Wednesday, January 14, 2015

Everybody In The Gene Pool - Plants That Swim

Biology concepts – botany, taxonomy, alternation of generations, cycad, gametophyte, sporophyte, gametes, motility, ginkgo, archegonium, antheridium


In the LOTR The Two Towers we find the tree herders
that can move on their own despite being plants. Today’s
exception is a version of this, if on a much smaller scale.
There are a few types of trees that have motile parts; they
don’t rely on wind, gravity, insects or anything else to
move from one place to another.
Plants are divided up into many categories, and few people agree completely on the groupings. I’ve got a new grouping – swimming plants versus non-swimming plants! It’s as good as anyone else has come up with – let’s investigate the plants that can move on their own.

Plants are most often called by their binomial system names (genus, species), but this is just naming, not categorizing in a large way. Animals, protists, fungi, etc. are all divided into different phyla based on their similarities ad differences. But for some reason (I hope there’s a reason) botany uses divisions instead of phyla.

There are 10-12 divisions of plants (we’ll use 10), covering everything from the mosses to the flowers. Compare that to 21 phyla of animals and it seems like the plants will be easier to classify – but not so fast.

Group plants according to various characteristics and you start to muddy the waters. You might divide them up according to whether they have vascular tissue or not. Non-vascular plants are short because they don’t have vessels to move water very high – these are the Anthocerotophyta (hornworts), the Bryophyta (mosses), and the Marchantiophyta (liverworts). Together they are called the Bryophytes.

The vascular plants are all seven of the other divisions – the Lycopodiophyta (the spikemosses and clubmosses), Pteridophyta (ferns and horsetails), Coniferophyta (conifers), Cycadophyta (cycads), Ginkgophyta (just one species, Ginkgo biloba), the Gnetophyta (a weird group), and Angiospermae (flowering plants).  The conifers, cycads, ginkgo and gnetophytes are often grouped together as the gymnosperms – you’ve probably heard of them.

On the other hand, you might divide the plants up into the seed plants and non-seed plants. In that case, you lump the club mosses and the ferns with the bryophytes, since they all reproduce using spores, not seeds.


Every plant alternates between versions of itself that are
diploid (sporophyte) and haploid (gametophyte). Different
types of plants spend different amounts of time as one or
the other. Mosses and other bryophytes are almost always
in their gametophyte state, while trees are sporophytes with
microgametophytes (antheridium and archegonium) located
in their flowers only.
Lest you think that all those divisions that are seed plants are the same, you can divide them all differently based on whether their seeds are naked (the gymnosperms) or those with fruit (parts of the ovary or accessory organs that overgrow – all in the angiosperms).  Or you could divide them on the basis of how many leaves the embryonic plants have; monocots have one while dicots have two. Angiosperms play by these rules, but gymnosperm seeds don’t, their embryos may have none, one, two, or dozens of cotyledons (embryonic leaves).

Here’s one classification method you may not have heard before – gametophyte dominant vs. sporophyte dominant plants. This has to do with the cycle of life of plants.

Every plant has two lives. Part of its life is spent as a haploid gametophyte (produces haploid gametes) while another plant of the species is a diploid sporophyte.  The sporophyte produces spores that grow into the gametophyte, then the gametophyte produces gametes that join together during fertilization to become a new sporophyte.

Some plant types (like bryophytes) exist mostly in the gametophyte stage and are therefore called gametophyte dominant. Other plants (like trees and flowers) spend all there time as sporophytes and only small parts of them become gametophytes (like pollen or cones).

One way you shouldn’t classify plants is based on their movement. Sure, some plants can grow in a certain direction, toward or away from some stimulus (tropisms, see this post), but plants aren’t motile. They don’t pick up and move themselves from one place to another under their own power.


The Himalayan Balsam is an invasive viny flower that has
become a problem in Europe and is invading the US as well.
Their seed pods contain fins under great strain when fill
with water. The slightest provocation will cause them to
explode, sending seeds more than 25 ft (7.5 m).
Plants also have many ways of moving their seeds and this is sort of a way of plants moving, but I think it’s cheating a bit. Seed dispersal mechanisms can rely on the wind (maples, dandelions) or water (cranberries, coconuts). They can use animals that eat them (many), or just grab ride on them (devil’s claws), or they can burst out (peas) or be shaken out (poppies) and use gravity. But this isn’t really a plant moving by it’s own power.

Plants disperse seeds as new plants, but they also disperse their male gametes in order to find the egg on another plant of their species. You have to get the pollen of seed plants (containing male gametes) or the male gametes themselves to the egg. Like seeds, pollen grains can be moved by insect, by wind, by rain, etc. These are the ways most plants get their male gametes to the egg in order to create a new plant, either in a seed or without a seed.

But there are exceptions, and this is weird exception. Some plants have male gametes that are motile. They swim to the egg! No big deal for animals, they pretty much all have motile male gametes (we’ll look at the exceptions to that), but it’s quite the stunner in plants.


Who knew SpongeBob cartoons were science lesson. Plankton
is green, a phytoplankton – an algae to be precise. Those two
antennae? Probably his two flagella, the way he would swim
around. The feet and the single eye-not so scientific.
Algae are probably the ancestors of all land plants, and we know their gametes have flagella for swimming from our post on them. But some land plants retain this method of male gamete dispersal, but they do include some weird twists. The plants that have motile male gametes cross many of the classes that we described above. There are some seed plants and some spore plants, some vascular and some non-vascular, some are gametophyte dominant and a few are sporophyte dominant – but no flowering plants do this.

Bryophyte males gametes are swimmers. The mosses, liverworts and hornworts  live close to the ground and must have standing water for the make gamete to reach the female gametophyte and egg. The haploid gametophytes are the moss that we usually see. The antheridium grow on the top of the male plants to produce male gametes, while the archegonium on the female plant tip produces the ovule with the egg. When the water is high enough the antheridium releases the male gametes and they swim to the egg using two flagella. The sporophyte (diploid) plant grows from the top of the female gametophyte.

Ferns, horsetails, and club mosses are taller than mosses because they are vascular, but they still require water for their male gametes to swim to the egg. The gametpophyte is a heart shaped leaf that lies near the ground. At one spot the archegonium grows the egg, while the male gametes in the antheridium grow nearby. Water resting on the leaf allows the male gametes to swim across the leaf to the egg (or from leaf to leaf). The sporophyte grows from the heart-shaped gametophyte and is the fern we usually think of.


Cycads (left) are gymnosperms whose trunk are formed from
the bases of the leaves as they grow and are lost. There are
about 300 species of cycads known, with several added every
year. The Ginkgo biloba is the only extant species of the
division. Because its wood is insect resistant, some trees may
be over 2500 years old.
Angiosperms and other seed plants use pollen to send the male gametes to the ovule. When the pollen reaches the archegonium, a tube grows into the ovule and to the egg. The male gamete cells are carried along by the pollen tube right to the front door of the egg. This is when fertilization occurs.  But not all seed plants work this way. A few of the gymnosperms still use a modified version of swimming to the egg.

Cycads (about 300 species) and the lone extant ginkgo, Ginkgo biloba, do have pollen grains that represent the male gametophyte plant. They get blow or carried to the female gametophyte cone and then it gets weird.

The ovule produces a drop of liquid that sticks into the air. The pollen gets caught in this drop and then the drop and the pollen are pulled back into the ovule. The pollen tube grows into the female reproductive organ, but not right to the egg. When the pollen tube reaches the entrance of the archegonium, it ruptures and the gametes are released into a watery fluid that surrounds the eggs.


Cycad and ginkgo male gametes move on their own, the only
exceptions in the seed plants. They have hundreds to thousands
of cilia, as opposed to flagella in bryophyte gametes, which
pull the cell forward. Ginkgo male gametes are huge (0.3 mm),
larger than an entire Wolffia globosa plant.
The male gametes have about a thousand of cilia (not flagella) that pull the cell through the watery environment inside the ovule toward the egg. Fusion and fertilization occurs when the male gametes find the egg – as always. The cycad and ginkgo male gametes swim, but they swim in the indoor pool, not out in the old swimmin’ hole like the bryophytes.

The male gametes of cycads and ferns are very different, from where they swim, to their relative sizes – ginkgo male gametes are HUGE compared to those of ferns, to the use of thousands of cilia as opposed to a couple of flagella.  However, research shows that they are remarkable similar in structure and function.

A 2006 study looked at the proteins involved in gamete movement in ferns and ginkgo. Their results indicated that most of the proteins in both were homologous enough that it suggested a direct descent from bryophyte to gymnosperm, not a case of parallel evolution.


In Guam, there is a neurologic disease that looks a lot like
Alzheimer’s. Research in 2004 found that it was actually
coming from cycad trees. Here’s how it happens. Cyanobacteria
live in the tree roots and put the toxin BMAA into the tree
tissues. Bats eat the fruits and people eat the bats. Than BMAA in
the brain causes disease.
One more cycad exception while we’re here. The cycads can do something that I thought was reserved only for philodendrons and a few relatives. These thermogenic plants can raise the temperature of their male cones by several degrees when the pollen is mature. A 2013 study showed that they can raise the temperature of male cones 2-15 degrees above ambient temperature.

This is believed to attract more insects as pollen distributors, and the researchers did find that more insects visited the plant when the temperature was increased. The mechanism may involve volatilizing more attracting chemicals though the added heat, which would then attract more pollinators (usually weevils).  Pretty advanced for a plant with a so-called primitive reproduction mechanism.

Next week – the base of the undulipodia has a special story all its own. Is it another instance of bacteria evolving into one of our organelles? And it has two very different jobs – which came first?



Suinyuy, T., Donaldson, J., & Johnson, S. (2013). Patterns of odour emission, thermogenesis and pollinator activity in cones of an African cycad: what mechanisms apply? Annals of Botany, 112 (5), 891-902 DOI: 10.1093/aob/mct159

Vaughn, K., & Renzaglia, K. (2006). Structural and immunocytochemical characterization of the Ginkgo biloba L. sperm motility apparatus Protoplasma, 227 (2-4), 165-173 DOI: 10.1007/s00709-005-0141-3

Murch, S., Cox, P., & Banack, S. (2004). A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam Proceedings of the National Academy of Sciences, 101 (33), 12228-12231 DOI: 10.1073/pnas.0404926101


For more information or classroom activities, see:

Alternation of generations –

Seed dispersal –

Pollen –

Cycads –

Ginkgo biloba –

Wednesday, January 7, 2015

The Fungus And The Frog

Biology concepts – common descent, evolution, direct descent, fungi, undulipodia, amphibians, phylogenetics

THIS IS NOT HOW EVOLUTION OCCURS!! What this
animation implies is that one type of animal became
another type of animal. It shows a chimp becoming a
human. If so, how come there are still chimps? This
suggests direct descent with adaptation and this is a
fallacy. What is correct is that the animals shown did all
share a common ancestor at some point.

The first life on Earth is a mystery to us. Our best guess right now states that whatever it was, it showed up about 3.5-3.7 billion years ago. It was a cell, let’s call him Luca (last universal common ancestor). Luca had DNA, or maybe just RNA. He had ways to harness and use energy for his purposes, to adapt to changes in his environment, and to reproduce. Luca possessed all seven of the characteristics of life.  

Every living thing you see around you, and all the living things you can’t see around you, are descended from Luca. But here is the part that’s a little harder to understand – it hasn’t been a straight line from Luca through all other life forms to you.

It’s the difference between common descent and direct descent. Just because humans and pine trees have a common ancestor, it doesn’t mean that we are direct descendents of the same organism.

At some point, about 3.5 billion years ago, archaeal prokaryotes were recognizable. Luca gave rise to archaea and also to bacteria, but we can’t say that bacteria descended directly from archaea. There are as many differences between archaea and bacteria as there are between you and a pine tree, maybe more. All we can say is that they diverged from a common ancestor, which is why they have some common characteristics (from a common ancestor), and many different characteristics (because they diverged).


This is a much better representation of evolution
through common descent and adaptation. We may not
know what exact organism was the last common ancestor
between any two branches since only the fossil record only
represents about 1% of species that lived.
Bacteria were, and are, just about perfect organisms. They were bacteria then, and they are bacteria now - why mess with perfection. They have diverged into many types of bacteria, and those types are diverging even today, but they have stayed as bacteria.

Archaea, as opposed to bacteria, diverged again and again, giving rise to the rest of the kingdoms we know today – protists, plants, fungi, and animals. The question is, why did they diverge so much, while bacteria stayed so much the same?

I don’t know the answer, but a good theory is the development of organelles. We have talked before about how an archaea swallowed a bacteria, but didn’t destroy it, and how that the eukaroytic nucleus. Another instance in this endosymbiosis theory formed the mitochondrion. The more complex something is, the more chance for it to respond to changes in the environment – more adaptation could have led to more divergence.

Through billions of years of struggle and adaptation, the eukaryotic kingdoms emerged – but again, you can’t say that one descended directly from another. Contrast evolution to the alphabet. C follows B, which follows A. Humans like to think linearly. But consider that there may be millions of A’s. Must they all become B’s and then C’s?

No, millions of A’s may breed and remain A’s over the years, while what became a B breeds and stays a B. Maybe later on a couple of A’s breed and have a little baby that looks like neither an A nor a B. Now we have C. B and C or both diverged from A, but B and C are different from one another. They are linked by common, but not direct, descent.


This is a phylogenetic map of the life on Earth. Notice that
we don’t know just what the last common ancestor was, but
you see that eukaryotes diverged from archaea and that
animals, plants, and fungi diverged from protists
(microsporidia, flagellates, ciliates, slime molds) rather
recently. Trees may look a bit different based on what DNA
target gene is being compared.
Scientists use changes in DNA over time to track just when two lines of organisms diverged from their last common ancestor. They can plot this out by time and distance, forming a diagram. This is the study of phylogeny (from Greek phylos = race, and genesis = birth of) and its tools are phylogenetics. Because the diagrams can look like trees, with the common ancestor as the base of the trunk, they are called phylogenetic trees.

A long time ago, a few archaeal descendents had diverged enough to be called protists. They were eukaryotic now, with organelles and special functions, and were starting to think about working together as multicellular organisms. The protists of that time were direct descendents of archaea, but the different protists we know today (see our last few posts here, here, and here) aren’t necessarily directly descended from one another or even from the same archaea.

Some protists diverged from one another. Many stayed as protists, even though they might have evolved to different orders or families over the years. However, others became animals, fungi, or the plants. Our last common ancestor with plants was a protist of some sort, so we have a common ancestor with a pine tree, we just can’t draw a direct line through humans and a pine tree to get to that ancestor.

Let’s use undulipodia (eukaryotic flagella and cilia) to illustrate, or confuse, the situation. We saw that protists – most all of the different protists, use flagella or cilia in one or several ways. Flagella and cilia are characteristics that have been retained in the various descendents of archaea…. But didn’t we also say that prokaryotic flagella and eukaryotic undulopdia are completely different in structure and genes? Yes we did - so what gives.


This is a typical fungus that someone might think of. This is the
basidiomycete mushroom, Phallus indusiatus. Fungi can range
from single cell yeasts (yeah beer!) to hyphal forms that make
your tongue fuzzy, to mushrooms that can take up thousands of
acres. By the way, in New Guinea they worship P. indusiatus as
sacred and that lacy web is called an indusium.
The archaea that diverged to become eukaryotes lost their flagella at some point, and then very quickly evolved them right back again. The structure of the new flagella were different; made from different proteins and having a different structure, but they did about the same job(s).  This re-evolving of a flagellum (and cilium) must have occurred pretty quickly, because all the kingdoms that descended from those early eukaryotes (protists, plants, fungi, animals) have them to some degree or another.

Yet, if you look for undulipodia in the fungal species on Earth today, you’ll find them in only one of the five phyla. Again, what gives? Didn’t we just say that fungi descended from undulipodia containing ancestors?

Four of the phylums of fungus are grouped by characteristics, both genetic and life cycle – the Chytridiomycetes, the Zygomycetes, the Ascomycetes and the Basidiomycetes. The fifth phylum is called the imperfect fungi because we haven’t found a life cycle in them that we can place into one of the other four phyla. But when we do, as we have for some individuals imperfect fungi, they usually fall into the ascomycete or basidiomycete phylum.

However, only chytrid fungi have flagella. Every species in every other phylum of fungi has lost their undulipodia. If you are thinking in terms of phylogenetics – what does this suggest to you?

Yes, very good – the chytrids are probably the common ancestor for all the other fungi. Those that didn’t diverge enough and stayed chytrids retained their undulipodia, but at some point, others lost their flagella and kept on changing into all the other phyla of fungi over time.


Here is a phylogenetic tree of the fungi, showing that flagella
were lost after the other phyla diverged from the
Chytridiomycetes. On the bottom right is a microscopic image
of the mature sporangium of a chytrid fungus. The
zoospores are inside the sporangium. The dark filaments are
rhizobia, not flagella.
You could do the genetics studies to find out which phylum diverged first, and then which one diverged from that and so on, but it would be a waste of time – it’s already been done. The picture to the right shows the phylogenetic tree for four of the phyla of fungi (minus the bothersome imperfect fungi).

What is so different about the chytrids that they kept their flagella, while the others were suited to live without them? There must be something about the chytrids life cycle and/or environment that required the retention of their eukaryotic flagella. Well, they all live in water, maybe they need flagella to swim around. But look at the picture of the chytrid on the right, I don’t see a flagellum anywhere there.

The chytridiomycete name comes from the Greek chytridion, which means little pot.  The pot holds all their zoospores, their reproductive form. It is the zoospores that have the flagella, so they can swim away and establish themselves somewhere with less competition. But that isn’t a good enough explanation. Many water borne fungi come from the basidiomycete or ascomycete phyla, and they don’t have flagella in any of their life cycle stages. Hmmm.

We have tens of thousands of extant (living today) fungal species, and only about 750 or so have any undulipodia. This makes the chytrids exceptional, and is directly related to their being the common ancestor for all the other fungi. If undulipodia are so important that animals, protists, some fungi, and even some plants have them, then why is it that so many fungi seem to get along fine without them? Maybe they’re the exception.

Let’s tell one story of how the chytrid flagella are important. A species of chytrid, called Batrachochytrium dendrobatidis, is responsible for perhaps the largest vertebrate mass extinction in the history of the Earth - and it's going on right now. Most chytrids are sabrophyitc, meaning they eat dead tissue, but a few are parasitic, mostly on plants.


Although the chytrid infection is a large reason for amphibian
collapse, there are others. Mutagens in pollution are responsible
frogs with extra or missing limbs. You can imagine how that
might interfere with long life and mating. It turns out that
amphibians, being in and out of water, are especially vulnerable
to environmental changes.
B. dendrobatidis, on the other hand, is the only known chytrid parasite of living animals - amphibians specifically. The fungi embed themselves in the keratinized skin of amphibians that find themselves in chytrid-contaminated water and then proceed to digest their skin. As many as 6000 species may be vulnerable to this fungus, and several hundred have gone extinct because of it.

You may have heard of the frightening loss of amphibian diversity on the past decades. The reasons for this are known to be several, including toxic pollutants, climate change, and habitat destruction. But B. dendrobatidis has played a significant role as well. Fortunately, a 2011 study showed that a water flea has a voracious appetite for our frog foe and might be used as a control measure. Unfortunately, a 2013 study showed that chytrid-susceptible amphibians may be succumbing to at least two different, and probably more, species of Batrachohytria. So the problem is probably more complex than we thought.

And yes, you read correctly a couple of paragraphs above. Some plants have cells that have flagella. There are moving plants cells! Those will be our exceptions for next week.




Martel, A., Spitzen-van der Sluijs, A., Blooi, M., Bert, W., Ducatelle, R., Fisher, M., Woeltjes, A., Bosman, W., Chiers, K., Bossuyt, F., & Pasmans, F. (2013). Batrachochytrium salamandrivorans sp. nov. causes lethal chytridiomycosis in amphibians Proceedings of the National Academy of Sciences, 110 (38), 15325-15329 DOI: 10.1073/pnas.1307356110

Buck, J., Truong, L., & Blaustein, A. (2011). Predation by zooplankton on Batrachochytrium dendrobatidis: biological control of the deadly amphibian chytrid fungus? Biodiversity and Conservation, 20 (14), 3549-3553 DOI: 10.1007/s10531-011-0147-4




For more information or classroom activities, see:

Common descent –

Fungi –

Amphibian collapse –

Phylogenetics –



Wednesday, December 31, 2014

It May Be A New Year, But It’s The Same Old Brain

Biology concepts – learning, habit, long term potentiation, neural plasticity

50% of Americans will make at least one New Year
resolution, but a quarter of them won’t even make it
one week before relapsing. However, those who write
down a resolution are much more likely to make
changes than those who don’t make a specific
demand of themselves.
I swear, this year I’m going to get these posts written a month in advance. Really, I mean it this time. I know I said the same thing last year, but this time I’ve got a plan in place –- yeah, sure. Biology is stacked against me here; making new good habits is definitely an exception. Our brains function to make it hard to change our behaviors – but it is possible.

First things first, I am not a neurologist. I don’t even play one on TV, but we’re going to delve into some neuroanatomy and neurochemistry here. I’ll try to keep it from making your brain hurt.

Before diving into the gooey mess inside our skulls, we need to know that keeping a resolution means creating a new habit, or breaking an old habit and replacing it with a new one. But, what is a habit anyway?

A habit (from old French meaning “to hold” or “customary practice”) is an extreme form of learning, ingrained to such an extent that we do not think consciously about performing the behavior. But we still have the ability to turn the behavior on or off consciously. This is what separates a habit from an addiction. A poor man’s definition – if you have to decide to do it, it’s not a habit, and if you can’t decide not to do it, it’s an addiction.

William James was trained as a physician, but was
the first professor to start offering psychology classes
at the college level. His brother was novelist Henry
James, who wrote about the social corruption of
England versus the brash selfishness of America. His
father was a theologian who worried about the moral
evil have thinking about oneself, and Sigmund Freud was
a family friend. No wonder William went into psychology.
The philosopher and psychologist William James said, “99% of our behavior is purely automatic ….. all of our life is nothing but a mass of habits.” This is mostly true, we need to save our thinking for things that are important and undetermined, not for everyday things for which we can easily predict the outcomes and do not threaten our existence. You don’t think about putting one foot in front of the other when you walk, you look for the bus that may stop you dead in your tracks.

Habits are important, they keep us safe and alive for the most part. Good habits aren’t easy to make, while bad habits seem so simple. Bad habits are rewarded at more primitive levels of the brain, and the rewards are more tangible and shorter term. Good choices may be their own reward, but in terms of our brains, they aren’t as strong as a big ice cream sundae.

Rewards reinforce our habits and learning in a chemical sense as well. The reward centers of the brain release a neurotransmitter called dopamine, and we will see below that dopaminergic neurons are very important in learning, memory and making habits.

We need to know how our brains make habits if we want to increase our chances of keeping our resolutions. First comes intent and motivation, then comes learning, then comes making the learned behavior an unconscious act. As it turns out, there are brain centers for all these things, and they're all tangled together.

Dopaminergic neurons release, and may respond to, dopamine. They are involved in reward, learning, and in reinforcing learning to make habits. Dopaminergic neurons are located in many parts of the brain and a new study shows just how important they are in forming habits.

To help uncover the mechanisms of habit making, a mouse model has been developed that can’t form strong habits. A certain receptor was eliminated from dopaminergic neurons, and then the mice were taught new conditioned behaviors, like stepping on a lever to give them food. They could learn that the lever motion provided food, but they stopped after a while. Normal mice will learn the habit, and just keep stepping on the lever to get more and more food.

NMDA receptors contribute to LTP by allowing calcium
into the cell. This stimulates a retrograde signal that
causes the presynaptic neuron to release even more
glutamate. This stimulates more NMDA action and even
more calcium influx. This loop can literally remain
turned on for months!
The receptors in question work with dopaminergic neurons to reinforce signals and strengthen nerve firing. They are called NMDA receptors, and they respond to glutamate, an amino acid and important neurotransmitter. In the synapses (gaps, Greek; syn = together, and haptein = junction) between neurons, NMDA receptors bind glutamate and then allow sodium and calcium into the downstream neuron. These work in different ways to make the firing of the neuron stronger. Calcium in particular can keep the upstream neuron firing and keep stimulating the down-stream neuron. This leads to long-term potentiation (LTP).

LTP results in repeated firing of those neurons, from minutes to months in duration. Every time they fire, that individual pathway gets strengthened. This is the key to learning, called neural plasticity. When neural pathways are repeatedly used, they become strengthened and a behavior is learned or remembered. If they are not used, the connections fade away. Dopaminergic neurons are especially important because they can generate LTP through NMDA receptors but can use additional mechanisms as well.

Many parts of the brain are involved in habit formation, like those that link intent with action. Peter Hall at University of Waterloo near Toronto has been looking at intent and brain function, specifically, a portion of the brain called the superior prefrontal cortex (SPFC), located just behind that place on our forehead where you smack yourself when you do something stupid.

Some people have better SPFC function than others, and they find it easier to act on intentions and make behavior match intention. But good habits can increase SPFC function – see the end of the post.

Adolescent brains are maturing at an astonishing rate
during the teen years, but the maturation is uneven. This
means that they often revert to the more primitive,
emotional brain for decision making. The emotional brain
includes the reward center, so teens are more likely to make
habits based on short-term rewards. Good school work and
behavior habits are tough to develop in these befuddled brains.
The prefrontal cortex is more than just the SPFC. A 2009 study showed that the ventromedial prefrontal cortex is important in self-control, while the dorsolateral prefrontal cortex is important in meeting goals. And we all know that we need some hefty self-control to keep resolutions.

The entire prefrontal cortex is a big player here, as this is the seat of the executive function, those functions of the brain that control and manage other thinking; like planning, problem solving, resisting immediate reward, and mental flexibility. It boils down to this: the PFC is the chief weigher of risk vs. reward and is the boss decision maker – although he often listens to the primitive brain that, “wants what it wants when it wants it.”

The signaling from the PFC communicates with other brain areas that are needed for habit formation. These include the nucleus accumbens and the ventral tegmental area that are deeper and older. These just happen to be those reward centers we talked about that reinforce actions based on the pleasure they bring.

Dopaminergic signaling in the nucleus accumbens has a lot to do with LTP and plasticity. A 2012 study shows that dopamine in the nucleus accumbens works to reinforce strong signals while inhibiting weak ones. So burgeoning habits get reinforced and become strong habits, while changing habits is difficult because the signals to do so are inhibited. Plasticity isn’t an easy thing to induce.

For every resolution you make, there is an unconscious
resolution not to change. One reason that habits
(good or bad) are hard to break is because they have been
successful to this point; you aren’t dead yet. Changing a
habit means a journey into the unknown, and change is
evolutionarily dangerous; why change what has hasn’t hurt
you yet? This is why bad habits that take a long time to
manifest are so insidious – like a chain-smoking 2 yr. old.
Another reason habits are hard to break is the reinforcers; those things that trigger the behavior are a part of our everyday lives. You need to stay away from these reinforcers (temptations might be a better word) because your brain remembers those reinforcers for a long time. It stores the contexts in which the habits are triggered and can bring back the behavior of the context is encountered again. It takes time for plasticity to weaken these pathways.

It takes willpower to keep yourself out of those situations where bad habits are reinforced. It turns out that your willpower is a real thing, requiring energy to work and it can actually tire out. First proposed by Roy Baumeister in 1998, he showed that when people are asked to employ willpower to resist a temptation, it became harder for them to resist a later temptation. We all know this is true.

In addition, it seems that people with the best self-control use their willpower less often. A 2012 study of Wilhelm Hofmann from U. Chicago showed that people should set up their environments to minimize their temptations, so their willpower was energized for when it was really needed. If you want to stop gambling, don’t go to the track – duh!

Let’s put together all we have learned and get some tips from the experts (Peter Hall at University of Waterloo, B.J. Fogg at Stanford, and others) on how to keep your resolutions.

Exercise affects habit formation. A 2012 study from Brazil
shows that running rats on treadmills induced plasticity
in the habit formation portions of the brain. Proteins and
genes that control the formation and function of synapses
were affected in the striatum – which includes the
dopaminergic neurons of the ventral tegmental area.
1) Make your goal something concrete, you can’t resolve an abstraction.

2) Focus on tiny habits that can be implemented in small doses until you can build it up to something bigger. Don’t say you will learn to play the banjo – say you will learn to play one chord. Then do it over and over.

3) Don’t just say you have intent, make the implementation concrete as well. Where and when will you practice that chord on your banjo?

4) Place your new behavior directly after a good behavior that is already a habit – you will be less likely to avoid it.

5) Reward yourself – even just a nice thought about your ability to meet your goal for that day. It will help reinforce the pathways.

6) Limit your temptations, this will help degrade the pathways that lead to the behavior you wish to change and reinforce the new pathways.

7) Get some exercise – superior prefrontal cortex function in making habits and good executive function improves with physical exercise.

Next week we go back to the undulipodia. Fungi can teach us alot about evolution by looking at which ones have flagella. And one is killing off all our frogs.


Wang, L., Li, F., Wang, D., Xie, K., Wang, D., Shen, X., & Tsien, J. (2011). NMDA Receptors in Dopaminergic Neurons Are Crucial for Habit Learning Neuron, 72 (6), 1055-1066 DOI: 10.1016/j.neuron.2011.10.019

Wang, W., Dever, D., Lowe, J., Storey, G., Bhansali, A., Eck, E., Nitulescu, I., Weimer, J., & Bamford, N. (2012). Regulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core The Journal of Physiology, 590 (16), 3743-3769 DOI: 10.1113/jphysiol.2012.235200


For more information, see:

NMDA receptors –

Long-term potentiation –

Neural plasticity -
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=10&ved=0CG8QFjAJ&url=http%3A%2F%2Fwww.acnp.org%2Fasset.axd%3Fid%3D852ca1c4-ece9-4f2b-988d-bd6b5222e5ac&ei=9Ty-UKeYM9S80QHLtYHgBQ&usg=AFQjCNER4QfEVPqNhq6jrFAXfcQE4DVN_A