#parallel science

It’s time to talk about some ion channels in neurons!

So first, we’ll talk about the fast sodium channel and the delayed rectifier, which is a potassium channel. These are important in action potentials! Both activate around -50 mV. The fast sodium channel activates in less than one ms, the delayed rectifier in 5-20. The fast sodium channel inactivates at around -60mV about as quickly as it activated. It is responsible for the upstroke of an action potential, the delayed rectifier for the falling phase.

Let’s talk about some other potassium channels! First, the A channel, which opens at a rate of about 1 ms. That’s very fast! It likes to open most negative to the threshold, around -60 mV. It usually inactivates negative to that, and at a rate of about 20-50 msec. It leads to a larger and slower undershoot and a higher threshold, so there ends up being a slow, steady rhythm of action potentials. The M channel is closer to threshold and slow, taking hundreds of milliseconds to open. It has no inactivation gate. It causes a delay between action potentials. The falling phase is much slower. 

Now for some calcium channels. We have the LVA, low voltage activated or T channel, and the HVA, or high voltage activated channels. Both take less than 5 msec to open. The LVA is activated negative to the threshold, around -60 mV. The HVA is activated around 0 mV, which we consider highly positive. The LVA inactivated negative to activation and at a rate of 30 msec, whereas the HVA activates around where it activated. Its rate is 500 msec or greater, very slow indeed! The LVA causes a burst of action potentials, then silence. There is a short depolarization bump, then silence, in effect. The HVA causes a slower falling phase, and a longer action potential, so fewer happen.

Finally, there’s the IH or IQ channel. It conducts two ions! It is about equally permeable to sodium and potassium. It causes a characteristic “sag” with some APs afterwards in a sort of group. (It looks like an anodal break, if that means anything to you.) (Look at figure 1c here). It is activated by hyperpolarization - -75 mV is good to activate it. It takes a long time to act, 100s of msecs. 

So. Sleep. It’s finals week, and you’re probably wondering if you actually have to sleep. You do. Let’s talk about how it works in the brain.

Rhythms control a lot of this action. Asynchronicity generally means awake (or REM sleep), and synchronicity generally means asleep (or having a seizure).

What happens when you’re awake? The reticular formation is very active, and the thalamus sends lots of information to the cortex. The reticular formation has lots of those diffuse modulatory system neurotransmitters, like serotonin and norepinephrine in the Raphe nucleus and the locus coeruleus respectively.

When you’re asleep, the thalamus starts to make a very synchronous rhythm that stops information from coming to the cortex. That makes you sleep.

Sleep has four phases that are called non-REM, then something called REM. 

In non-REM sleep, a place near the thalamus called the VLPO. It has GABA that inhibit the brainstem arousal neurons of the reticular formation. Interestingly, older adults have slight problems here, which leads to a different sleep pattern with lots more wakings.

REM sleep is different. Acetylcholine in the subcoerulear nucleus goes to the magnocellular nucleus of the medulla, which inhibits spinal cord motor neurons. This paralyzes you while keeping your mind dreaming.

this is really short sorry! if anything’s wrong tell me xo

fun side note: i just read a paper that says that when you sleep your brain cells get smaller and toxins are flushed out? cool

Let’s talk about the brain’s response to stress (and along the way, we’ll talk about anxiety and depression, which are really closely related to stress and to each other)! As always, if something’s wrong, you should tell me.

First, let’s define stress.

1. Stress requires increased excitability and measurable increased arousal.

2. The experience must be perceived as aversive - an example of this would be avoidance behaviour.

3. Controllability determines the magnitude of the stress response.

The brain responds to stress in three ways.

1. The autonomic nervous system is activated. The sympathetic nervous nervous system activates quickly and uses norepinephrine and epinephrine (also known as adrenaline).

2. Hormones are released - a slower response, but it lasts a while.

3. Avoidance and vigilance behavior starts.

The autonomic nervous system is always on in one way or another, whether sympathetic or parasympathetic. They’re usually arranged in opposition to each other - the parasympathetic will, for example, relax something the sympathetic nervous system constricts. Cell bodies are in the brainstem, spinal cord, and sympathetic chain ganglia.

There’s a two neuron system: one has its body in the spinal cord and ends around the sympathetic chain or other peripheral ganglia, where the other starts until it goes to, say, the liver or heart. The first one, since it’s the ANS, uses acetylcholine, the second norepinephrine (the parasympathetic second neuron uses acetylcholine as well.)  Norepinephrine and epinephrine (from the adrenal medulla and also called “adrenaline”) are released in times of stress.

Sometimes stress is good - if a rat is in a situation where it can press a lever to avoid a painful shock, it has high dopamine levels, moderate cortisol, and low epinephrine. If the bar pressing no longer works, cortisol and epinephrine shoot up and dopamine levels fall. If this keeps happening, the rat keeps at very high cortisol, high epinephrine, and very low dopamine levels.

These high cortisol levels can damage the brain. Usually, cortisol goes back to the hippocampus, making it tell the hypothalamus to stop making CRF. But if it goes too much, it will actually kill the cells by elevating glutamate so high that they are poisoned. Severe stress disorders can even do this some in humans. Cortisol injections impair verbal declarative memory, for example.

The amygdala, which also regulates the hypothalamus, is important in avoidance behaviors and such. When it positively regulates the hypothalamus, the HPA axis that produces cortisol is activated, and the sympathetic nervous system’s response starts. When it goes to the periaqueductal gray matter, avoidance behaviour starts. When it goes to the diffuse modulatory systems, vigilance is increased.

This stress behaviour that’s so heightened can cause anxiety or a mood disorder such as depression. There are many types of anxiety disorders, and lots of treatments. One that’s often used for social phobias is called a beta blocker. It blocks the beta-adrenergic receptor, which means that the sympathetic reactions are all gone. There are also benzodiazepines like diazepam (marketed as Valium), and barbiturates. 

Barbiturates came first, but are no longer used as much, as the dose difference between relief from anxiety and coma is too small. When combined with alcohol, they are extremely dangerous. Benzodiazepines have a larger difference. Both work on the GABAA receptor, as do many anxiety medications. The benzodiazepine receptor can also be bound to by beta carbolines, which actually do the opposite and increase anxiety. That’s called an inverse agonist.

Depression can also come from too much stress, especially if you have a genetic predisposition. That’s called the diasthesis-stress hypothesis - other ones include that depressed people do not have enough BDNF, which nourishes neurons, and that they don’t have enough monoamine neurotransmitters (serotonin, dopamine, norepinephrine). It and anxiety can be treated with therapy, especially cognitive behavioral therapy (which I can personally vouch for).

Antidepressants are also used. The first one was a monoamine oxidase inhibitor (MAOI) called iproniazid. It was intended as a tuberculosis drug, but it made the tuberculosis patients “too happy”. It was then used as an antidepressant until it was discovered to cause liver damage. Other MAOIs took its place. Side effects of MAOIs include agitation and sleep disturbances - which can actually be beneficial, and weight gain. If someone taking one eats too much tyramine, they may go into a hypertensive crisis, which means their blood pressure is too high and can damage their organs. MAOIs work by making sure monoamines are not broken down as quickly, so they are in the synapse longer. At first, you have more neurotransmitter, and then you actually get fewer receptors that are more effective.

After this was found, another type started to be used called tricyclics. They were initially intended as antipsychotics, which they did not work as. They caused sympathetic nervous system symptoms like dry mouth, and various sorts of gastrointestinal problems. They also were sedative for patients. Overdose could cause death, which was worrisome enough that another drug was looked for.

This drug class, serotonin selective reuptake inhibitors (SSRIs), was supposed to be faster, have fewer side effects, and more effective. The first one, Prozac, was none of these, but the side effects were less dangerous. Immediately, these increase serotonin by making sure it stays in the synapse longer, but over time, there are actually fewer serotonin receptors, though they act more effectively, much like with MAOIs.

Electroconvulsive therapy is also extremely effective, though since it makes seizures in the temporal lobes, it can cause memory impairment. It is actually more effective than antidepressants. It’s administered three times a week for three weeks.

Another mood disorder is bipolar disorder. It is characterized by mania, which is an extremely elevated mood state. The first drug to treat it was called lithium chloride, though other lithium salts that are safer are used today. It increases serotonin, decreases monoamine release, interferes with intracellular calcium, and interferes with second messenger cascades.

That’s all for now! (Sorry that the end parts are all so short, it’s getting late here.) If anything’s wrong, please tell me!

Now for the molecular mechanisms of learning and memory!

Long term potentiation (LTP) is what I last talked about with the neurons firing together and then wiring together. Its effects are to make the synaptic strength stronger, and to increase the size of EPSPs. That’s an excitatory postsynaptic potential - and having a lot will lead to an action potential! We are pretty sure it does learning and memory, because chemical manipulation of it so it can’t happen prevents memories from being formed.

In the hippocampus, there’s an important pathway here that starts at the entorhinal cortex perforant, going to a granule cell in the dentate nucleus (this is excitatory), which then goes to CA3 in Ammon’s horn via a mossy fiber, which goes to CA1, which uses a Schaffer collateral to go to the fornix. The fornix goes out of the hippocampus. 

The CA1 neurons are often used to study LTP, because of how easily and reliably it can be induced. When given a tetanus at a specific input, tetanus here meaning a series of (high-frequency) stimulations, a large magnitude EPSP occurs.

The input specificity is important - this is what lets you make specific memory connections, such as between a rose and its scent, versus an onion’s smell and a rose. The first would cause a large EPSP, the second would not. That’s why the tetanus has to be applied to just the right part of the neuron 

The way this works on a molecular level involves two special glutamate receptors. The first is AMPA - it works by opening when glutamate binds to it, and causes depolarization, which is pretty typical. The second is NMDA, and it’s different. It requires that magnesium is cleared from its opening for calcium to come through. This calcium activates a protein kinase, which phosphorylates important proteins, notably more AMPA receptors to be placed in the membrane. It also increases dendritic spikes.

Given a low frequency tetanus, what will happen to these neurons? Between the Schaffer collaterals and CA1 cells, the opposite will happen - a decrease in synaptic strength and EPSP size called a long-term depression (LTD). A little calcium actually does come through NMDA receptors, but it only activates protein phosphatases. They remove phosphate groups - so AMPA receptors come inside the neuron. It might be important for forgetting.

That’s my last learning and memory post! If anything’s wrong, do tell me <3

A quick post about locomotion, the movement of an animal between different places!

(image source here)

Hummingbirds can beat their wings 75 times per second, and stay basically still in the air! Hover flies can hover, too - they beat their wings 1000 times per second! Hummingbirds and hover flies use flight to get from place to place. Only birds and insects have (independently!) evolved true flight. That’s called convergent evolution, by the way! But what does the hummingbird use to make its wings do that?

Muscles! Muscles are the effectors - the causers - of locomotion. Specifically, skeletal muscles. These muscles have three main characteristics:

1. They are anchored to a skeleton, whether an endoskeleton, like ours and the hummingbird’s, or an exoskeleton, like an insect’s.
2. They work in antagonistic pairs - one will relax while the other contracts.
3. They contract, then relax, then contract and relax again. Becaust that’s all they can do. Contract, then stop contracting.

Annelids are pretty interesting in that they have neither an endoskeleton nor an exoskeleton. They just have a really stiff body surface. Each of their segments has its own set of muscles. These segments can coordinate to make them crawl. The segments also have bristles to help them grip the surface.

Next, how muscles work!

Let’s talk about photoreception! That’s how light is made into a neural signal in the primary visual cortex of your brain. 

First, let’s talk about arthropod compound eyes. They have lots of ommatidia, or simple eyes, which each are attached to one axon. One ommatidium is one image. They also have ocelli, which sense light versus dark. These compound eyes mean they sense motion amazingly well!

Human (and all vertebrate) eyes are different. They have image formation and light detection! We have a sheet of specialized cells called the retina on the back of our eyes. 

There are a couple important types of special cells here: rods and cones. Rods are good at low light. They see in black and white. Cones require more light - but their three types of photopigment (the thing that helps them get light!) lets them do colour.

(image source here)

They’ve also got something in them called rhodopsin, which you can see above. It’s made out of two parts - retinal and opsin. Retinal comes from beta carotene, which is why everyone tells you carrots will improve your vision. There are a few basic steps:

1. The photoreceptor (rod or come) is exposed to light.
2. The rhodopsin changes shape.
3. A signal transduction cascade happens. 
4. The release of the neurotransmitter glutamate stops. That’s because sodium flow’s interrupted.

The baseline of vision is dark! When light happens, it turns that off. Light actually has to go all the way to the back of the eye for any of the signalling to happen. 

There’s also focussing with your lens! If you’re nearsighted, the front of your eye is football shaped. That means light can’t hit your retina right. That’s why everything looks so blurry!

And a final list on how vertebrate eyes are optimized for vision.

1. We’re well adapted to light and dark.
2. You can either have monocular or binocular vision. Flat faces like ours in humans lead to binocular vision! (The example that comes to mind for monocular vision is deer for some reason???)
3. We have different opsins for different colours - three, to be exact.
4. We have special places in our retinas for detail called foveas - raptors have two!
5. Some animals have the tapetum lucidum, which reflects dimmest light! Happens in cows. And raccoons.

Anyway vision is really cool! I probably didn’t do it justice here because I’m tired, but I do love it.

Along that vein (that xylem? :p), let’s talk about angiosperm reproduction! (As always, if I mess up, tell me! This is all for me studying.)

Angiosperm reproduction is mostly sexual. Gametes are deposited on another flower (well, hopefully another one for the sake of genetic diversity.) Some are entirely sexual, some entirely asexual, many both. 

Some forms of asexual reproduction are vegetative reproduction and apomixis. Vegetative reproduction is making a new individual from another non-flower part of the plant. Differentiated plant cells can de-differentiate more easily than fully differentiated animal cells. Some plants use the leaves for this, like this beautiful plant!

Mother of thousands plant (image source here)

Other plants use special underground structures to make new versions of themselves. These aren’t roots - they’re really more like stems, but underground! We call them rhizomes. A new plant from root tissue is called a sucker. That leads to aspen forests like this one.

(image source here)

There’s also apomixis (‘without mixing") - it’s like parthenogenesis in animals. An embryo is made without sex - eggs are already diploid. There is no meiosis in the megaspore mother cell.

Why would asexual reproduction be a good thing? Well, for one thing, it increases fitness - if you’re already perfectly adapted, sexual reproduction will mess that up for you. If one genotype works, here you just make a lot of it, and then you’re set! (for now)

But then why sexual reproduction? The genetic diversity is helpful long-term. Say that environment your asexually reproducing plant was perfect for changes a lot, and it no longer works. Sexual reproduction would ensure there’s a chance one genotype will work now.

Pollination is the most important sexual reproduction strategy in flowering plants. There are a couple of main types - animal and wind pollination. 

With animal pollination, you have to attract your pollinators, and animals want a reward. This doesn't have to be a real reward if they think it’ll be one.

This plant attracts wasps! It smells like a female wasp - so male wasps come and try to mate with it. This doesn’t work out, except for the plant, which puts pollen onto him. He’ll fly to another plant and try again - and he’ll pollinate that one! (image source here)

You have to signal that rewards are present. This is why flowers are so beautiful! And finally, you have to get the pollen onto the pollinator. Animal pollinated plants generally have less pollen per flower.

A pretty moth and a pretty flower <3 (image source here)

Wind pollination does not make flowers with sepals and petals - they’re not colourful and pretty. That would waste energy for these plants, which just want to make more pollen. They make tons of pollen per flower, because with wind, most of it’s not going to go anywhere near the right place. 

So now that we’ve gotten those choices down, let’s say our plant has pollinated another plant successfully. A plant baby is coming! How does this work?

A zygote divides into two cells, then four, and so on. Eventually you’ve got two parts - an embryo with its callose coat (prevents chemical signals from coming in, actually!) and the suspensor (basically the umbilical cord - get sugar from parent). This becomes an embryo, cotyledons, and a seed coat down below (from parental tissues). Cotyledons are “seed leaves” - they store food and are the very first surface that does photosynthesis for the plant!

All of that wrapped together makes a seed. The first part of the shoot apical meristem is actually here! So now, we have our baby plant, but what are we going to do with it? We have to get it somewhere! It’s probably in a fruit with lots of other seeds. 

Again, we have a few choices! Unsurprisingly, they’re wind and animal dispersal, with the addition of water dispersal! Wind dispersal leads to beautiful “engineering” like this.

Look at the fluff on this dandelion…

(image source here)

…or the wings on this maple seed!

(Image source here! Has other examples of seeds dispersed various ways. Warning for trypophobia a little while down.)

Animal dispersal either sticks to the animal with burrs or some such thing, or tastes good enough that they eat it and…disperse the seeds at a later time. 

Water dispersal is cool! Basically, seeds float on water till they reach dry land. Coconuts might be an example of this. (Another warning for trypophobia: a lot of water dispersal plants, like water lilies and lotus seed pods, have lots of holes. Don’t look up water dispersal, because one of the first images on Google is a lotus seed pod.)

So that’s about it for angiosperm reproduction! Hope you enjoyed it :)

Let’s talk about the plant life cycle! As always, if I mess up, tell me. Today we’re going to talk about two types of plants - angiosperms, which flower, and ferns. 

Plants are a bit different from animals in terms of their life cycle. They have something called alternation of generations. Generations are phases in the life of a plant. They have a diploid generation - with two sets of chromosomes - and a haploid generation - with one set of chromosomes.

At the end of meiosis, animal cells differentiate and become something else. Plant cells divide. This leads to the haploid generation from a spore, which produces a plant called a gametophyte. Cells divide (via mitosis), but do not separate. Moss is an example of what this can look like. After a little while, a haploid egg and a haploid sperm will, like in us, combine to form a haploid zygote (fertilized egg). 

Remember those spores from earlier? Well, there are different types (at least sometimes). There are microspores, which become pollen, and megaspores, which become the sac for the embryo. Microspores are made in a part of the anther called the microsporangium. Megaspores are in the megasporangium, which is in ovules in the pistil.

(Image source here)

Those are both gametophytes! Pollen is a male gametophyte, and the megaspore is a female gametophyte. Via meiosis, the microspore becomes four, then each divides once. This forms pollen. The megaspore also divides into four by meiosis! Then there’s an embryo sac, which has multiple parts. 

(image source here)

The two nuclei in the central cell are called polar nuclei. The other ones make the egg cell. This will all be more important later, so just remember this!

All this is in the pistil (“female” part of a plant) It has a long stalk called a style, with a receptive surface called a stigma on top. Down lower is the ovary, which contains ovules. Each ovule has one embryo sac. 

The pollen leaves the anther and lands on the stigma. It then germinates, and a pollen tube grows down. It actually has two sperm nuclei (from one generative nucleus) and one tube nucleus. One sperm nucleus fertilizes the egg to make the zygote and the other one fertilizes the polar nuclei, making the endosperm. It actually has three sets of chromosomes (triploid!) and provides energy to the plant. 

An embryo has now been formed via embryogenesis! (Cell division and differentiation) This embryo will keep dividing via mitosis until it becomes an adult sporophyte plant. The embryo, along with the aforementioned endosperm and a seed coat, makes a seed. The seed coat is actually from the mother! Lots of these seeds are in the ovary, which becomes a fruit.

A beautiful adult plant! These flowers can help make new plants :)

Now let’s talk about ferns! 

(Image source here)

As with angiosperms, the sporophyte is the phase you see right there. One difference right away is that it has just one kind of spore it makes, as opposed to the two types angiosperms make. They come from sporangia, which are on the bottom of the leaves.

(image source here)

A unicellular spore is released into the air, and hopefully, it’ll end somewhere wet. Then, mitosis happens! A visible gametophyte called a prothallus is made. It has sperm-producing and egg-producing parts. It is photosynthetic and can live on its own as long as it has to. If there’s enough water, the sperm can swim to the egg-producing section. A diploid zygote is then formed. After some mitosis, you get a sporophyte!

So those area couple of important plant life cycles! Of course, this is not every plant, but just two that are pretty cool :)