Are you feeling sleepy yet?

Today I found myself almost unable to control my dozing during my early morning classes.  It was a struggle to keep my eyes from drooping as my professor went on about the differences between mean and median.  Having the covered the information before in middle school, my sense of focus was severely limited.

While this may seem the every day experience for many college students, I found myself mentally drifting into a train of thought composed of how tired I am and how I can get more sleep when really I need to be spending so much more time studying.

No matter how much coffee I have, I sometimes end up like this.

I've often wondered about the healthy balance between sleep and pulling those late nights to cram for an impossible test.  But because of a little good luck and some diligent hard work, I'll finally get to find out.

In other words, I'm currently serving as an RA (research assistant) for Professor Schnyer of the Psychology Department here at UT.  I found out about the opportunity last fall but only this spring have had the chance to really get my feet wet.

The current project I'm focused on is called the chronic sleep restriction study.  I'll be tracking 10 participants through the semester by measuring the amount of sleep they get each night and comparing it to cognitive functioning.  I really ought not to say anymore in case there's someone reading this who'd like to participate.  Can't skew the data after all.

But really I'm just so thrilled to be doing real research and getting real hands-on experience.  As the only RA involved with this particular study, I'm taking the lion's share of the work.  I've become acquainted with EEG (electroencephalogram- which measures brain waves off the surface of your scalp) protocols and soon I'll be moving on to the actual data processing portion.  I find it absolutely astounding to be doing real research and not some monotonous, lackey's task.

We use a more modern EEG but this particular readout is
showing the alpha wavs which occur right before sleep
(or when you're drowsy).

And for all those UT students out there who worry about the future, I have some simple advice to give.  Go out and seek opportunities in the areas you're interested in.  The fact that we attend such a big school just means there's even more variety and opportunities to discover.  And if you end up finding what you're doing isn't your passion, at least you got to find out early on.  I can't stress enough how getting actual experience outside of class is important!  It's more applicable to what you'll actually be doing in the future and will impress future employers to give us that leg up in life.

It's a brain, not a computer

Analogies serve as great teaching tools.  They help you piece together how a system works by comparing to something you experience in everyday life.  I use heuristics all the time to help get the main points from my lectures in school.

But there's one comparison I hear in the every vernacular which sort of drives me crazy.  Your brain is not a computer.

Your brain can't be simplified to a few gears either.

I can appreciate people comparing the body to an organic machine.  Many of our systems are similar to something you'd see an engineer working on.  We have a bone structure like the metal frame of a building. We "burn" food through metabolic processes to make energy much like a car burns gasoline.

But a brain is so much more than a computer!  A computer can only fulfill the tasks it's programed to do. It can't rewire itself to account for damage or learn new behavior patterns.  True, the brain uses massive parallel processing which can make it slow as compared to the modern laptop or even iphone.  But part of what makes the brain so beautiful and amazing is its capacity for change.

This change happens at all levels, from full circuits partially or fully reconstituted after damage to the individual neurons.  In fact, recent research has found that individual synapses are capable of change.  You literally can rewire your brain by individual cells.

Today my class went into the mechanisms for some of this long-term/short-term potentiation and just how the ions (yep, more ions) lead the cells to physically change and make the signal stronger or weaker.

If our cells can change, why can't we?

But what I really take away from this is our capacity for change.  Too often I hear people use the excuse "this is just how I am."  But we are malleable creatures.  We live and thrive by continuing to change.  I take this scientific message to mean to me that I can change on even the most biological level.  And if that's possible, why can't I make a concerted effort to always have those changes push me to be a better person?

It's a philosophical take on a scientific phenomena but appreciable all the same I think.

Channeling my Inner Ions

Ok, so I'm not sure that I made this hugely clear in my last blog post but the topics I'll be covering for about the next week will be a little on the detailed side.  It's important to delve into how a neuron works individually before plunging into the complicated world of systems and such.  Most of this will be a bit tough for the layperson to understand unless you've had a grounding in biology but I'm going to try to make today's post more about the interesting ways this information can be applied.

In particular, I want to talk about snails.

No, not these garden variety species you can find in your yard on a spring morning.  I mean the kind that can kill you.

http://www.pbs.org/wnet/nature/episodes/the-venom-cure/video-cone-shell-conotoxins/4416/

I bet you didn't know that there's a whole genus of snails called cone shell snails with deadly venoms, huh?  There are actually hundreds of varieties and each species has it's own unique blend of toxins.  It's used both defensively and for hunting prey as shown in the above videos.

So what the heck does this have to do with ion channels?  Well as you read in my last post, channels are what create the voltage along the cell membrane to send messages down the axon in a neuron.  Here's the thing, without the channels properly functioning you can end up dead.

Ion channel diseases, called channelopathies, are quite numerous.  They can cause heart arrhythmias, epilepsy, osteopetrosis (unwanted extra bone growth), and some kidney diseases.  They can also lead to malignant hyperthermia and paramytonia and a host of other medically diagnosable problems.

In all of these channelopathies, they have one thing in common.  They all have lost proper functioning of an ion channel.  Whether this allows too much of an ion to flow (aka- "leaky channels") or blocks them completely- they both change the permeability to cells to a single type of ion and the phenotypic results are staggering.

Now back to our story of the killer snail.  The cone snail's primary toxin affects the calcium channels of its prey.  It paralyzes the fish and then swallows it whole to be digested- yes, while it's still alive.  One might think the story ends there, but enter the pharmaceutical companies and researchers.  It turns out the con snail is a wealth of pharmacological discoveries waiting to found.  One of the most recent drugs developed from the cone snail's deadly toxin is called "ziconotide."  This drugs blocks calcium receptors, just like the original compound, but does so in a way that serves as a highly effective pain killer.  In fact, ziconotide is between 50 and several thousand times stronger than morphine!

General chemical formula for ziconotide.

So why isn't it dosed out to any patient that comes in with a stubbed toe?  Well such a powerful pain killer comes with its own set of problems.  The drug is not specific enough to target only the calcium channels involved with pain perception. (Keep in mind there are many varieties of every kind of ion channel with different levels of permeability.)  It actually can affect the calcium channels of muscles.

Calcium channels here are used to regulate muscle tone.  So if the conotoxin affects the muscles, it makes them relax.  This isn't a huge issue until you apply it to the smooth muscle of your artery walls.  If those muscles relax too much, your blood pressure will drop dangerously low, possibly to the point where you can't get proper circulation and you die.

Hence, the current research being done with conotoxin involves refining the compound to only affect specific calcium channels.

I bet you didn't think such a "small detail" as ion permeability could make such a big splash in the modern world.  But without knowing how ion channels work, many diseases would be untreatable and many medications unavailable.  I personally enjoy the bigger picture when it comes to biology.  I like knowing how systems work.  But if you're interested to learn more about ion channels, check out this website.  http://clm.utexas.edu/aldrichlab/ Professor Aldrich is a leading authority on the subject and a great lecturer/teacher as well.

The Wires in my Head

Today marks the beginning of our review in my neural systems class on the most basic principle of the neuron- the action potential.  It's a surprisingly complex phenomena which most people only understand as "a spike in electrical current the sends the signal down the axon to the terminal end."  You could see a series of spikes drawn in a textbook and anyone with a small background in biology could name it as an action potential.

This is a standard action potential drawn the
world over in physiological and biological
and neurological classes the world over.

But do they understand what it actually is caused by?  In my biopsychology class I was told the neuron receives chemical signals which when there are enough different signals from other neurons (spacial summation) or when it got enough signals within a certain time constraint (temporal summation), the signal would be passed along the axon of the cell in the form of an action potential to be used to spread the signal to the other cells.

So what's actually happening when an action potential occurs?  Well I'm by no means a teacher or a
professional writer but I'll try to explain to the best of my knowledge.  Bear in mind, this subject will be covered in multiple lectures in class so I suspect it will take me several blog posts as well.

Let's just start with the basics shall we?  The first question to really ask is what is an action potential?  Sure we all see the spikey line on a graph but what does it mean?  What you are seeing is actually the membrane voltage of the neuron change in response to the influx and efflux of ions.  Which ions? you might ask.

Well there are actually many ions involved with the regulation of cellular membrane in a neuron.  But for the most part, the work of the action potential is being done by two main ions: potassium and sodium.

Let's start with sodium (Na) since it's what initiates the action potential.  As the cell is receiving signals from the network, it starts to open (primarily) ligand-gated Na channels.  When enough of these are open, sodium -which is normally pumped out of the cell- begins to flood the cell.

Here's where it gets a little tricky.  The important things to remember are:

1. Sodium is being constantly pumped out of the cell (when there's no action potential) which sets up a gradient.  This "makes" sodium want to flow into the cell to put the ion at equilibrium but it must have specific gates open in the membrane to do so.

2. Potassium is being constantly pumped into the cell (except when, once again, the neuron is experiencing an action potential) which also causes an unequal distribution of the ion.  This gradient wants to move in the opposite direction of sodium.  That is, potassium wants to flow out of the cell if it can find the opening to do so.

3. Sodium is more positive than potassium.  Hence, because these two major ions have differing charges a voltage is created across the membrane with the inside more negative than the outside.

This image depicts the traditional sodium-potassium pump
which maintains the cell's membrane potential by keeping most
of the sodium on the outside and the potassium inside.

Now back to our story.  When enough of these sodium channels open, they set off a special kind of sodium channel which is voltage-gated.  That is, when the cell becomes positive enough, tons of these sodium channels open.  This is the upward part of the spike on an action potential.

The cause of the fall of the spike is for the exact opposite reason.  The sodium channels have a time-dependent element which makes them inactivate shortly after opening.  This stops the "depolarization" of the cell which is that upward part.  And as the sodium channels inactivate, potassium channels open up and potassium leaks out.  That changes the cell's membrane back to being more negative than the surroundings.  However, these additional potassium channels usually overshoot (though not in all neural cells) and hence you see the action potential dip below the line it started at.  This is called hyperpolarizing and it's during this period of time that the sodium channels are re-setting themselves for the next spike.  It's often called the refractory period because during this time the cell cannot fire because it's still resetting its various gates.

I know this is a lot of information to try to understand clearly but those are the bare bones of an action potential.  In actual life, there are an unbelievable number of variations on this general theme.  Some cells use chloride ions and some have different types of gates.  The numbers of the different gates vary across cell types and the overall population of these channels is only just being investigated.

I hope I've provided a little clarity on reading and understanding the picture of an action potential for those new to the topic.  I hope my further posts are more interesting and maybe a little more detail-oriented.

If you're more into circuits like some of my electrical engineer student friends,
this might be a little easier to understand. But honestly to me it looks super confusing.

A one (train) track mind

Today represented my first day of real classes for the new semester.  I know it's a friday, but with most of the week dedicated to syllabi and such it took until today to really get the ball rolling.  But I will say while my 8 am classes are rough (I'm a really huge fan of sleep), my neural systems class is promising to be enlightening and entertaining.

But onto the "meat" of my experience.  As my attempted-witty title implies, today's topic revolved around a train track.  Or the creation of a train track I guess.   It's a famous story I first happened upon in middle school.  My close friend, Max, was telling me at lunch one day about this guy who had a railroad spike go through his head and survived.  At the time, we just grossed each other out with our speculations about the amount of blood spilled during the accident and left it that.

The only known picture of Phineas Gage.

I don't think I could've realized how this little memory would reappear in such force 7 years later.  But there I sat in class and listened to the story of Phineas Gage.  It runs a little something like this:

Phineas Gage was a railroad constructor in the 1840s.  In fact, he was a well known foreman who was praised for his hard work and personable handling of his workers.  Well in the area he was working, the land was extremely rocky and hilly so they would blast the hills with explosives.  The procedure was in the dimple form of drill a hole, fill it with explosives, pack sand over that, leave blast zone, and blow the thing up.  However, the 1800s aren't lauded for the safety concerns shown by the working class.  And as luck would have it, Phineas Gage was in the process of packing in the powdered explosive with a tamping rod when his attention was distracted.  The rod scraped against some of the rock and created a spark which ignited the powder.  The explosion forced the rod up through his cheek and out the top of his skull.  According to witnesses, he fell to the ground and convulsed a few times but quickly regained consciousness.  His fellow workers carried him to an ox-cart by which he was taken into town to be cared for by a physician.

But the amazing part isn't just that he survived the massive blood loss.  Nor are we simply stunned that he could find a sense of normalcy after having a gaping hole left in his skull.  What truly fascinates me and my fellow neuroscience enthusiasts are the cognitive changes which resulted from his "run in" with the tamping rod.

Though our data comes from merely 2 reports given by the physician who first cared for Phineas and did a single follow up 14 years later, the reports are fascinating.  It seems after the injury Phineas became childish, obstinate, impatient, and lacking self control.  He lost his job and friends described him as no longer himself.  It was like he had become a whole new person.  So what elicited this radical change?

Enter modern technology.  Thanks to some sophisticated software, scientists were able to trace the pathway the tamping rod cleared in Phineas' head.  According to their measurements, it pushed directly through his ventromedial prefrontal cortex.  Though the prefrontal cortex is generally considered one lobe, it can be broken into different regions which process different types of information.  For Phineas, the part that he lost is highly tied to emotion regulation.  And believe it or not, emotion is extremely important for making good judgements!

The computer reconstruction of the
damage caused by Phineas' tamping rod.

Sadly, it was at about this point that the bell rang.  As engrossed in the story that I was, the next the class was filtering through the door and my stomach rumbled loudly in protest to the light breakfast from that morning.  So, my dear reader, I will leave you here.  I hope I've provided some food for thought!

Neural Systems II

Though I posted about wanting to send this blog in a new direction over the break, I was never really able to settle on how I wanted to go about it.  But thanks to my current favorite class, I have a "game plan" to make this blog both an interesting read (hopefully) and an excellent study tool for myself.

Because today in my Neural Systems II class, my professor made the point that we've properly learned when we're able to explain material covered in class to others.  In this past fall's class, I simply talked though the information with my classmates.  But many of the topics we'll be covering this spring are of intrinsic interest for most people.  Questions regarding memory, learning, and consciousness will all be brought up on multiple occasions.

This is the textbook we'll be using this semester- just as a little background.

Hence, to increase my comprehension on these subjects as well as help spread some neuroscience love- I'll be posting on this blog at least once a week concerning the material taught in class.  Please feel free to leave any comments or questions about the subject matter (though let me get going first).  Please be patient with me as I get this project started and I hope I'm able to convey some of the most interesting studies and research from the world of neuroscience!