put your science panties on (part 2)

 Last time, we covered the first part of the journey a neural signal takes on the way to becoming muscular movement.  We started at the brain and made it all the way down the nerve highway to a muscle. And it is here at the neuromuscular junction that you have been waiting with bated breath for the tale to continue.

When an action potential makes it to the end of the nerve road, it must make something happen in your muscles. The electro-chemical energy of the action potential must be somehow translated into kinetic energy. While your muscles are capable of creating large-scale movements like swinging a golf club, the tiny movements of the molecular structures of your muscles is where this kinetic energy is translated. So let’s get up close and personal with muscle structure.

Your muscles are like bundles of cords within bundles of cords- kind of like Russian nesting dolls- bound together by connective tissue. When you get down to the cellular unit, a single muscle cell is called a muscle fiber. A single fiber is made of smaller units called myofibrils. It is in these myofibrils that the basic contractile units of muscles are found. This basic contractile unit is called a sarcomere. Sarcomeres are made up of long proteins that slide past each other to make the muscle contract. These two stringy proteins are actin and myosin.

A relaxed sarcomere

Myosin filaments have these little bulbs hanging off called “myosin heads.” The myosin heads like to link up with the actin filaments. Through a process involving some supplementary energy molecules (holla, ATP!), the myosin heads creep along the actin filaments, bringing them closer together. Think of a little army guys (myosin heads) climbing along a rope (actin). This is muscle contraction on the tiniest level.

Contracted sarcomere

Just watch this. http://www.youtube.com/watch?v=zQocsLRm7_A&feature=fvwp

So, imagine that a whole bunch of sarcomeres are crammed into a muscle fiber. And a whole bunch of fibers are crammed into a single muscle. You’ve got tons of sarcomeres, working simultaneously, causing a whole chunk of muscle to squeeze in on itself.

Well that’s all well and good. But how is it that we’re so coordinated? I wouldn’t call Beyonce’s performance in the video for Single Lady “chunks of muscle squeezing themselves.” I mean, one muscle group is capable of a wide variety of motion, so there must be more nuance to it than  “chunks of muscle squeezing in on themselves,” right?

Right. This is where we go back to part 1- the innervation of the muscle. The complex maze of nerve fibers feeding muscle is responsible for the precise control we have over our movement. Your brain can selectively fire the pathways that feed just part or parts of a muscle. These different combinations are what make a smile different from a frown, from an inquisitive facial expression, from an embarrassed expression, from an amused expression. All use the same muscle groups, but each stimulates them in a different pattern.

The complex neural to motor pathway, to me, is one of the most intricately wired processes in all of Vertebrata, but always funnels down to one of the most basic: the little sarcomere. 

put your science panties on (part 1)

Let me warn you before you embark on this post: it’s a little more technical than usual. We’re going to cover the mechanics of both your nervous system and your muscular system, in our first ever two-part blog post (ooooh, aaaaaah!). So unless you have a solid 20 minutes or so, I suggest saving this one until you are at home with a cup of hot tea with Wheel of Fortune on in the background.

It’s easy to avoid thinking about how your muscles work because it can be an overwhelming thought. How complex they must be to be capable of lifting heavy things and also finite tasks like writing! And even MORE mind-boggling is the system that connects your brain to each and every muscle cell in your body. How in the cornbread hell can a simple thought turn into an intent, and then turn into an action? How can you go from thinking about scratching your head, to intending to scratch your head, to scratching your head? It is confounding.

Your brain has highways reaching out to all of your skeletal muscles. These highways are your nerves. Most of them exit your skull and travel along your spine in that clump called the spinal cord. From there, they branch out to your muscles.  A single one of these nerve cells is called a motor neuron, and is not a blob of a cell like you usually think of.  It has a body and a long skinny “stem” called an axon. They’re long and skinny because- well, they’re highways! In fact, the longest single neuron you have runs from the base of your spine to your toes- up to a meter long. Think of the motor neurons a giraffe has!

Figure 1: A single neuron.

These highway nerve cells are uniquely structured for carrying signals- chemo-electric signals- from your brain to your muscle cells. Your brain tells your muscles what to do via your nerve signals. But these signals are not “encoded” with information- one signal does not vary from the next, nor do they vary in strength. It’s kind of like binary code- it’s either a 1 or a 0. In this case, there’s either a signal, or there’s not. Your neuron fires, or it doesn't. One single signal is called an action potential.

An action potential is basically a change in voltage of the membrane of a nerve cell. It’s like this wave of voltage that travels along one nerve cell, setting off the one after that, and the one after that, and the one after that, and- well, you get the picture. But these nerve cells- their membranes in particular- are specially built for carrying action potentials.

Alright y’all. Time to put your science panties on. It’s about to get real up in here.

The inside of the cell is negatively charged, in respect to the outside of the cell. Positively charged potassium (K) and sodium (Na) ions are floating around, both inside and outside of the cell. There are little pumps in the membrane are constantly pumping these ions against their concentration gradients in and out of the cell to maintain a high concentration of K and low concentration of Na inside the cell- which maintains an internal charge of about -70 millivolts. This is called resting potential.

Figure 2: The basic set up of the axon of a neuron: The movement of Na+ and K+ ions  through channels and a pump
across a the membrane cause depolarization, repolarization, and hyperpolarization of the cell membrane (aka an action potential)

Now, let’s say the neuron’s dendrites become excited enough to set off an action potential. Little voltage-dependent sodium channels will open up, allowing sodium ions to diffuse along their gradient- into the cell. This influx of positively charged ions raises the inside voltage. This part is called depolarization, since the cell is becoming, well, depolarized.

Once the inside of the cell reaches about 40 mV (notice, that number is now positive!), sodium channels close and their neighboring voltage-dependent potassium channels open. Then, the potassium ions have their turn to diffuse along their gradient- out of the cell. This exodus of positively charged ions then causes the intracellular voltage to drop- bringing it back down into the negatives. These potassium channels are a little sluggish, though, and take a while to close. The cell hyperpolarizes a little past the original -70 mV, but is corrected quickly by the trusty Na/K pumps.

This process happens as a wave, traveling down the axon of a neuron. To help the process, a material called myelin wraps around the axon (Fig.1- the white bead looking things). Myelin is white (that’s why the neural tissue of your brain is white… white matter!) and is an insulator. This allows the action potential to skip right through the insulated bits, speeding up transmission to lightening fast speeds. That time you almost dropped your phone in the toilet but caught it right in time? Yeah, those lightening fast reflexes were thanks to myelin.

Once a neuron propogates an action potential all the way down to the terminal buttons, it sends chemical signals (neurotransmitters) out to the next neuron in line and excites its little dendrites- starting the process over. This occurs all the way down to the intended muscle site. And there, the muscle must take this action potential and turn it into kinetic motion. And kinetic motion is WAY more exciting than ion diffusion- so, stay tuned!

Now, I know that if you’re reading this part, you’ve read this entire blog post. And for that, faithful reader, you deserve A TREAT. To claim your treat, simply leave a comment stating your name, and I will write you a poem. And yes, it will hurt my feelings if no one takes me up on my poetry offer. FYI.

cheers to love

You know the moment you meet a special someone and your face flushes when your eyes meet? Or the accidental brush of a hand that makes you jittery and you start to sweat? That hug that makes your heart pound? These are all perfectly normal responses to being smitten.

In the spirit of Valentine’s Day and romance, we’re going to talk about what happens when you get a little frisky. As embarrassing as the topic may be, sexual arousal brings about fascinating responses, born from primal origins long ago in our evolutionary history. Don’t worry; it’s all PG-13.   

Get it girl. (sheknows.com)

Flushing is an especially functional reaction. Increased heart rate forces blood into vascular dermal tissues such as your cheeks. A nice rosy glow communicates to your crush that you are interested, healthy, and sexually operative. (And thanks to the makeup industry, you can now fool people into thinking you are all of these things! Stupid suckers.)

Sweating may seem like a sexual deterrent (after all, pit stains don’t really say “come hither”), but is actually working for you in a romantic setting. You have two types of sweat glands. Eccrine glands are all over your body and really only secrete water and salt. Appocrine glands are found in your armpits and crotchal area and are connected to hair follicles. It is from these appocrine glands that pheromones are emitted. When sweating increases upon sexual arousal, it is your body’s way of dispersing those pheromones into your immediate environment. Though it may be only subconscious, the person of interest will pick up on these smells and (hopefully) react positively to your smell.

When you let your honey into your personal space, you are certainly allowing yourself to be vulnerable. Goosebumps that arise from this sort of closeness are remnants of the ancestral reaction to a potential threat. Think of a porcupine putting up its quills, or a cat’s hair standing on end. You’re on guard and your senses are heightened. Makes sense.

Thank you for setting
unachievable pupil standards,
Belle. Thanks.

My favorite sexual reaction is pupil dilation. Pupil dilation occurs as a means to heighten sight sensitivity, and functions similarly to the goosebumps as a way of being “on guard.” Studies show that men consistently prefer women with big ole’ cartoon pupils. The bigger the pupils, the stronger the attraction. However, this is not mutual. Studies by Tombs and Silverman (2004) show that women prefer men with moderately dilated pupils. They suggest that men with fully dilated pupils are more emotionally charged and pose more of a threat, tending towards violence or forcible acts. It has also been shown that females’ pupil size varies on a monthly cycle- peak size correlating with peak fertility (Caryl et. al).

Our bodily systems are amazingly and elegantly coordinated. Pupil size changing with fertility? That's amazing.

All of this being said, I think the distinction between lust and love must be made. All of these physiological responses are lustful. Love requires some extra ingredients that I’m not sure biology can explain.

Cheers to cool biology and love, friends. Hope you have a wonderful Valentine's Day.

Caryl, Peter G. Jocelyn E. Bean, Eleanor B. Smallwood, Jennifer c. Barron, Laura Tully, Michael Allerhand. Women’s preferene for male pupil-size: Effects of conception risk, sociosexuality and relationship status. Personality and Individual Differences. Volume 46 Issue 4, March 2009. Pg. 503-508.

Tombs, Selina, and Irwin Silverman. Pupillometry, a sexual selection approach. Evolution and Human Behavior 25 (2004), Pg. 221-228.

cwelling

Currently, I am lying on my couch eating King Cake and watching The Two Towers (extended edition, eh hem). Just now, Merry and Pippin escaped the dinner conversation between the quibbling Uruk hai and orcs, and haunting Fangorn Forest towers in the background. Ah, Fangorn Forest- home to that loveable Treebeard. He’s so funny. Mostly, because he is a tree. A walking, talking, poetry-loving tree, who thinks it’s easier to travel south because “somehow, it feels like going downhill.”

A big part of Treebeard’s strength as a character is just this- he is a tree that can move and walk and talk. In the films, his entrance surprises and delights us when Pippin realizes he is clinging onto the face of a conscious tree. It seems contrary to us that a plant should locomote and exhibit behavior of any type. While I am (sadly) unaware of any actual Ents in existence, I am aware of a few plants that are capable of motion.

Sensitive plant, Mimosa
(0364920.netsolhost.com)

Those cute little sensitive plants that grow in the grass, Venus Fly Traps snapping their prey, fields of sunflowers that begin the day facing the east and end it facing west; moonflowers that close up at dawn and reopen at dusk; the world of plants is surprisingly animated.

Without muscles, ligaments, or tendons, how do they do it? When you touch the leaves of a sensitive plant and they close up in a matter of seconds, what do you think is causing the motion?

In most cases, a change in turgor pressure is the mechanism. Turgor pressure is simply the water pressure within a plant cell. By localized swelling in turgor pressure, the shape of a leaf may be altered. For instance, if the cells of just one side of a leaf swells, the whole structure will become bent (Fig. 1). Conversely, if a bunch of cells expel their water, that area of the plant will collapse.

Figure 1: A.) Even turgor pressure B.) Increased turgor
pressure on top layer forces leaf to bend

The stimuli for these pressure changes vary. Sometimes, sunlight exposure will trigger cell swelling (cwelling, new word? I think so). Other times it is a reaction to sensory hairs called trichomes, or simply pressure setting off an ionic message through the cells like dominos. It varies from species to species.

If we could ever get our hands on an Ent, wouldn’t it be something to see if their physiology operates on a turgor pressure differential system? That Isengard and Soromon were defeated basically by the simple act of water diffusion? 

Why yes, Aragorn. We should go get drinks later.

no more flat tires

One weekend when I was sixteen, my family was loading up the car to go visit my grandparents. As I climbed into the backseat, a stabbing pain in my chest hit me. My left shoulder cramped and my left arm was painful to move.  I told my dad about what I was feeling, and we both dismissed it as a random cramp. Five minutes later, the pain was worsening and I wondered if I was having a heart attack at only sixteen years old. We decided to swing by the emergency room just to be sure.

Come to find out, my left lung had spontaneously collapsed. As doctors with x-ray machines and pokey things began to swarm around, I looked at my unshakeable father standing in the corner of the room. He was looking at me and shifting his weight from side to side, with a furrowed brow and crossed arms. This meant he was confused.

It just so happened that my best friend’s father is a pulmonary specialist. As the drugs began to cloud my head, I watched Dad pacing outside of the room with a cell phone to his ear, talking to my friend’s dad, Dr. Liendo. A man with a well-placed sense of humor, he told my dad that I was experiencing a “flat tire,” and after several minutes of conversation, my dad was clear on what was happening.

One of the most misleading physiological comparisons is that of a lung to a balloon. (If I could legally encourage you to deface every balloon/lung demonstration you see at science education centers, I would). A balloon inflates by air being forcefully pushed into the vacant space inside. This is a positive pressure system, since the balloon inflates by air being pushed into it. But lungs do not work like this. They work on a negative pressure system, meaning that air is pulled into the spongy tissue that is the lungs- not an empty cavity like a balloon. What does the pulling, then? Lungs are not muscularized- but your chest cavity is.

Your diaphragm is the muscular floor of your chest cavity. When it is relaxed, it bows upwards. When it contracts, it straightens out and lowers down- making your chest cavity bigger and therefore expanding the lungs, pulling air in. Ahhh, yes. Your lungs are attached to the walls of your chest cavity. At least they’re supposed to be.

They are attached by a thin layer of moisture called the pleura (imagine two sheets of plastic being stuck together when they get wet). Should this adhesive moisture break contact with the lung surface and the chest wall, air will leak from the lung into this pocket, forming what’s called a “bleb” between the lung and chest wall.  Sometimes, the bleb heals and the pleura reseals itself. No harm no foul.

Left: A tiny bleb at the top of the lung
Right: The lung continues to collapse

Other times, the pleural break is large enough that the lung continues to pull away from the chest wall and collapses. Your diaphragm continues to expand the chest cavity, but the lung is a pathetic, shriveled, useless raisin. (This hurts a lot). This can be fixed by inserting a chest tube so that it rests in the chest cavity, allowing the air pocket to escape and the pleura to reseal. If it’s a stubborn one, they might even hook it up to a vacuum and suck it out.

Dr. Liendo likened this system to a tire (the chest cavity) and the innertube within (the lung). To this day, Dr. Liendo tells me that I am allowed “no more flat tires.” I will always be grateful to him for unfurrowing my dad’s brow that day.

And if a rash of vandalism against balloons being used as demonstration lungs breaks out after this, I will not be upset.

eyes on the horizon

Horizontal pupil of a goat (flickr.com)

 Literature and lore often depict satanic or demonic animals as having hooves, horns, and elongate pupils. But my experience with goats, their delicious cheese and cute little tongues lapping up food at a petting zoo suggest otherwise. So I’m going to go ahead and make a bold statement: maybe these attributes are not markers of a demonic origin, but adaptations for predator avoidance and feeding.

You’ve probably noticed that livestock animals like horses and cows have horizontally rectangular pupils? Admittedly, this difference from our own eyes can make them seem unrelatable and a little spooky… probably interpreted as “demonic” by scribes of old. But look at the eyes of an animal, you can make inferences about where they spend most of their time, and what sort of predation they are likely to face.

Wide-angle view of ungulates, thanks to eyes being on
either side of the head and horizontally stretched pupils.

Ungulates (hoofed animals like deer, goats and sheep, bovine, horses, etc. that graze on grasses) all have the horizontal pupils, and eyes generally situated on either side of the head. This adaptation gives them an expanded range of peripheral vision. As grazers that must keep their heads down in open fields and grass plains, they have to be able to keep an eye on the horizon for Mufasa and Simba coming to eat their asses, even as they are munching on grass. Once motion is spotted, the zebra/sheep/antelope/whatever is equipped with long legs and speed that usually gets them out of hot water.

Reduced angle view that carnivores
experience.

The predators of these ungulates have vision adaptations of their own. Their eyes are situated more on the front of their head, causing the images seen by each eye to overlap. This is called binocular vision, and allows the animal keen depth perception fitting for a hunter. Of course, they trade wide-angle peripheral vision for their depth perception. But as predators and not prey, they don’t need to monitor the expansive horizons for danger as attentively. In addition, rounded pupils allow for super-tight focusing, perfect for spotting a tasty morsel off in the distance. Great depth perception + focusing power = zebra for dinner.

Can you think of any other animals with crazy eyes? Or eyes placed on the head differently than they are on yours? What do these things tell you about the animal's role in the food web?

try to b positive

Do you know your blood type? I do. Turns out, I’m a proud B positive. Representin’ homies.

A few years ago, I had my blood typed out of curiosity. They had to take three vials of blood to complete the test- which I initially found absurd. But when I stopped to think about how the blood typing system works, three vials made sense.

You’ve heard the blood types before: A, B, O, or AB with a positive or negative stuck on the end. What these letters really represent are proteins that belong to the ABO blood group. You see, on the surface of all your red blood cells are imbedded little proteins in the membrane. These are fittingly called- wait for it- surface proteins. They act like identity badges, marking the cell according to which protein floats in the cell membrane. Maybe you have A proteins, or B proteins, or both, or neither. If you have both, you are an “AB” blood type. If you have neither, you are an “O” blood type (O really stands for “none”). So, if you’re “A,” you are technically either “AA” or  “AO.” At the end of the day, you only have “A” proteins so you are just called an “A” bloodtype. Same thing goes for us B types.

There’s another category of surface proteins, known as the Rhesus blood group, or “rh” for short. If you have rhesus proteins, you are “rh-positive.” If you don’t, you are “rh-negative.” This is where the positive/negative part of your blood type comes from.

When blood transfusions take place, phlebotomists must make sure to not give blood with any proteins that the recipient does not originally have. For instance, if you were to give A positive blood to a B negative person, their body would be all “what are these B proteins?! And rh proteins?! Ah HELL no!” and attack those cells. Give that very same person A negative blood, and there’s no problem. Their body would not detect any proteins with which it was not already familiar.

With this knowledge, you can figure out that O negative blood would be accepted by anybody, since it has no proteins for a donor to reject. This is why O negative people are called “universal donors.” Conversely, AB+ blood may only be accepted by AB+ people, since it has all possible surface proteins that could cause a immune reaction. Likewise, AB+ people can accept any blood, since their bodies are already familiar with all three of the possible surface proteins. Ah lah, AB+ people are called “universal recipients.”

All of these proteins are inherited genetically. Each parent can contribute one protein of each category. An “AB” parent can contribute either their A or their B, while an O parent has nothing to offer. So, if Judy (O negative) and Bill (O negative) have a B positive child, Judy got some ‘splainin to do. Blood types were historically used as paternity tests, but as you can see, can sometimes be inconclusive. They are only able to rule out, not determine, a parent- and only part of the time at that.

Armed with the knowledge that there are three possible proteins that may determine a blood type, I understood why that vampire nurse bled me like a stuck pig when I went to get my blood typed. They needed one vial to test for A proteins, one to test for B proteins, and one to test for the rhesus group.

Do you know your blood type? Go find out. Then, I dare you to figure out all the possible blood types your parents could be. It’ll be so much fun!