Showing posts with label sleep. Show all posts
Showing posts with label sleep. Show all posts

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 (http://www.moonlightsys.com/themoon/flower.html). 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 (http://www.youtube.com/watch?v=ymnLpQNyI6g). 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. and Y. Nakamura. 2006. Metabolites involved in plant movement and ‘memory’: nyctinasty of legumes and trap movement in the Venus flytrap. Natural Product Reports, 23 (4): 548-557.

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

nastic movements –

turgor pressure –

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 –
nwabr.org/sites/default/files/learn/bioinformatics/AdvL5.pdf
 

The Best Cure for Insomnia Is To Get A Lot Of Sleep

Biology concepts – theories of sleep, REM sleep, circadian rhythms, neural plasticity

You open the door to your house and find your roommate sprawled out on the couch. Is he sleeping, unconscious, or dead? Knowing your roommate, you figure it could be any of them – you stop yourself short of naming a preference.


You find your roommate passed out in his underwear,
and can’t decide if he is sleeping, unconscious or dead.
If you have chosen Homer as a roommate, you have
already clued us in to your decision-making abilities.
The live/dead question is easy; hold a mirror under his nose and see if it fogs up. If he’s not breathing, there’s only one thing to do – go through his pockets and look for loose change (with a nod to “The Princess Bride”). But if you do see condensation, how do you decide if he is passed out or just sleeping - or are you considered unconscious when sleeping?

Sleep is voluntary, at least most of the time. I try to stay awake at the ballet, but I don’t always succeed. But besides drinking yourself into a stupor, going unconscious is usually not voluntary. Unfortunately (or fortunately), you weren’t there to see what preceded the crease marks on your roommate’s face or his drooling on the couch pillow, so how can you identify his state?

Sleeping implies that one has a diminished ability to respond to external stimuli with reduced sensory perception. However, unconsciousness appears much the same. The difference lies in the degree of diminished capacity; you can be roused more easily from sleep and perhaps not at all from deeper unconsciousness. Some people I know must pass out every night, because they are tough to wake up. You might parse the difference and just say that sleep is more easily rousable unconsciousness.

Sleep has stages and these stages have cycles. If deprived
of a particular stage the night before, your body will
change your cycles so that you make up the lost time in
that stage on the next night. Source for image: http://xavier 
appsychology.wikispaces.com/Chapter+5,+ Period+6
A more profound difference between the two exists, but you won’t be able to detect it in your roommate without monitoring his brain waves. In sleep, you go through different phases, each with characteristic brain wave patterns. In 2007, a revised set of sleep stages was published, identifying 4 distinct phases, although stages 2 and 4 are repeated more than twice. Stage 4 is REM sleep, in which many many animals dream.

In general, the safer an animal is, the more it dreams. Predators dream more than prey and big species dream more than small species, though there are several exceptions to this rule. For example, ruminants (cows, deer, goats, and buffalo) dream very little (about 5 minutes/night), and cetaceans (whales, dolphins, porpoises) may not dream at all.

In contrast, animals that are born immature (not able to live on their own) tend to experience lots of REM sleep. These altricial (meaning “requiring nourishment") animals, including marsupials, cats, dogs, and most rodents, may have 6-8 hours of REM sleep a night. What is more, as adults they continue to dream heavily – about what, I have no idea.


Do you know the differences between dolphins and porpoises? Dolphins have longer bodies and snouts, and porpoises have a straight front edge on their dorsal fin. But, they are both cetaceans and have the same sleep patterns. Opposums, the only marsupials in North America, have immature young, and for some reason they dream much more. They are probably dreaming about the day their kids will get off their back.
 But even this exception has an exception. Many birds are born very immature. They have no feathers, they can’t fly, they usually have their huge eyes closed, so they are definitely altricial species. But, birds have extremely short cycles of non-REM and REM sleep. Avian REM cycles might total only 5 minutes in a night, and each episode might be only 9 seconds long. What can you get done in a 9 second dream?


Brain waves recorded on an electroencephalogram
(EEG) show that dolphins and birds have normal
activity in one hemisphere while the other is at rest.
The heartbeat is constant showing that there is
normal body rhythm. This is unihemispheric sleep.
Image is taken from: Ridgeway, S. et. al. J. Exp. Med.
209:2902-2910, 2006.
REM sleep is deeper and harder to be roused from compared to non-REM sleep, the short cycles might be related to birds’ sleep pattern, which is unihemispheric (one half of the brain) in non-REM sleep, and is probably related to their need to keep watch for predators. Birds don’t lose muscle tone when they sleep; often they have to remain on a perch while they sleep. How embarrassing it would be for a bird to fall asleep and then fall off their branch- they would deserve to be eaten.

Other species of bird can sleep while flying, the arctic tern for example, whose migration can be as long as 22,000 miles one way. During flight, the eye connected the active half of the brain will remain open to navigate, but the bird will not dream, since both hemispheres are required in all animals for REM sleep.

Dreaming less doesn’t necessarily correlate with sleeping less. Animals that dream little may still sleep a considerable amount. For prey animals, sleep may represent a dicey time when they must be on the lookout. But it might also represent a way to stay motionless, blend in, and avoid predators. Either theory is practical, since predators seem to take the old, young, and diseased, whether sleeping or not.

Indisputably, every animal needs to sleep to survive, but why? It is interesting that science hasn’t quite figured this out yet. It is known that many beneficial events occur during sleep, but just being good for you doesn’t make them vital. But it must be vital, since even hibernating animals will cycle from hibernation to sleep in order to reap the benefits. Several theories exist for the necessity of sleep:

Energy conservation theory of sleep. Smaller animals carry less fat than large animals, which means they have a smaller margin of error in energy usage – they must conserve energy or feed more often. By sleeping longer, smaller animals keep their metabolic rate low and conserve more energy for when they need it, like for finding more food.

Related to this, animals with fewer predators seem to sleep longer than animals who may be hunted by many other species (as discussed above). However, since resting saves 90% as much energy as sleeping and that animals could watch for predators while resting, there clearly must be additional reasons to sleep instead of just rest.

Repair theory of sleep. This theory contends that non-REM sleep is important for repairing the physical body. Indeed, cell division and protein synthesis increase during non-REM sleep. On the other hand, REM sleep is necessary for restoring mental function, but we will leave the reasons for why we dream for another discussion.

Information packaging theory of sleep. You may sleep in order to provide the brain with time to process all that occurred the previous day, and be ready to take in more the next day. This relates to something called neural plasticity (new connections, ie. learning) and memory consolidation. Recent evidence shows that sleep deprivation harms recall, so sleep may help move information from short-term to long-term memory.


One theory of sleep is that your brain returns to a set
point so you can learn things the next day. Learning
means making new connections between neurons;
these connections are reinforced by neurotransmitters
being released to stimulate the next neuron in series. If
the neuron isn’t fired, it will not release neurotransmitters
to stimulate the next neuron in the path. If they are not
repeatedly fired, the pathway will no longer exist, and
new connections can be made.
In terms of plasticity, a 2007 study indicated that the slow brain waves in non-REM sleep are linked to our ability to learn new information. Dr. Guioli Tononi stated that neural connections become progressively weaker during slow wave sleep, so that by morning, the connections are ready to record new information, but still strong enough to hold the old memories. 


An extension of this study, published in 2011 by the same group showed that in some groups of neurons, synapse size and number was affected by the amount of sleep that fly and the amount of experience that the fly had. More experience required more sleep in order to prune the connections and strengthen those that were used repeatedly. After a few hours of wake, synapse size and number increased, and sleep was required to reduce those that are weak and strengthen the remaining circuits.

If sleep provides all these benefits, and higher animals can’t survive without it (even insects and worms have periods of inactivity that look a lot like sleep), then how is it that the giraffe sleeps only 2-4 hours per day? As prey, nature may have deemed it more important to stay alert; or maybe they just can’t find a long enough blanket.

Cetaceans, like birds, only let half their brain sleep at a time, so they probably don’t dream either. Being mammals, they still have to be able to surface to inhale and exhale while sleeping, called conscious breathing. This might require that some part of their brain be active at all times.

I say might because most cetacean sleep studies have been done in captive animals (the smaller species). But in 2008, the boat of a cetacean research team accidentally floated into the middle of a pod of inactive sperm whales. The whales were unresponsive to the researchers and had both eyes closed. This agreed with another observation that electronically tagged sperm whales spent about 7% (1.68 hr/day) of their drifting with the tide. If this is true sleep (not unihemispheric), it would be a new finding in cetaceans and would indicate that that sperm whales sleep less than any other mammal.


The American bullfrog is fully alert when inactive, so is it
asleep? Scientists think that the bullfrog is so territorial and
is such a good parent that it will not let its guard down until
it dies.
An even more amazing exception to the sleep rule is the American bullfrog (Rana catesbeiana). Brain wave studies (electroencephalography) of the nocturnally active bullfrog did show signs of rest during the day, but bullfrogs had no loss of sensory perception. They could react to stimuli just as if awake. Other frogs show similar brain waves, but are much harder to arouse. The bullfrog might be the only animal to pull a lifetime all-nighter. He should really be ready for that math test.

Nobody yet knows exactly how sleep restores the brain or why bullfrogs and giraffes need so little, but we do know that people who are deprived of sleep suffer physically, emotionally, and intellectually – or worse. How would you like to be condemned to death for not taking a nap? We’ll talk about this next time.

Daniel Bushey, Giulio Tononi, Chiara Cirelli (2011). Sleep and Synaptic Homeostasis: Structural Evidence in Drosophila Science DOI: 10.1126/science.1202839

For more information, classroom activities, and laboratories on theories of sleep, and sleep in animals, see:
sleep –


stages of sleep and REM sleep –

sleep in animals –
http://thebrain.mcgill.ca/flash/capsules/outil_jaune07.html
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