Wednesday, February 3, 2016

Plants That Don’t Sleep Will Take The Dirt Nap

Biology concepts – nastic movements, turgor pressure, evolutionary pressure, tropism, osmosis

If you don’t let a Mimosa pudica (sensitive plant) plant rest at night, it will wilt away to nothing. A plant that needs a good night’s sleep? Really? We have talked about how sleep revitalizes different brain functions, especially within the hypothalamus (The Best Cure For Insomnia Is To Get A Lot Of Sleep), but plants don’t have a hypothalamus or any brain for that matter. So why does it die if it can't rest; is it out of its mind?

The prayer plant on the left is how it looks during the day, but
on the right, the leaves have folded or curled up. They also stand
straight up, as if at attention. A tough way to spend the night, but
it must serve some purpose.
The prayer plant (Maranta leukoneura) folds up its leaves at night and tilts them upward. When morning comes, the leaves tilt back into their day position and unfold to catch as much sunlight as possible. The folded leaves might look like they are praying (hence the name), and it may appear that they are sleeping, but this is just anthropomorphism.

Humans have a need to feel connected to the rest of Earth’s life, and in the process, we tend to see the behaviors of other organisms in human terms, trying to assign some human motivation to them. So, is the plant sleeping? Does it need to rest? No. Sleep in animals implies inactivity and neural rearrangement, and these don’t occur in plants.

Charles Darwin performed crucial experiments
in plant movement in his later life, including the
identification that chemical signals moving in the
plant are responsible for growth toward the light
(heliotropism). Notice that his son got pretty good
billing as an assistant.
However, the fact that the plant carries out this activity every night suggests that it has evolved in response to some pressure, some need. Surprisingly little is known about why plants move their leaves at night, but there are a few hypotheses. Some scientists believe that changing the angle of the leaves helps funnel dewdrops and overnight rain down the trunk or stem to the roots. Charles Darwin published two books on these plant movements, his theory being that the behavior reduced the chance of chill or freezing.

Another hypothesis suggests that leaves fold up to keep the rain from pooling on them and promoting bacterial or fungal growth. Or perhaps, apposing one leaf closely to the opposite leaf reduces the amount of water lost overnight. However, aquatic plants don’t have to worry about loss of water, but some immersed plants, like Myriophyllum Mattogrossense, still fold up at night. It may be a holdover from their terrestrial days, as most of today’s aquatic plants evolved from terrestrial plants.

My personal favorite proposes that by folding up their leaves, the plants give nocturnal predators a better shot at seeing, hearing, and smelling nocturnal prey. By helping the predators, plants are indirectly protecting themselves from animals that would eat them- plants are sly little devils (more anthropomorphism). It is probable that different plants move for different reasons, so one hypothesis almost certainly won’t cut it for all organisms.

Plants have night moves other than folding leaves. Morning glories (Ipomoea violacea) close their flowers overnight. The reasons for this movement may be a little plainer. Dry pollen sticks to pollinators better than wet pollen, so closing off the stigma to rain or dew keeps the pollen dry. It also takes energy to maintain an open flower; this energy would be best spent when pollinators are around. If the plant’s pollinators are diurnal, they why leave the buffet open all night?

Just as animals have an internal clock, plants gauge
their movements according to the circadian period.
Often plants match their rhythms to pollinator animals
they depend on or to avoid the active periods of
predators. Anyway, I like the picture.
There are also flowers that have the exact opposite behavior, opening their flowers as the sun sets. Philodendron selloum (Is It Hot In Here Or Is It Just My Philodendron) is a classic example, with its spathe closing down in the early morning hours.

Moonflowers (Ipomoea alba) are another example.  At about 8:00 pm, the moonflower opens. A single flower can go from completely closed to fully open in less than a minute ( The morning glories and the moonflowers are both of genus Ipomoea, but they have opposite behaviors – different pressures lead to different adaptations, even in closely related species.

These movements of plant structures are independent of the direction of the stimulus, ie. they are not following the sun or being blown by a particularly wind, so they are called nastic movements. Nyctinasty (nyc = night or darkness, nastic = firm or pressed close) is the specific movement of leaves or flowers in a daily pattern, open during the day and closed at night. If directed by the position of a stimulus, the movements are called tropisms (heliotropism, thigmotropism, gravitropism).

The left picture shows that changes in the pulvinus shape could affect the direction of the entire petiole and all the leaves, or individual leaves (like on the sensitive plant). The middle cartoon indicates that filling the central vacuole with water can change the shape of the cell, pushing in one or more directions. The right image shows just how the extensor cells on the bottom must be inflated to lift the petiole, while turgidity in the flexor cells makes the leaf drop.
Nyctinastic movements are accomplished by the flow of water in and out of specific cells in the pulvini (swellings, singular is pulvinus) at the base of the petioles (the stalk that attaches the leaf blade to the stem). It is not unlike our muscle movements in that there is an extensor and a flexor pair. When K+ and Cl- are pumped into the extensor cells on the bottom of the pulvini, they become hypertonic and water follows the ions through osmosis. This causes the extensor cells to swell due to increased turgor pressure.

Turgor pressure refers to the pressure of the cell contents against the cell wall. This increased turgor pressure at the bottom of the petiole pushes the leaf up. In an opposite fashion, night causes a movement of ions to the flexor cells on the top of the petiole. Water flows out of the extensors and into the flexors by osmosis, causing the stem to droop. Flowers and leaves open and close by the same movements, with the extensor and flexor cells located at their bases.

Turgor pressure is the same mechanism which causes the venus flytrap (Dionaea muscipula) to snap closed its jaws of death when an insect disturbs its trigger hairs. These hairs are located on the nectar laden, red lobes of the trap. Touching just one trigger hair doesn’t spring the trap, two must be displaced within 20 seconds of each other. This saves energy and unnecessary trap closings; each trap snaps shut only four or five times, then dies. If you thought the moonflower moved fast, check out the venus flytrap ( I’m just surprised we can’t hear the water shooting into the flexor cells!

The venus flytrap supplements its diet of water and carbon
dioxide with proteins from the insects it catches and digests.
The bright surface with nectar draws them in, where they trigger the
mechanosensor hairs. The magnified image on the right shows a
trigger hair with its hinge that transmits a signal to the pulvini to
swell quickly and snap the trap shut.
The trigger hairs are mechanosensors. The stimulus that trips the trigger and causes the flow of ions and water in the extensor and flexor cells of the hinge region is directionally irrelevant; therefore, the snapping shut of the trap can be considered a nastic movement. In this case, as with the sensitive plant (Mimosa pudica), the movement is called haptonasty (hapto = touch).

A small percentage of plants have nyctinastic movements, so they are an exception to the rule that plants don’t move actively, but even a small percentage means that thousands of species do have these movements. This many exceptions underscores the point that nyctinasty must perform an important function.

Just as humans with fatal familial insomnia die from a lack of sleep (An Infectious, Genetic Disease), the sensitive plant has a much shorter lifespan when nyctinasty is prevented. A plant hormone that stimulates leaf opening was identified in 2006. When given to plants continuously, it caused the leaves to remain open. When nyctinasty was prevented in this way, the leaves were noticeably damaged within a few days, and the plant was dead in less than two weeks. It may not be sleep, but whatever it is, it is just as important.

Some plants are open during the day and some are open at night, just as some animals are active during the day and some during the night. And just as plants adapt to a time schedule to promote survival, animal adaptations are crucial to life in the light or the dark. But that doesn’t mean that some organisms won’t throw us a curve, as we will discover next time.

Ueda, M., & Nakamura, Y. (2006). Metabolites involved in plant movement and ?memory?: nyctinasty of legumes and trap movement in the Venus flytrap Natural Product Reports, 23 (4) DOI: 10.1039/b515708k

For more information, classroom activities or laboratories on nastic movements or turgor pressure, see:

nastic movements –

turgor pressure –

Wednesday, January 27, 2016

An Infectious, Genetic Disease? Better Sleep On It.

Biology concepts – thermoregulation, sleep, genetic disease, infectious disease, central dogma of molecular biology, form follows function

Even rats have to get some sleep. It was nice to have the sleeping cap,
but unnecessary for a sleep deprivation study. Not a good use of
research dollars.
“I’m dying for a good night’s sleep.” Is this just hyperbole, or an impending warning of death? For laboratory rats, sleep deprivation does kill. During their insomniac downward spiral, the rats tend to get hot and can’t cool down – you know, they can't thermoregulate (see Can’t We Just Go With The Flow). This doesn’t mean that a loss of the ability to thermoregulate is what kills the rats, but it does suggest a connection between sleep deprivation and the hypothalamus.

We looked at the hypothalamus in our story of endothermy. This evolutionarily old brain structure implements a set point temperature for the body and receives information about the temperature of different parts of the body. When the body temperature deviates from the set point, the hypothalamus initiates bodily mechanisms to normalize the temperature.

Apparently one of the effects of sleep deprivation is that you
become semi-transparent.
People with severe insomnia tend to sweat more and have higher core temperatures even though they say they are cold. They also have extreme high blood pressure, pulse, and appetite. These symptoms suggest that sleep deprivation messes with the hypothalamus, since functions of the hypothalamus include themoregulation, sleep, hunger, thirst, reproductive readiness in females, and stress responses. What scientists don’t know yet is just how sleep deprivation actually kills the rats or harms people.

Dying from a lack of sleep is not just a rat problem, a few very unlucky humans die from it as well. Fatal familial insomnia (FFI) is a very rare genetic disorder; it has been reported in only 40 families worldwide. Before describing the truly horrible way these patients die, let’s look at what causes the disease.

FFI is caused by a point mutation in the gene for the prion protein PrPc. A point mutation means that one nucleotide on the DNA is changed, which leads to a change in the protein coded for by the DNA. Three unit (nucleotides) segments of the RNA (made from the DNA template) work together (called a codon) to code for one protein building block (amino acid). In the case of FFI, the amino acid called aspartic acid is changed to one called asparagine, and this changes the protein’s shape. 

The left image shows mRNA bases recognized in sets of three
(codons) by tRNAs with amino acids attached (Ser = serine, tyr =
tyrosine). The amino acids are linked to because proteins. The
lower section is the genetic code, showing which amino acids are
coded for by which codons. The right image shows how proteins
fold. The primary structure is the amino acid sequence. The
secondary structure comes from interactions of adjacent amino acids,
including spirals called helices or sheets. The tertiary structure comes
from the folding up of the entire protein, while the quaternary
structure comes from the interaction of different proteins into a
larger complex.
PrPc is made up of 250 amino acids linked together in a chain. Each different amino acid carries a different shape and charge and will interact with every other amino acid differently. The sequence of amino acids in a protein cause it to fold into a specific shape. It is the protein’s conformation (shape) that determines its function. This is the opposite of what we determined for evolved organism characteristics, where form follows function (see Do You Have To Be Ugly To Hear Well?). With proteins – function follows form!

Mutation of that single amino acid at position 178 (aspartic acid is negatively charged, while asparagine is positive) causes the folding, and therefore the function, of the protein to change. Aspartic acid is sometimes abbreviated "D", while asparagine is called "N"; therefore, the mutation is often indicated as D178N (D at position 178 is changed to N).

Many genetic mutations result in no change in amino acid, or a change that bring a large enough change the shape to cause a change in function. But when it does, good or bad things can happen. On one hand, the altered protein might confer an advantage to the organism, one that promotes survival in the environment or after an environmental change.This positive selection through reproductive advantage become the new normal – and this is evolution

On the other hand, the change in amino acid sequence, form, and function could be destructive. Disease might be the result, or perhaps a change in the organism that reduces reproductive success. One of these two results is what occurs with the FFI mutation of the prion protein.

When the mutated prion folds differently, it forgets its day job and moonlights as a sinister evil force. Every other prion protein it contacts, WHETHER MUTATED OR NOT, is coaxed into changing its shape. The new prions turn to the dark side, then change other prion proteins they contact, multiplying the effect. The poorly folded prion proteins will stick together, come out of solution, and form solids (plaques) where they settle out. In different prion protein diseases, this settling out occurs in different parts of the brain. In FFI, it is the hypothalamus.

In the top image, the PrPc on the left is properly folded. The green
represents alpha helices and the blue arrows represent beta-pleated
sheets. The right image shows the malfolded version of PrPsc. It is a
tighter structure, which partially explains why protein-degrading
enzymes don’t work on it. . The lower cartoon shows that the PrPsc
can force the PrPc to assume the improper form, and these then
aggregate into plaques.
The prion plaques are longer lived then the regular prion protein; normal cellular enzymes whose job it is to degrade proteins won’t work on prion plaques. And worse, if some of the malfolded protein is transferred to another animal, the recipient will develop plaques and disease as well. That makes this an infectious disease that isn’t caused by a bacteria, fungus, parasite, or virus. The prion is an infectious protein! What a terrible exception to the rules of infectious diseases.

We see here a protein that can replicate itself (not by building more of themselves, but by changing the form of normal proteins), and that makes it a repository of biologic information. This is an exception to the central dogma of molecular biology, which says that DNA is the sole information storing material.

FFI moves from person to person through heredity, but if a non-affected person comes into contact with some brain material from an FFI patient and that material entered their bloodstream, it can be transmitted this way as well. A prion protein disease called Kuru is famous for being transmitted from person to person.

The Fore tribe in Papua New Guinea once observed a ritual wherein they honored a dead tribe member by eating part of their brain (called ritualistic mortuary cannibalism - gasp!). Because of this, there was an epidemic of Kuru in this tribe in the early 1900’s. Over a period of 3-6 months victims would become unsteady, irrational with bouts of laughter, and then degrade mentally and physically to the point of death. There are more than twenty known prion diseases (mad cow disease, Creutzfeldt-Jakob, scrapie, etc.), and Kuru suggests that some might have no genetic component, only person to person transmission.

A member of the Fore tribe is shown on the left. This tribe used
to celebrate the lives of departed members by eating their brains.
This spread a prion protein disease called Kuru, a protein disease
that is infectious! The Fore tribe still lives in Papua New Guinea,
although there are fewer of them than before Kuru.
The differences between the various prion diseases are based on the specific prion protein mutation, what part of the brain is attacked, and how potent the prion is at refolding normal prion proteins. For instance, the D178N mutation in FFI also occurs in Creutzfeldt-Jakob Disease (CJD), but a normal polymorphism (an amino acid change that doesn’t change form or function) at position 129 determines the fate. If amino acid 129 is methionine, the the person gets FFI, if it is valine, then they get CJD. 

The families that suffer from FFI have the D178N mutation, and also pass on the polymorphism for methionine (M) at position 129. Even more gruesome, some cases of prion protein diseases can be sporadic, not associated with either an inherited mutation or transmission. The malfolded prion can very rarely arise out of nowhere in isolated individuals.

The mutated PrPc is passed on via inheritance. You get one copy of each chromosome from each of your parents, so for an individual gene, you might get two normal copies, 1 mutant copy and 1 normal copy, or 2 mutant copies. Some diseases require that you must inherit two mutant copies for symptoms to show (recessive), but other require only one mutant copy (dominant, it dominates the trait from the other parent).

FFI is autosomal dominant (not associated with the X or Y sex chromosomes), so the chance of getting a mutant copy and the disease if one parent has it is 1 in 2; these are bad odds. But, if everyone with FFI dies, then why is the disease still showing up in families. Remember that we said above that some genetic diseases can, but don't have to, affect reproductive success. Unfortunately for those with FFI, the symptoms appear in the victims’ fifties, after they have had children. Natural selection doesn’t eliminate FFI from the population because FFI doesn’t appear affect reproduction.

The first symptoms of FFI include sweating while feeling cold. Later, the ability to get a good night’s sleep is lost, followed closely by the inability to nap. As the disease progresses, there are panic attacks, phobias, and no sleep whatsoever. After 4-6 months, mental abilities start to degrade. In its final stages unresponsiveness precedes death. 

This is especially sad way to die, because during the majority of the disease course the patient is aware of everything going on. At least with middle to late Alzheimer’s disease the patient is blissfully unaware of their dementia.

For both the gross and microscopic images, the left example is from prion protein disease victim, while the right example is from a normal brain. The brains on the left show how great the loss of tissue can be in Creutzfeldt-Jakob disease. The microscopic image from the diseased brain shows the plaques and the resulting holes in the brain structure. The small gaps in the normal brain on the right are a result of shrinking of tissue after it was on the slide.
On autopsy, the hypothalmus of an FFI sufferer looks like it has been hit with a shotgun blast. Holes are present in the tissue, representing areas where neurons have been lost due to inflammation and triggered cell death. The affected area of the brain takes on a spongy appearance, so prion protein diseases are lumped together and called transmissable spongiform encephalopathies (encephalon = brain and pathy = disease). Unfortunately, there are no cure, treatments, or vaccines for any of these prion diseases.

It is the hypothalamus' control of sleep cycles and circadian rhythms that promotes survival in animals. But what about plants? They don’t have a hypothalamus. Can they suffer from loss of circadian activity? In a word – yes!  And this will be our starting point next time.

For more information or classroom activities on prion proteins, central dogma, infectious or genetic disease, the genetic code or protein structure, see:

Prion protein and diseases –

central dogma of molecular biology –

infectious disease –

genetic disease –

genetic code –

protein structure –

Wednesday, January 20, 2016

Pump Up Your Brain

Biology concepts – learning, memory, attention, concentration, hippocampus, neurotransmitters, neurotrophins, executive function, processing speed, exercise

Many people exercise because of how it makes them feel,
or just because they think it helps them think more
clearly - maybe by reducing stress. They will be happy to
know that exercise actually increases the power of your
brain, everything from learning, to memory, to attention,
to decision making speed.
Many years ago, my father told me the story of how he studied while in college. He would hit the books in a solitary, silent room and just cram until he couldn’t concentrate anymore. Then he would get up, go outside, and run laps around his dorm for a while. Then he would come back and start again. Study, run, repeat. Turns out, the running makes a true difference. Exercise can actually make you smarter!

In a study from 2011, researchers took overweight kids and had them start exercising. Those that had at least 30 minutes of physical activity each day showed increased hippocampus size, and significant improvement on a CAS planning test, an alternative to the standard IQ test.

Planning basically means that their executive function (planning, reasoning, and decision making skills) had improved markedly. They also performed much higher on a math test, even though no additional math instruction had been given.

Exercise has impacts on memory, learning, attention, concentration, and processing speed. So now we know what we are talking about when we say exercise helps learning. Oh – you won’t just take my word that exercising helps? Good, always ask for evidence.

Let’s look at studies just from 2013, although there are many older studies. One study found that a single bout of moderate exercise allowed participants to more accurately complete a test on memory, reason, and planning - and it took them less time. Another study indicated that exercise reduced the loss of cognitive function in middle-aged women. Yet another publication talked about how master athletes (over 50), have a larger brain volume and better cognitive function as compared to their sedentary counterparts.

We can go on. Exercise has been shown to support the cellular structure of the white matter (myelinated) neurons of the cerebral cortex in patients with vascular disease, important for higher thinking functions. And another study shows that processing speed is increased after starting a regular regimen of cardiovascular activity.

The upper image shows where the hippocampus is located
within the brain. There are two, one in each hemisphere.
They are connected as well. The lower image shows the
regions of the hippocampus, including the dentate gyrus
(DG) the area where much of the neurogenesis after
exercise is found.
Finally, we will mention just one of the many 2010 studies. Nine-ten year old kids that exercised regularly had 12% larger hippocampi (plural of hippocampus, part of brain for learning and memory). They were faster on recall tests and they learned new information faster.

So now that you are convinced that exercise does help cognitive functions, the question still remains as to how exercise carries out this miracle. The first thing to get clear is the difference between memory and learning. It might seem that they are the same thing; you have some experience, either verbal, aural, visual, etc. and if you remember it, then you have learned it. But there are subtle differences.

Specialists define learning as a process that will modify a subsequent behavior. Memory, on the other hand, is the ability to remember past experiences. Memory is the record left by a learning process, so you need to have memory to learn. You learn to play piano by studying the notes and the instrument, but you then play it by using your memory to retrieve the notes and fingering that you have learned.

Back to the mechanisms of how exercise help memory and learning. The easy explanation is that exercise helps you sleep, improves your mood, and drives more oxygen to the brain. These undoubtedly help you study better or even notice more that can be used to build knowledge. These are the factors my dad counted on when he went running. But there’s much more.

The hippocampus is important for learning and memory. Many studies of exercise and cognitive function have shown increases in the size of this part of the brain in exercise participants. Those kids that increased their “IQ,” they had an increased hippocampus. So did mice from studies in the 1990’s.

Neurogenesis is the production of new neural cells from
stem cells. There are stem cells located in the brain. They
can become any type of brain cell, depending on stimuli in
the local area. Normally, only a small percentage of
stimulated stem cells will become neurons, but after
exercise the number that survive goes up dramatically.
Exercise upregulates neurogenesis, oxygenation, synaptic plasticity, neurotransmitter populations, myelination, processing speed, and long-term potentiation (LTP). O.K., that’s a lot of big words, so let’s take them one at a time. Remember that all these things are linked together. Plasticity, neurogenesis, and LTP apply to memory. Neurogenesis and processing speed apply to new learning and executive function. Neurotransmitters, plasticity and oxygenation combine to affect attention.

A lot of the benefits from cardiovascular exercise come through the making of new neurons (neurogenesis). Yep, this is a huge exception to the rule that central nervous system neurons last your entire life and can’t be recovered or new ones produced. Neurogenesis is how the hippocampi of all those exercisers got bigger.

Regular exercise induces neurogenesis through action of brain chemicals, trophins and NTs. We talked about brain-derived neurotrophic factor (BDNF) 2 weeks ago with respect to mood and we said we revisit this factor. This neurotrophin actually stimulates your brain to make new neurons! More neurons means more connections, and more potential learning.

For most all of the cognitive functions, the lynchpin seems to be BDNF. How does exercise increase BDNF? We aren’t sure yet. It may be that exercise is a stress, this increases the calcium flowing into the brain. The calcium activates many transcription factors, and BDNF is known to require calcium for transcription.

But nothing is ever simple. It is probable that serotonin, IGF-1, and BDNF are all needed to increase neurogenesis in the hippocampus. Inhibitors of any one of these drastically reduce the amount of exercise-induced neurogenesis.

Think of plasticity as a general process, the altering of neurons and their connections. It involves making more neurons (neurogenesis) and the number (developmental plasticity or synaptogenesis) and orientation of the dendritic connections with other neurons (synaptic plasticity).

The images show the increase in the number of dendrites and
possible synaptic junctions over time. The increase in dendrites
is called arborization (arbor = tree) for obvious reasons. The
increase in synapses is called synaptogenesis. Exercise increases
both of these. This image isn’t a result of exercise, but it would
be is similar.
BDNF doesn’t just induce new neuron formation, it can increase the number and size of the connections (synapses) between neurons. IGF-1 is probably involved in this as well, as its main function is to support the growth of fragile, newly formed neurons and connections.

Plasticity is crucial to learning and to memory, since all learning and memory is just a map of connected circuits that work together to access certain information. It is the number and pattern of the connections that determine the amount retained. More connections must help this process.

Long term potentiation
LTP is for memory and learning – the reinforcing of neural connections to make them stronger. Exercise increases LTP, probably through synaptic plasticity, more connections between two neurons would help reinforce each other when they fire. We talked about LTP last year, so read that post and know that exercise increases it.

Unfortunately, for best increases in memory the exercise must be long term. In a 2013 study, neurogenesis was apparent only 14 days after initiation of exercise, and these were immature neurons. LTP wasn’t increased appreciably until 56 days.

Processing speed
Increased speed probably comes through increased IGF-1 and oxygenation, and their effects on the support cells in the brain. Oligodendrocytes and astrocytes help the neurons do their job at peak efficiency. In particular, oligodendrocytes make the myelin sheath that increases transmission speed.

Meet the glial cells. Astrocytes mediate the travel of fluids
and nutrients from the capillaries to the neurons and
between the neurons and the cerebrospinal fluid.
Oligodendrocytes make the myelin sheath around some
axons. Microglial cells are the immune system of the brain,
they phagocytose intruders. Finally, the ependymal cells
line the ventricles in the brain, the spaces that hold the
cerebrospinal fluid.
Astrocytes, on the other hand, are important for blood flow to neurons, and cerebral spinal fluid movement. These two functions would be particularly important for moving neurotrophic factors toward the neurons.

Attention and concentration
Exercise also helps your attention and concentration. And no, these two aren’t exactly the same. They’re more closely related than memory is to learning, but there are still some differences. Both are important for making you smarter, because only by focusing do we take information in – you have to notice something to learn it.

When you are in a room full of people talking, you can still follow the conversation between yourself and one other person. This is one of several different forms of attention. In general, attention is a thinking process for directing and maintaining awareness of stimuli in one’s environment.

Concentration is the ability to control attention for a sustained period. Attention shifts as we wander from thought to thought about different things in our mind or environment, but concentration requires attention to one thing without wandering. In more clinical terms, concentration is a combination of two types of attention; sustained attention and selective attention.

Sustained attention is staying on task, keeping your mind on a single task over time. Selective attention is more about how you pick what you pay attention to. If there are many activities going on within range of your sense, but you focus on one thing and pay no attention to the others, that is selective attention.

Attention span is not equal to sustained attention. It is
focused attention; how long until your brain diverts to
some other stimulus. In 2000, Americans had a 12 second
attention span on average. In 2010, it was down to 8
seconds. Heck, a goldfish has a 9 second attention span,
and we make fun of them!
Attention is centered in the reticular activating system (RAS), near the brain stem. But it connects to other centers that work in attention as well, like the prefrontal cortex and the parietal cortex. The RAS accounts for shifts in levels of awareness to different things. Exercise activates the RAS, which increases alertness, and therefore attention and concentration – my dad was ahead of his time.

It turns out that increased dopamine, serotonin, and norepinephrine in the brain, and particularly the RAS is crucial for attention and concentration. And we talked two weeks ago about how exercise increases all these. In ADHD, they give drugs (methylphenidate) that increase the apparent levels of dopamine. This helps us make sense of studies that show regular exercise alleviates the symptoms of ADD/ADHD.

One last point that I find interesting. The type of exercise seems to make a difference for the increase in neurotrophins. A 2012 study showed that rats that ran on exercise wheels had increased BDNF in the hippocampus, but rats that lifted weights (climbed ladders with weights on their tails) increased only IGF-1. The two proteins work in different pathways, so rat studies show us that it is best to include both aerobic and resistance training in your exercise program. And a rat shall lead them.

Next week, can you die from not getting enough sleep. Yep, and that's not the weirdest part of fatal familial insomnia.

For a good resource on brain structure and function, see the Open College’s interactive brain.

Patten AR, Sickmann H, Hryciw BN, Kucharsky T, Parton R, Kernick A, & Christie BR (2013). Long-term exercise is needed to enhance synaptic plasticity in the hippocampus. Learning & memory (Cold Spring Harbor, N.Y.), 20 (11), 642-7 PMID: 24131795

Cassilhas RC, Lee KS, Fernandes J, Oliveira MG, Tufik S, Meeusen R, & de Mello MT (2012). Spatial memory is improved by aerobic and resistance exercise through divergent molecular mechanisms. Neuroscience, 202, 309-17 PMID: 22155655

Davis CL, Tomporowski PD, McDowell JE, Austin BP, Miller PH, Yanasak NE, Allison JD, & Naglieri JA (2011). Exercise improves executive function and achievement and alters brain activation in overweight children: a randomized, controlled trial. Health psychology : official journal of the Division of Health Psychology, American Psychological Association, 30 (1), 91-8 PMID: 21299297

Tam ND (2013). Improvement of Processing Speed in Executive Function Immediately following an Increase in Cardiovascular Activity. Cardiovascular psychiatry and neurology, 2013 PMID: 24187613

For more information or classroom activities, see:

Most of the information for this post comes from recent scientific journals, here is more general information from the internet.

Memory classroom activities –

Hippocampus –


Neuroglia –