this world”

–William Shakespeare

Yawning is very much on my mind today, as I settle in to write the last blog entry in this particular series.  I recently decreased my caffeine intake, from four large cups in the morning and several sodas or cups of coffee during the day to two large cups of coffee in the morning.  Two things inspired the change.  First, I was beginning to have a lot of difficulty falling asleep, and would often find myself awake at 4am with a morning class looming on the horizon. Since I am not a morning person, this became increasingly uncomfortable, not to mention all that yawning (sometimes in the middle of lecturing!).

Secondly, I discovered the wonders of French press coffee by whim shopping online one night when I couldn’t sleep.  Yes, the irony that I bought something to keep me awake one night when I couldn’t sleep was not lost on me. The French press I bought was a 32oz pot, which is two cups worth in my favorite coffee mug.  I can’t begin to describe how delicious French press coffee is—I can’t drink coffee any other way now.  Of course, I could just buy a bigger French press, but I figured it was good way to motivate myself to cut down.  It seems to have worked, since my sleeping patterns have normalized, and I have less trouble falling asleep when I go to bed.

The other reason yawning is on my mind today, in particular, is due to a text message from a friend who is a morning person who doesn’t realize that not everyone is awake at 7am when there are no classes in session.   So I’ve been yawning up a storm today, despite trying to keep my mouth closed and breathing through my nose (which really does work to decrease the frequency of yawning; I’ve been informally tracking that all summer in myself).

For this last entry, I want to take a look at yawning as a symptom.  Yawning is a seemingly simple behavior, though as we have learned over the last several weeks  it is a complex and little-understood behavior.  All humans, as far as we know, yawn, and we all yawn in the same, stereotypical way.  Even people who are profoundly paralyzed and can barely move a muscle still yawn (though not contagiously) as well as people who have had everything but their brainstem removed (Provine, 2005).  Interestingly, Cattaneo, Cucrachi, Chierici, and Pavesi (2006) document two patients who suffered strokes in their brainstem who developed excessive yawning as a result, further suggesting that the control of yawning is located in the brainstem and medulla.

Changes in yawning frequency are also associated with certain medications, particularly SSRIs, which are used to treat anxiety and depression.  Taskapilioglu, Akkaya, Sarandol, and Kirli (2009) documented the case of a female patient who began to yawn excessively while taking an SSRI for anxiety.  Other researchers have noted excessive yawning for patients taking SSRIs (Chen and Lu, 2009; Gutiérrez-Álvarez, 2007).  Beale and Murphree (2000) took a closer look at this side-effect in two case studies for individuals being treated for major depression using SSRI’s fluoxetine and sertraline, among other medications.  Both developed excessive yawning within 14 days of the start of treatment.  In one of the cases, the excessive yawning continued across three SSRIs and only went away when the medication was discontinued.  Yawning is such a notorious side effect of the drug Lexapro that the symptom is often referred to as The Lexapro Yawn.

Daquin, Micallef, and Blin (2001) provide a nicely detailed overview of various other pathologies that are associated with excessive yawning.  The disorders cover a broad spectrum of categories, and include neurological and psychiatric pathologies as well as physiological, infectious, and metabolic.  Lets take a look at some of the pathologies associated with central nervous system disorders.  People who suffer from migraines often experience yawning before, during, or after an attack.  Research has indicated that people who suffer from migraines may have a hyper-sensitive dopaminergic system.  We learned in an earlier blog entry that dopamine plays a role in yawning as well, with yawning often triggered in humans and animals by the administration of a dopamine agonist, such as apomorphine.  As an added bit of evidence, people who have Parkinson’s Disease tend to yawn much less frequently than normal, due in part to the dopamine deficiency that is a hallmark of the disorder.  Given that dopamine levels in the brain are also related to schizophrenia, yawning is often seen as a symptom in that disorder as well.

As I mentioned earlier, in the blog post about causes of yawning, I think neurotransmitter regulation, or at least neurotransmitter levels, is the place to look for causes.  There is a very long list of neurotransmitters associated with yawning, particularly dopamine and serotonin, and the appearance of excessive yawning as a side effect in many disorders, either as a natural part of the disorder or as a result of medication seem to support the idea.  I’ve really enjoyed reading and writing about yawning, and haven’t even really scratched the surface of the phenomenon.  I will probably update this blog on yawning research as I come across it in the future.

To close out this round of blogging, I’d like to thank my students in the Summer II 2012 session of PSY 229 Introduction to Biological Psychology at Cedar Crest College, who have been blogging on a variety of topics along with me.  It’s been fascinating to read your blogs on many levels for me.  Since this is an online class it’s hard for us to get to know each other.  Your blogs have told me a lot about who you are as people and what you find interesting about brain and behavior.  I appreciate all your hard work on this assignment, as well as your insight and research that you have all so enthusiastically shared with each other.  I hope you have found the assignment as enjoyable as I have, not only in terms of sharing your interest and knowledge, but also reading the blog posts of your fellow students.  I especially hope that some of you will continue the practice of blogging, if not necessarily about brain and behavior, at least about those things you find especially interesting as you continue your education.  Writing about something is a tremendously beneficial scholarly activity and I encourage all of you to do it regularly.  You will not regret it.


Beale, M. D., & Murphree, T. M. (2000). Excessive yawning and SSRI therapy. International Journal Of Neuropsychopharmacology, 3(3), 275-276. doi:10.1017/S1461145700001966

Cattaneo, L. L., Cucurachi, L. L., Chierici, E. E., & Pavesi, G. G. (2006). Pathological yawning as a presenting symptom of brain stem ischaemia in two patients. Journal Of Neurology, Neurosurgery & Psychiatry, 77(1), 98-100. doi:10.1136/jnnp.2005.075267

Chen, C., & Lu, M. (2009). Venlafaxine-induced excessive yawning. Progress In Neuro-Psychopharmacology & Biological Psychiatry, 33(1), 156-157. doi:10.1016/j.pnpbp.2008.10.014

Daquin, G., Micallef, J., & Blin, O. (2001). Yawning.  Sleep Medicine Review, 5(4), 299-312. doi:10.1053/smrv.2001.0175

Gutiérrez-Álvarez, Á. M. (2007). Do your patients suffer from excessive yawning?. Acta Psychiatrica Scandinavica, 115(1), 80-82. doi:10.1111/j.1600-0447.2006.00856.x

Provine, R. R. (2005).  Yawning.  American Scientist, 93(6), 532-539 doi: 10.1511/2005.56.980.

Taskapilioglu, O. O., Akkaya, C. C., Sarandol, A. A., & Kirli, S. S. (2009). Pathological yawning in a patient with anxiety and chronic disease anaemia. Journal Of Psychopharmacology, 23(2), 211-213. doi:10.1177/0269881108089812