Are you a prairie vole or a meadow vole?

Can you believe that less than 5% of all mammals are long term monogamous?  Whereas 90% of birds stay with their mate for life.  These are a few of the interesting tidbits I came across while doing some reading homework on sexual motivation.

I think voles are much cuter than lab rats, don't you?

But I think the most interesting story starts with a couple of voles.  Voles are small mammals similar to mice.  The genetic variation between a meadow vole and a prairie vole is nearly zero yet they display almost completely opposite behavioral characteristics.  Prairie voles are how we human would like to view ourselves.  They pair-bond with their mates and act more or less monogamous by sharing a nest and defending one another.  When they have a litter, they demonstrate better parenting and care for their young for a longer time than their meadow counterparts.

In fact, I think this song fits my characterization of meadow voles:

They don't make for life, share a nesting ground, or care for their young any longer than is strictly necessary.  Yet these two species are nearly identical in genetic make up.  What's causing the difference in their behavior?

Well a bit of research into their brain structures revealed a rather interesting set of differences.  The prairie voles had more receptors for two very specific signal molecules when compared with their meadow counterparts.  In the female prairie voles, there were more oxytocin receptors in circuits related to the reward pathways in their brains.  I mentioned oxytocin in a valentine's day post so feel free to reference back to that for more details on its effects.  But the basics show that it increases motherly behavior in the females.

The other change was found in the male prairie voles.  They show increased numbers of vasopressin receptors in the ventral pallidus.  This signal has sometimes been linked to aggression in the context of mate-protective behavior.  Thus it makes the males more likely to stick around and protect the family.

The brain images on the left are of the males and on the right are the females.

Turns out, there's a short "microsatellite" piece of DNA code that allows for the additional production of these receptors and the bonding behavior seen in the prairie voles.  And while you may think, what's this got to do with me?  Well, there's currently evidence coming to light that that these same systems are in play in human systems as well.  Surely it's a more complicated system but what does your DNA code your behavior towards?  Do you know?

Science on the Radio

I'll be the first to admit that I'm in love with NPR.  My childhood revolves around car trips listening to Prairie Home Companion and long summer afternoons in the garage surviving the Texas sweltering heat by turning up Car Talk.  But while these will always be a part of my identity and connection to my family, I've found a whole new program which meshes beautifully with my passion for neuroscience.  I am referring to, of course, the wonderful programming of radiolab.

I first heard the program while driving home on a pleasant spring day.  It was either their program on sleep or stress but what I really recall was my inability to tear my ears away from the speakers.  I rushed indoors and immediately turned on the stereo inside the house, not wanting to risk missing a single bit.

Really, I just can't support the program enough.  Jad Abumrad and Robert Krulwich have this great interplay between each other.  One plays the cynic while the other holds out for the brightest conclusion on the many scientific discoveries and experiments explored in the show.  I love that they characterize inanimate things like genes to make biological processes become a beautifully woven story.  I would kill to become one of their researchers and get to interview all the fascinating folks of the science world which they bring in.

I'm sure I seem to be rambling but if you're reading my blog I assume you have an interest in biology or neuroscience or just like to expand your horizons.  If any of these are true, I highly suggest tuning into radiolab.  You can get free podcast versions on itunes, play them directly from the sight, or donate to WNYC to help support the show and get several episodes on a complimentary thumbdrive.

Let's support those who help bring science into the modern world!  It's a complicated story but when told right, it becomes a work of art.

Blame my genetics

I must say, for as hard as I work out I'm always sorely tempted to over eat.  There are so many savory, delicious places to eat in Austin that I'm only beginning to discover.  Gourdough's elaborate donuts covered in all sorts of things (brownies, bacon, gummy worms and more!)  But while I can get myself to salivate over these fabulous treats, I know I can make myself sick from eating too much.  But not everyone can sense that line of where to stop and it's in part due to their genetics.

An example of Gourdough's extravagant donuts.

And while  know the idea that genetics controls your overall body type and weight, I never understood the specifics until now.  Gordon Kennedy was the first to describe the "lipostatic hypothesis" which states brain receives signals about the fat storage of the body and tries to keep it in equilibrium with either feeding behavior or lack of eating.

But sometimes the brain can't receive this signal.  Certain genetic variations lack a specific piece of code that produces a protein.  This protein, now known as leptin, sends the message to the brain that you're full and to stop eating behavior.  But if you lack the genetic code to produce leptin, you're brain thinks you are in a constant state of starvation.  Not only do you feel constantly hungry, your metabolism slows down (as if you are trying to hang on to those last bit of energy producing fat).

Now I'm not here to say that this explains the obesity epidemic in America.   A complete genetic knockout of leptin is fairly rare and can be treated with hormonal replacement therapy.  And of course there are numerous other processes, both in the brain and the gut, that regulate body shape.  But I find it fascinating that we don't have as much control over our appetite.

With all the current hype on the
movie, I couldn't help including
one of my favorite books.

And a special shout out to my friends cutting weight for Taekwondo National Collegiate Competition.  You might be fighting your genetic homeostasis but those few pounds lost will make all the difference in the ring!  Not to mention, we'll be sure to indulge in some of the best food Austin has to offer to bring those leptin levels back up.

Motivation reward? Or frustration?

*Note: Apologies!  I know I usually post 3 times a week but it's been a bit of a trial getting back into the swing of class after spring break.  Not to mention I had a major paper due this week but I will be much more consistent in the future.

At first, I wasn't sure which topic I wanted to discuss as I enter the subject of motivation.  But as I read my Neuroscience: Exploring the Brain, I stumbled across a rather fascinating example of the disconnect between animals studies and application to the human system.

The setup starts with a simple rat test of motivation.  A rat is implanted with electrodes in its brain which, when the animal shows a specific behavior like pressing a lever, it receives a jolt of current in that brain region.  When the electrodes are properly placed, they affect the dopamine pathways between the VTA (ventral tegmental area) and the striatum or prefrontal cortex.

This has long assumed to be a reward pathway due to the behavior of the rats once they learn the trick.  After the rats connect pressing the lever with the stimulation, they will continue to press the lever as much as possible to get that "fix."  It can even get to the extent that the animals with ignore food and water and exhibit only the trained behavior until they collapse from exhaustion.  But what if what the rat is experiencing isn't actually pleasure?

This diagram helps clear up the basic
pathways of dopamine.

Human trials of this nature are (obviously) unexploited.  But the few times that scientists have implanted electrodes into human brains, it has been to deal with disorders like schizophrenia and severe epilepsy.  And when we sample this population, their self stimulation doesn't seem to be providing that orgasmic reward as expected.

The two examples I read describe the observations of Robert Heath on a couple of patients he assisted at Tulane School of Medicine n the 1960s.  One man, when asked what it felt like to self stimulate the  septal area of his forebrain, reported that it was similar to the feeling of building up to an orgasm.  However, when he tried to repeatedly use the stimulation he was left with the frustrated feeling of incompletion.

The other man focused on medial thalamus (though he had other electrodes in different parts of his brain which he could stimulate).  When asked why he repeatedly stimulated this region when it left an irritable sensation, he replied that it was like the feeling of that moment before you recall a memory.  He would continue to self stimulate on the hope that  it would finally dawn on him, though it never did and he was left as frustrated as the first man.

Robert G. Heath of Tulane

Of course, these case studies are no where near perfect.  Both subjects had severe mental discrepancies from the average population.  And the location of their electrode implants are not identical to those found in the rats.   Lastly, it's a very small subject pool shown here.  But we must admit that the experiences of these men leave room for doubt.  Maybe the rat pushing the lever isn't feeling pure euphoria.   Maybe it's just on the cusp and frustratingly can't reach the peak.  We can't be completely sure.

British Virgin Islands

Sorry I've been away for so long but this past week was my university's spring break.  To celebrate the freedom from school, my family took a trip to the British Virgin Islands to sail the seas for a week.  It was an amazing experience where I got to learn to sail, spent hours viewing reefs and their inhabitants, and finally catching up on my much needed sleep.

But while I was snorkeling my time away with all the tropical fish, I found some of the invertebrates didn't have the most savory reputation.  No, I didn't run into any sharks or jellyfish (which are actually my greatest fear).  But I did spot a small, rather unassuming fish which was none other than the puffer fish.  Sometimes called the "fugu" (or 河豚 in Japanese), this fish carries a toxin in its liver, intestines, and skin.  Some Asian countries treat the fugu as a delicacy though chefs must be specially trained to cook the less tainted parts and know just how much is safe to serve.

I don't know the species but this is the exact type of puffer I
saw 3 separate times.

The toxin, called tetrodotoxin, induces light-headedness and a numbing of the lips.  Often this is why the fish is consumed, sort of like imbibing alcohol for the less toxic effects.  But if too much is consumed, it leads to vomiting, a prickling sensation all over the body, rapid heart rate, and some paralysis of muscles.  In bad conditions, it will paralyze the person's diaphragm, making it impossible for them to breath on their own.

Another toxic critter I saw was the cuttlefish.  During our swim around the Baths on Virgin Gorda, we saw a school of 5 cuttlefish swimming along the sandy part of the ocean floor.  I recalled hearing they were poisonous as well so I did some research when I got home.  These guys have a powerful neurotoxins contained in their saliva produced by the bacteria that make their home in the mouth.

I rather thought these little guys were cute!

So I guess my trip wasn't completely devoid of learning.  Next time I'll have to make it a point to do my research before hand and see what other interesting animals surface.

Bicycles and the Basal Ganglia

When I first understood that the basal ganglia is necessary for creating procedural memories, I immediately thought of learning to ride a bike.  Nothing could be more iconic of a learned behavior in humans than those first few tentative pedal pushes as you learn to navigate the two-wheeled beast.  Personally, I'm an avid cyclist both as a commuter and for simple pleasure.  I ride my bikes every single day, yet if you asked me I would be unable to explain all the minutiae of adjustments my body makes to keep me in the seat.

One of my friends plans a monthly ride to explore the city and hit up
some of the coolest bars of Austin.

The ability to ride a bicycle, along with many other habitual actions, rely on the processing of the basal ganglia.  This collection of nuclei are vital for what I consider "physical memory."  The basal ganglia receives general input from the cortex, processes it, and then sends it through the ventral lateral nucleus of the thalamus and on to the frontal cortex.  The frontal cortex is then responsible for issuing a command via the motor cortex for the body to actually do something.  This integration with the motor circuit explains why procedural memory is affected when the basal ganglia is damaged and not declarative memories.

The type of damage that the basal ganglia can receive changes how the afflicted person or animal will act.  Two classic diseases- Parkinson's and Huntington's- have symptoms at opposite ends but due to damage in the same structure.  While it's true that each lose function in a slightly different pathway, it would be a little ambitious of me to try to explain the circuitry with only words.

Let's just leave it with the understanding that the diseases cause damage in slightly different ways.   With Parkinson's, the damage leads to a slowing or even lack of movement.  These are called, respectively, bradykinesia and akinesia.  And at the other end of the spectrum is Huntington's where patients experience hyperkinesia.  It's as if they can't stop themselves from making too much movement.

This figure helps identify some of the structures
within the basal ganglia.

In these two diseases, the ability to moderate inhibition or disinhibition seems to be lost.  So there's either a surplus of movement or a dearth of it.  Research into how the damage occurs and ways to prevent it continue.  But I'm happy to say I have a well-functioning basal ganglia and I can continue to ride my bike to my hearts content!

Science is Hard!

Remember back in the good old days when teachers said "Here's how this works! Just learn the process." and that was it?  I wont disagree that there's a certain element of boredom involved with that style of learning.  But this semester is teaching me that performing real science is so far beyond rote memorization.

It's not easy to get access to up there, huh?

Currently I'm working in a lab on my college campus.  I'm just an undergraduate research assistant but our project is relatively small so I get to handle all aspects of the actual research.  When I first volunteered for the position, I thought all the procedures and general direction of the project were pretty obvious.  We're doing a longitudinal study so it breaks up into neat little chunks.

But halfway through the semester I'm seeing all these sources of error!  I have a bit of OCD and sometimes I wonder whether that's a blessing or a curse for doing academic research.  Let's start with the fact that I do human research.  So we had to start by getting a big enough sample size.  We didn't have grandiose expectations yet you'd be surprised on how difficult it is to even get 10 people to it your research criteria.  There are all sorts of things that can eliminate a person from a psychology study.

And even when they do make it past initial screening, you have to remember that these are people you're dealing with.  People, unlike lab rats, have schedules and plans and can't be kept in a cage in the lab.  So you have to keep an eye on your participants and make sure they keep up with the requirements of the project.  This is particularly important for longitudinal studies.

Ah, and we must also remember the fallibility of technology.  For all the good its done us, our tech is never perfect.  You can have faulty wires or computer programs that wont run or even run out of materials.  Just today, my lab ran out of circular adhesives to use with the EEG and had to run a makeshift version of our preferred methods.  And I've had times when batteries nearly died and the electrical leads on the EEG decided to stop working.  There's just so many little places for a slip up to affect your data.

Obligatory cute baby picture!  Though really I meant to
say I'm still young in my training.

Yet, in a weird way I love that variability.  It makes science hard, but it also keeps it interesting.  You're always striving for the perfect run and the most accurate results.  And a truly good scientist learns to compensate for all the possible external factors.  Trying to design the cleanest. most efficient, most reliability study appeals as an interesting study for me.  But for now, I hope to continue to learn in my current position.

Why Cab Drivers Have Better Hippocampi

Ok, so the title is a little ludicrous.  Cab drivers don't necessarily have better hippocampi.  However, there is evidence that they have better trained hippocampi, so to speak, which allow them to process spacial information in a more efficient manner than the average person.

The hippocampus is a structure in your brain that looks a bit like a couple of protruding fingers horizontal with the temporal lobes.  It's primary function has to do with memory, both consolidation and recall.  In my previous posts I've mentioned examples such as H.M. (Henry Molaison) and others like him who suffered from a deficit in the hippocampus.  But now I want to show how a brain structure can also become better at its function, not  just worse.

The hippocampus is here hi-lighted in blue.

This study originated in the ancient city of London.  Like most old cities, the roads don't form a grid pattern.  Instead they form curves and loops in a jumbled mess like a knotted ball of string.  Also, the streets are not numbered in sequential older like the modern cities of today.  The names are assigned from times long past which makes for some confusing navigating.

Yet a recent study found that the cab drivers of London have more developed hippocampi than those of the average person.   The first instinct was to say that people who have better spacial memory naturally would become taxi drivers.  In other words, a simple correlation could be responsible for the connection they observed.

But further testing allowed for a more definite picture.  The researchers took participants who were training to become taxi drivers in London. (The test to become a cab driver requires that you know 320 routes, 25000 streets, and 20000 landmarks.)  The measured the participants early in their training and found average hippocampi.  But after the participants earned their cab license, the researchers took a second measurement system.  Indeed, the hippocampi of the newly minted cab drivers were more developed, proving it was the training leading to causation of brain change and not just correlation.

Just looking at this map of London increases my respect
for the cab drivers who navigate it.

So next time you think that taxi driving is a brain-rotting job, remember that your cab driver probably has a bigger hippocampus than you do.