There’s nothing in this world so sweet as love. And next to love the sweetest thing is hate.
– Henry Wadsworth Longfellow
I stare hard into his hazel eyes. Those damned eyes. I blink, and I’m bombarded with flashes of those eyes through lenses of love, trust, fear and anger. My blood is pumping with passion, sped on by norepinephrine and vasopressin. The neurons in a round structure at the base of my forebrain are firing like crazy, a cacophony of neural activity. I glance down at his lips. Half of me wants to kiss him – half of me wants to break his jaw.
Part of the problem is that for intense emotions, my body reacts in a similar way. Heart rate and blood pressure skyrocket, driven by stress hormones. My muscles tense. My palms sweat. My cheeks flush. Objectively, it might be hard to tell what I am feeling. Subjectively, it’s hard, too.
Love him or hate him, two regions of my brain – the putamen and the medial insula – activate when I look at his face. Some have suggested that since the putamen regulates motor functions and contains neurons that activate when we plan actions, perhaps it is helping me decide between that punch and that kiss, but there seems to be more going on. The putamen is highly regulated by dopamine, one of the neurotransmitters linked to intense romantic feelings and the messenger of our neurological reward system. I smirk at the idea that, perhaps, I just find the thought of cold-cocking him deeply rewarding.
It is the activation of the insula, though, that is most intriguing. The insula is a bit of a neurological slut, and is intimately involved in our experience of number of basic emotions, including anger, fear, disgust, happiness and sadness. Scientists believe the insula acts as a translater, connecting sensations in our bodies to emotions in our brains. The insula turns a bad taste into disgust, or a gentle touch into arousal. But what makes the insula so interesting is that many believe these connections go both ways. Not only are my feelings affecting my body, the very act of processing my body’s reaction to the situation – my fast pulse, shallow breaths, sweaty palms – is changing how I feel.
As my sensations surge, parts of my cortex responsible for judgement and reason shut down – love and hate really are blind in that way. Studies have suggested love is more blind, though, as larger areas of the cerebral cortex deactivate. I know my thoughts aren’t logical anymore. They’re at the mercy of neurotransmitter tides, waxing and waning. Confusion is an understatement.
I blink hard and try to focus.
Even my hormones are flirting with both sides of the emotional spectrum. The flushed skin, pounding heart and rapid breathing are the fault of norepinephrine and adrenaline kicking on my fight or flight instinct. Passion is passion, and the same hormonal system is triggered by fear, anger, lust and desire. Whatever the fueling emotion, my body is primed, ready to spring into action.
Similarly, the anger-pumping hormone testosterone has a romantic side. Testosterone levels strongly control feelings of lust and desire, but more importantly, women falling in love have higher circulating testosterone. Thus even a hormone so intertwined with agression and hate is instrumental in my experience of romance and pleasure. I briefly wonder if the increased testosterone level in my body is having side effects as I clench my fist.
Sure, love and hate have their differences, too. The giddy, happy romantic feelings come from different parts of the brain than deep passion. But as the intensity of the emotion rises, the fine line between love and hate blurs. It’s no wonder philosophers have been lumping them together for centuries, two sides of the same coin. As glorified as our idea of love might be, passionate love has the same biomarkers as addiction and obsessive compulsive disorder – and like with addiction and obsession, when the stakes are high, the smallest thing can push a person over the edge.
He shouldn’t have pushed me.
My amygdala turns on. Today, the dark side wins. I close my eyes as aggression ripples through my body. I didn’t want a fight, but my body disagreed. Rage fueled by love overwhelms me. It takes everything in my power not to fly at him. Feeling my self-control waning, I clench my teeth. Then, slowly, I open my eyes to see his have hardened, too. Alright, then. Here we go.
Despite only being around for the past century or so, plastics have become ubiquitous in modern life and for good reason: the final product is incredibly versatile. From grocery bags to IV bags to the teflon on non-stick pans, plastics really do make almost everything possible.
But, such a useful product comes at a cost. One of the chemicals used in making certain plastics, BPA, has been linked to a suite of ecological and human health problems. Now, scientists have discovered that the effects of BPA are so strong, certain species of fish lose their ability to tell their own species apart from another.
BPA is the building block of polycarbonate plastics, and is used in other kinds of plastics alter their flexibility. The trouble is, BPA doesn’t stay neatly locked in – it’s known to leech out, contaminating food and liquids that come in contact with BPA containing plastics. Studies have shown that BPA is now in our lakes and rivers, affecting all kinds of creatures that rely on those water sources.
The real trouble with BPA is that it looks a lot like one of the most potent animal hormones: estrogen. It tricks animal cells. Because estrogen controls a number of very important bodily functions, the potential affects of BPA on animals – including us – are severe and range widely.
Jessica Ward and her colleagues were particularly concerned with how BPA is affecting fish in contaminated waters. In Georgia waters, an introduced species of fish – the red shiner (Cyprinella lutrensis) – is encroaching upon the habitat of a native species, the blacktail shiner (Cyprinella venusta). To determine the short term effects of BPA exposure on these two species, the research team placed male and female fish in BPA and control treatments for two weeks, then looked for physical and behavioral changes.
Males that were exposed to BPA changed color, losing some of their distinctive coloring that females use in mate choice (image from the paper on the right). This loss of color affected the females’ behavior: they were less choosy when it came to their mates. Exposure to BPA led to more mixed-species pairings.
“This can have severe ecological and evolutionary consequences,” said Ward, “including the potential for the decline of our native species.” Already, hybridization with red shiners is altering the community composition of native shiners in southern waterways and facilitating the invasion. With BPA and other hormone-mimicking pollutants speeding up the process of invasion, our native species are in for the fight of their life.
While we knew BPA was a problem, this is one of the first studies to reveal how broad its effects really are. “Until now studies have primarily focused on the impact to individual fish, but our study demonstrates the impact of BPA on a population level,” said Ward. Additional studies like this one on other species, from insects to mammals, will help us better understand how BPA and other hormone-mimicking chemicals are affecting our ecosystems. Given the dire situation many of our ecosystems currently face, such knowledge is vital in the effort to protect what biodiversity we have left for further generations.
Citation: Ward, J.L. & Blum, M.J. (2012). Exposure to an environmental estrogen breaks down sexual isolation between native and invasive species, Evolutionary Applications, n/a. DOI: 10.1111/j.1752-4571.2012.00283.x
After a long, cold winter, nothing says spring like the hopeful songs and dances of horny male birds looking for mates. Throughout Europe and western Asia, the blue tit is one of the most colorful birds to engage in this annual hormone-driven spectacle. The males bring their A game, flitting about, singing beautiful songs, and offering gifts, trying everything in their power to convince their potential mates they are the best man around. One thing is for certain when it comes to blue tit love: it’s ladies’ choice. But, as a new study published today in Frontiers in Zoology found, the guys do have minds of their own: they’re better dads when they’ve landed an attractive mate.
Why should looks matter after the kids have been born? Well, from an evolutionary perspective, animals are attracted to individuals that make the best mates. Thus, in turn, attractiveness is a basic assessment of mate quality (though, certainly, other factors carry weight, too). Over a female tit’s life, she may mate with a number of different males that vary in their attractiveness. If the most attractive one she ever mates with is the healthiest, or the one with best genes, or in whatever way produces the best kids, it’s worth her while to make sure that any babies she makes with him are given the best odds of surviving – which would mean putting more effort in to caring for her young when her partner is sexy, and less when he’s just so-so. This change in effort based on mate quality is known as the Differential Allocation Hypothesis (DAH).
Since the female tits are making the decisions, you might think their looks aren’t as important. But once the babies are born, both parents shoulder the burden of caring for their young – and there’s reason to believe the guy’s parental care efforts may contribute more toward baby bird survival. While the female tits spend more time tidying their nest, evidence suggests that when it comes to bringing home the bacon, male blue tits bring in more food – and specifically more high quality food – than their mates. Furthermore, hungry baby tits beg dad for more instead of mom, suggesting that the young instinctively trust their father to feed them when times get rough. Which begs the question: do males slack on their fatherly duties if their mate isn’t pretty? That is exactly what Katharina Mahr and her colleagues at the Konrad Lorenz Institute of Ethology wanted to know.
To test the Differential Allocation Hypothesis, the research team took female blue tits and used UV-blocking chemicals in duck gland oil to dull their pretty color. On others, they placed the same oil, but no blocking chemicals, so their plumage still shone brightly. The UV-blocking chemicals didn’t alter the females behavior in any way, only made them look less ornate to their mates. So how did the males react?
While all males protected their mate and chicks with equal fervor, the males with the less attractive mates made significantly less foraging trips to feed their chicks. Less food means the young are not as strong, healthy and competitive as others, lessening their chance of surviving and reproducing themselves. “The UV reflectance of the crown plumage of female blue tits significantly affected male investment in feeding nestlings,” explain the authors. This decreased parental investment wasn’t compensated for by the female, and thus the chicks are directly and negatively affected.
“This is the first study to show that male blue tit behavior depends on female ornamentation,” said Matteo Griggio, co-author of this study, in the press release. The male tits are likely using attractiveness as a measure of the health of their mate. “Females in bad condition might not be able to provide sufficient parental care, which in turn affects nestling body mass and growth [of the young],” explain the authors. Since getting food for chicks costs the male both food and energy, the male can’t afford to waste his time feeding chicks that might not make it. Instead, he cuts his losses without completely sacrificing his young, and keeps himself healthy and strong for the next set of chicks that will hopefully be with more suitable mate.
Of course, it’s hard to resist the temptation to draw human parallels. After all, blue tits are considered monogamous, though they cheat on their partners and divorce bad matches like we do. However, no evidence for DAH in people has ever been presented, and designing such an experiment would be extremely difficult. Unlike many animals, though, humans are remarkable parents even in extreme biological circumstances. Adopted children and stepchildren receive a lot of parental care from their non-biological parents, for example. It’s unlikely that this kind of differential allocation plays a large role in human parenting. That said, this study of tits does make you wonder…
Citation: Katharina Mahr, Matteo Griggio, Michela Granatiero and Herbert Hoi. Female attractiveness affects paternal investment: experimental evidence for male differential allocation in blue tits. Frontiers in Zoology (in press)Photo of blut tits ‘kissing’ from Wikimedia commons.
Photo of an adult blue tit feeding its young by David Friel via Flikr.
Rafflesia cantleyi, perhaps better known as the corpse flower for its pungent scent, steals everything from its host. Though each blossom can be in excess of three feet across, the massive buds cannot support themselves, and have no leaves, stalks or true roots. Instead, they rely entirely upon their vine host, Tetrastigma rafflesiae, for survival. Harvard researchers have now discovered that food and water aren’t the only things the corpse flowers steal – over the course of evolutionary history, Rafflesia has also stolen Tetrastigma‘s genes.
The corpse flower and its host have a very intimate relationship. From the start, Rafflesia burrows into the Tetrastigma‘s tissues, growing as thread-like strands in direct contact with the surrounding vine’s cells. They are so dependant on their host that the corpse flowers have even lost the ability to make chlorophyll, a requirement for photosynthesis, and thus defy the very nature of being a plant by being unable to produce food from sunlight. These parasites feed off their host vines, growing and growing until they finally erupt, dramatically if briefly, into large, rubbery flowers that stink like rotting flesh.
Somehow, after generations and generations of intimate contact between parasite and host, Rafflesia has ended up with more than the usual parasitic spoils. As a new study published today in BMC Genomics reveals, the parasite expresses dozens of genes that it has co-opted from its host.
The passage of genes from distant lineages, such as the corpse flower and its vine host, is known as horizontal gene transfer. Though common in bacteria (e.g. the transfer of antibiotic resistance), it is much rarer in plants and animals, and we still don’t fully understand how it occurs.
Scientists were first alerted that something was a little off with Rafflesia several years ago. At that time, they were looking at a much bigger picture – the overall evolution of parasitism in plants – when they noticed something a little odd in their data. For one of the genes, Rafflesia and similarly deeply-embedded parasites didn’t appear to be related to their closest kin, and instead, appeared to be cousins of their hosts. They hypothesized that such a strange evolutionary relationship could only have evolved in one way: if the parasites had stolen that gene.
Now, the Harvard team has sequenced all of the active genes of both the corpse flower and its host to determine how many genes were stolen. Researchers found that 49 of the proteins expressed by Rafflesia – 2% of its transcribed genome – are bootlegged.
“We found that several dozen actively transcribed genes likely originated from the flower’s host,” said Zhenxiang Xi, first author and a graduate student at Harvard University. They also found that most of these genes were incorporated into the parasites own DNA, even replacing similar genes, and another third of Rafflesia‘s own genes have evolved to look more like the vine’s.
The genes that were stolen perform a wide variety of cellular functions, including roles in respiration, metabolism, mitochondrial translation, and protein turnover. Their active expression suggests that they play a key role in the parasite’s survival, but the researchers hope that future research will determine exactly how important these genes are and whether they help the parasite evade detection by the host’s immune system. “These findings might reflect a sort of genomic camouflage, or genomic mimicry for the parasite,” says Charles Davis, co-author and head of the lab at Harvard. A bacterial pathogen of citrus trees, for example, produces a hijacked protein which limits the victim’s ability to detect and remove the intruder.
What’s truly remarkable about this study is that the rate of gene transfer between the vine and its parasitic corpse flower is as high as rates of lateral gene transfer seen in bacteria. Never before have scientists thought that horizontal gene transfer could play such a pivotal role in the evolution of plants and animals, let alone in parasite-host relationships. Given that parasites make up for an astounding 40% of the species on Earth, these findings are bound to transform our understanding of evolutionary processes and how we ended up with the diversity of life we see today.
Reference: Xi, Z. & et al, (2012). Horizontal transfer of expressed genes in a parasitic flowering plant, BMC Genomics, 13 DOI: 10.1186/1471-2164-13-227
Our sense of smell is often overlooked. After all, our 20 million smell receptors pale in comparison to the 220 million found in the noses of man’s best friends. We don’t take credit for our ability to distinguish thousands of different smells, even in minute quantities, or how our brains can form strong and lasting memories of scents from a very young age. Yet of all our senses, smell is the first to develop, and before we can feel or see, our noses are hardwired into our brain’s limbic system and amygdala, the parts of the brain where emotions are generated and emotional memories are stored. Since smell detects chemicals in the air, it can warn us of dangers at a distance, even when our eyes and ears are unable to detect them. But more importantly, because it relies on chemicals, smell is one of the most honest ways animals communicate. Human odors, from the smell of tears to underams, have been shown to affect how we think, feel and act, and although we don’t often realize it, our noses play a key role in how we recognize and communicate with one another.
So perhaps it shouldn’t be surprising that scientists have discovered we can distinguish a person’s age by scent alone. In a study published today in PLoS ONE, scientists document how our noses are able to distinguish older people from middle-aged and younger ones not based on the scent mothballs or denture cream, but based on the smell of their body odor.
While we tend to think of B.O. as a reason to wear deodorant, the chemical complexity of Eau de Self is remarkable. Our personal scents can convey a biological and social information, and are thought to play a role in who we like, how we recognize others, and even how we tell men from women. Babies know their mother’s smell shortly after birth, and at a young age we can distinguish between family members and non-family based on their scent. Research has even suggested that we really do have ‘chemistry’ with the people we like, as we can smell immune system differences that might factor into attractiveness, and that we might even be able to smell differences in personalities. Yet there is a lot we don’t understand about how our olfactory system works and exactly what information we obtain through our sense of smell. Given that other animals have been shown to distinguish older animals based on smell, Susanna Mitro and her colleagues from Swarthmore College and the Karolinska Institute in Sweden wondered if smells help us distinguish a person’s age.
To find out, the research team placed pads under the armpits of people in three age groups: young (20–30 years old); middle-age (45–55 years old); and old-age (75–95 years old). Young research participants were then told to discriminate between age categories in side-by-side comparisons and to group the smells according to age as well as rate their perceptual properties like how pleasant or strong the smell. The researchers were startled to find that the participants rated the older aged group’s smell as the most pleasant and least intense. “This was surprising given the popular conception of old age odor as disagreeable,” said co-author Johan Lundström. “However, it is possible that other sources of body odors, such as skin or breath, may have different qualities.” Participants also rated the smell of women to be far more pleasant than the smell of men. But what the researcher’s really wanted to know was whether they could tell the difference between age groups in head-to-head comparisons – and they could.
While the participants were unable to distinguish between young and middle-aged scents, the smell of old age was distinctive. “These data suggest that, akin to other animals, humans are able to discriminate old individuals from younger individuals based on body odor,” write the authors in their conclusion. “The modest effects suggest a limited impact on our everyday interactions but does support previous reports of a unique ‘old person odor’.”
Scientists aren’t entirely sure what makes the smell of older adults different from that of younger people. Studies have found that certain chemicals are present in different levels in older body odor, suggesting that these compounds may serve as biomarkers for old age, but the relevance of these chemicals to age determination has yet to be tested explicitly, and it is unknown whether these chemicals can be detected well by our noses. It’s also unclear whether the ability to distinguish age changes over time. This study focused on young participants as the odor-sniffers, yet it’s possible that the ability to tell age is age-dependent. Older people may lose this ability, or people may be more able to tell ages that are strikingly different from their own. It’s also unclear if the ability to distinguish age has any evolutionary relevance, or if it is simply a byproduct of our more-acute-than-we-think sense of smell.
The researchers also expressed that their study was careful to keep the body odors pure, and thus it is unclear how the scents of hygiene products might affect their results. Does wearing Old Spice actually make a guy appear older, for example? Or does a flowery perfume enhance the youthfulness of a woman? While this study did not explore these questions directly, it has created a foundation for future studies, which may lead to a better understanding not only of our innate ability to determine age by smell but also how our hygiene routines and how product choices affect how we are perceived by others. I can’t wait to see scientists build off these results!
Reference: Susanna Mitro, Amy R. Gordon, Mats J. Olsson, & Johan N. Lundstrom (2012). The Smell of Age: Perception and Discrimination of Body Odors of Different Ages PLoS ONE : doi: 10.1371/journal.pone.0038110
Weighing in at only 40 grams, brown mouse lemurs are one of the smallest species of primate in the world. Their diminutive size as well as their nocturnal, tree-dwelling lifestyle makes them difficult to track and observe. It would have been completely understandable if Sarah Zohdy, a graduate student at the University of Helsinki, had simply given up her quest to understand the social structure of these elusive creatures — but she didn’t. Instead, she and her colleagues came up with an ingenious way to study the interactions of these small lemurs: they followed their lice.A mouse lemur and a close-up shot of lice on its ear. Photos by Sarah Zohdy
For as long as there have been mammals, there have been lice. Though it’s hard to find lice in the fossil record, scientists have estimated that the group originated at least 130 million years ago, feeding off feathered dinosaurs, though they now live on just about all species of birds and mammals. Lice tend to be very host-specific, meaning they only live and feed on one species or a set of closely related species. Furthermore, lice can only survive a limited time without their hosts, and must quickly find a new one if they leave or are forcibly removed. This means that for lice to reproduce and spread, their hosts have to be in fairly close contact (like, as many parents know, kids in a kindergarden classroom). In wild species, lice rarely switch hosts unless the animals interact physically, whether through wrestling, nesting together or mating.
It was that requirement for close contact that made Zohdy and her colleagues think they might be an ideal proxy for investigating social interactions that can’t be viewed directly. They had already been collecting data on the mouse lemur populations in Madagascar using traps to monitor their movement. But while the researchers knew certain lemurs spent a lot of time together if they were caught together in traps, the researchers figured they were probably missing a good amount of social interaction. So, they decided to follow the lemur’s lice as well.
Mouse lemurs are parasitized by a particular species of louse, Lemurpediculus verruculosus, which feed off the lemurs’ blood. The researchers were able to track the transfer of these lice between lemurs by tagging lice with a unique color code using nail polish, so they could tell what lemur each louse started on. Over time, they continued to trap lemurs and look at their lice to see if any of the tagged ones had switched hosts.
In total, they tracked 76 transfers between 14 animals — all males — over the course of a month, which happened to be during the breeding season. The researchers hypothesized that the male-only transfers likely occurred during fights over females. But perhaps more interestingly, the lice data only supported 8 of the 28 expected social interactions predicted by trapping data, and found 13 new ones, suggesting the louse marking technique was able to uncover lemur social activity that the researchers have never observed. They also found that some animals shared more lice than others. Sarah Zohdy explained, “The youngest male in the study had the worst louse infestation, but only donated one louse, indicating a low number of interactions, while the eldest male, who also had a heavy infestation, appeared to be more sociable, collecting lice from many donors. Other males appeared to be ‘superspreaders’ donating but not collecting lice.”
The lice also revealed that lemurs travel more than the researchers had thought. “Most of the louse transfers occurred between lemurs over 100 m from each other, and one transfer spanned over 600 m,” the authors write. “The transfers therefore demonstrate a degree of lemur ranging far greater than anticipated.”
Overall, these data provide new insights into the social interaction of mouse lemurs as well as the relationship between the lice and their hosts. This isn’t the first study that used lice to look at a bigger scientific picture. Because of their host-specific nature, scientists have used them to map ancient speciation events, and even determine when humans first wore clothes. But never before have lice been used to study behavior in a living wild species, though the team hopes their study shows the usefulness of this technique. “The approach developed here has potential for application in any species parasitized by sucking lice, including the many trappable species of cryptic, nocturnal, subterraneous or otherwise elusive mammals in which host social contact and parasite exchange data are difficult to obtain.”
Reference: Zohdy S., Kemp A.D., Durden L.A., Wright P.C. & Jernvall J. (2012). Mapping the social network: tracking lice in a wild primate (Microcebus rufus) population to infer social contacts and vector potential., BMC ecology, PMID: 22449178
“He caresses every bottle like it’s the first one he’s had, saying it ain’t love, but it ain’t bad.”
– Ani DiFranco
Rejection stinks. It literally hurts. But worse, it has an immediate and negative impact on our brains, producing withdrawal symptoms as if we’re quitting a serious addiction cold turkey. It’s no wonder, then, that we are tempted to turn to drugs to make ourselves feel better. But we’re not the only species that drowns our sorrows when we’re lonely – as a new study in Science reveals, rejected Drosophila do, too. Scientists have found not only will these sexually frustrated flies choose to consume more alcohol than their happily mated peers, sex and alcohol consumption activate the same neurological pathway in their brains.
Drosophila melanogaster males sure know how to woo a lady. When placed in the same container as a potential mate, a male fly will play her a delicate love song by vibrating one wing, caress her rear end, and gently nuzzle her most private of parts with his proboiscis to convince her that he is one heck of a lover. But even the most romantic fly can’t convince an already mated female Drosophila to give up the goods, so scientists were able to use the girls’ steely resolve to see how rejection affects fly drinking behavior.
“Alcohol is one of the most widely used and abused drugs in the world,” explains lead author Galit Shohat-Ophir. “The fruit fly Drosophila melanogaster is an ideal model organism to study how the social environment modulates behavior.” Previous studies have found that Drosophila melanogaster exhibit complex addiction-like behaviors. So in the controlled setting of Ulrike Heberlein’s lab at the University of California San Francisco, researchers paired male fruit flies with three types of females: 1) unmated females, which were willing and happy to mate; 2) mated females, which actively rejected the men; and 3) decapitated females, which didn’t actively reject the guys but, well, weren’t exactly willing partners either. After the flies were satisfied or frustrated, they were offered regular food and food spiked with ethanol, and the researchers measured which type they preferred to see if there was any connection between sex and drinking.
The flies that were rejected drank significantly more than their satisfied peers, but so did the ones paired with incapacitated girls, suggesting that it wasn’t the social aspect of rejection but sexual deprivation that drives male flies to increase their ethanol consumption (see the video at the end!). This alcoholic behavior was very directly related to the guy fly ever getting laid, for even after days of blue balls, if he was allowed to spend some time with a willing woman, he no longer preferred the spiked food.
What the scientists really wanted to understand, though, was why. What drives a frustrated fly to the flask? So to look at the underlying mechanism of this phenomenon, the scientists examined the flies’ brains. A body of scientific literature has connected one particular neurotransmitter, neuropeptide F (NPF), to ethanol-related behaviors in Drosophila, so it was a logical place to start. A very similar neurotransmitter in our brains, called neuropeptide Y (NPY), is linked to alcoholism.
Increased expression of NPF in mated male brains, as shown through immunochemistry.
The team found that sexual frustration caused an immediate decrease in the expression of NPF, while sex increased expression. Furthermore, when they used genetics to artificially knock down NPF levels in the satisfied flies, they drank as much as their not-so-satisfied friends. Similarly, when the researchers artificially increased NPF levels, flies stayed sober. This is the first time NPF levels have connected sexual activity to drinking. Clearly, NPF levels controlled the flies’ desire to drink, so the team further explored how NPF works in the fly’s brain.
Many animals, including ourselves, possess a neurological reward system which reinforces good behavior. Through this system, we ascribe pleasure or positive feelings to things we do that are necessary for species survival, including sex, eating, and social interaction. Drugs tap into this system, stimulating pleasure which can lead to addiction. Previous studies have shown that flies find intoxication rewarding, so the researchers hypothesized that NPF may play a role in the reward system.
Preference tests showed that artificially increasing NPF levels in the absence of sex or ethanol was rewarding to the flies, confirming the scientists’ hypothesis. This was further supported by the discovery that constantly activating NPF abolished the flies’ tendency to consider ethanol rewarding.
“NPF is a currency of reward” explains Shohat-Ophir. High NPF levels signal good behavior in Drosophila brains, thus reinforcing any activities which led to that state. This is a truly novel discovery, for while NPF and the mammal version, NPY, have been linked to alcohol consumption, no animal model has ever placed NPF/NPY in the reward system.
Understanding the role of NPF in reward-seeking behaviors may lead to better treatments for addicts. “In mammals, including humans, NPY may have a similar role [as NPF],” says Shohat-Ophir. “If so, one could argue that activating the NPY system in the proper brain regions might reverse the detrimental effects of traumatic and stressful experiences, which often lead to drug abuse.” Already, NPY and drugs that affect the function of its receptors are in clinical trials for anxiety, PTSD, mood disorders and obesity. This study suggests that perhaps they should be tested as treatment for alcoholism, too, as well as other reward-based addictions.
Research: Shohat-Ophir, G, KR Kaun & R Azanchi (2012). Sexual Deprivation Increases Ethanol Intake in Drosophila. Science 335: 1351-1355.
A picture of a hydra, from the Encyclopedia of Life
Upon first glance, hydra seem like remarkably simple creatures. The basic description of a hydra would be a tube closed at one end with tentacles surrounding a mouth on the other, made of fragile tissue that can be as slim as two cells thick. No gills, no heart, no brain, no eyes – of course, it would be hard to pack all those organs into a creature a few millimeters long, and hydra certainly seem to do well enough without them. These small relatives of jellyfish are found worldwide, and are some of the only members of the phylum Cnidaria to be found in fresh water.
Yet their modest body plan is misleading. Hydra have fascinated scientists for centuries, for they have a phenomenal capacity to regenerate and may even be immortal. In 1744, Swiss naturalist Abraham Trembly was one of the first to be entranced by these simple animals and reflected, “It seemed to me from the start of my observations that knowledge of the remarkable properties of the polyps could bring pleasure to the inquisitive and contribute something to the progress of natural history.”
The hydra’s simple nature is also belied by their tentacles, which inject a potent neurotoxin into unsuspecting prey using extremely sophisticated cells called cnidocytes. For decades, scientists have sought to understand how these specialized attack cells are triggered. Now, evidence published in BMC Biology suggests these primitive creatures may ‘see’ more than we realized, as the firing of these prey-catching stinging cells is regulated by the same chemical pathway used in our eyes.
Ever since the genome for Hydra magnipapillata was published in 2010, it was known that hydra possess the genes for opsins, the photosensitive protein family found in all animals that can see, but no one knew exactly what they do with them. Unlike other animals, hydra don’t have eyes or eye spots, or any kind of centralized visual sensory area, although they have behavioral responses to light. When David Plachetzki teamed up with Caitlin Fong and Todd Oakley’s lab at UC Santa Barbara, they found that these light-sensitive proteins were clustered on the hydra’s tentacles and around the hydra’s mouth, suggesting that they might be involved in feeding behavior.
Fluorescent picture of hydra tentacle bulbs; Musculature is stained green, neurons, including cnidocytes, are stained red and nuclei are stained blue
In hydra, potent stinging cells are grouped with other neurons in what are called “battery complexes” on the hydra’s tentacles, forming one of the most intricate systems of neurons in an organism that lacks a central nervous system. Using fluorescent molecular probes, the researchers were able to show that opsins are expressed in the same locations. They also discovered that other proteins that are part of the response to light, cyclic nucleotide gated (CNG) ion channel and arrestin, are found in these battery complexes, too. In other words, the stinging arsenals are completely equipped to react to changes in light.
Just because they have the parts, however, doesn’t mean they use them. So to see if the stinging cells themselves, the cnidocytes, are regulated by light, the researchers exposed hydra to LED lights of different intensities, then prodded the animals’ tentacles with gelatin-coated fishing wire as if they were being touched by potential prey. After, the team was able to count how many cnidocytes were embedded in the line as a way of measuring whether the stinging cells were triggered.
They found that bright light decreased the firing of stinging cells – which makes sense, really. “Cnidocytes are expensive to make for a hydra; a significant proportion of their cellular mass is comprised by these cell types. Therefore, it is important these austere animals to discharge them in an economical manner,” explains Plachetzki. Hydra and their relatives in the phylum Cnidaria are known to feed in daily patterns, becoming especially active at dawn or dusk, so it’s logical that they would be less inclined to feed in bright light, which might be perceived as day. Of course, there is an even more straightforward explanation as to why cnidocytes fire when the lights go out – shadows. “It could be that hydra use this sensory function to detect the shadows cast by prey on feeding tentacles, just when the moment is right to strike.” The researchers were able to directly connect the opsin signaling cascade to this change in feeding behavior by introducing a blocker of opsin signaling, cis-diltiazem. In the presence of the blocker, light had no affect, confirming that opsin-based signaling is required for this light-mediated change in cnidocyte firing.
Since hydra have been extensively studied for centuries, it is a bit surprising that we are only now learning how light affects their feeding. “It is strange that nobody had discovered this before,” remarked Plachetzki. “Folks have been playing around with hydra and their photobehavior for greater than 200 years, why didn’t they notice this?” But, he says, when you look at some of the older observations of these creatures, “you get the impression that others might have had this hypothesis as well, but there were until now never any data to support it.”
These findings reveal one of the earliest uses of the chemical pathways that were co-opted to create vision. By learning more about these signaling cascades, we can begin to glimpse back at the very beginnings of sight, and slowly learn more about the evolutionary steps that led to our eyes. Aside from the interesting evolutionary implications, this research may also lead to more direct benefits to humans. Cnidarians, including hydra, jellies and corals, are responsible for tens of thousands of stings every year, a handful of which are fatal. The more we know about how these stinging cells are triggered, the better we can prevent these stings, or even develop a way of protecting swimmers against them.
Reference: David C Plachetzki, Caitlin R Fong and Todd H Oakley (in press). Cnidocyte discharge is regulated by light and opsin-mediated phototransduction. BMC Biology
Lots of animals use chemical cues to avoid danger. Mice will run from the smell of cat urine, for example. But one particular instance of chemical fear signaling has been stumping scientists for 70 years; the release of Schreckstoff by schooling fish.
For some species of fish, when a predator swoops in and injures one fish in a school, the rest will take off in fear. This much we know. In 1938, Austrian ethologist Karl von Frisch claimed that at the root of this behavior was a chemical alarm signal which he referred to as “Schreckstoff,” which means “scary stuff” in German. Since von Frisch’s seminal work, over 100 published studies concerning Schreckstoff have demonstrated that certain fishes have some substance in their skin cells which is released when that fish is injured and causes other fish to scatter. That much, we know, too.
This has perplexed scientists because it seems strange that any animal could evolve to give off that kind of chemical alarm. The other fish aren’t fleeing from blood or any clear signals of death, so what are they so afraid of? And if it’s not a signal of death but instead a signal of danger, as many scientists have argued, where is the benefit to the dying fish? You see, as much as we love the idea of altruism, it’s not very common in the natural world – at least not in its pure form. Doing something purely for the sake of others is of little benefit to an individual from an evolutionary perspective. So, hypotheses have been thrown around wildly to explain this kind of altruistic signaling – perhaps the alarm is to protect close kin, or, somehow, the chemical actually attracts the would-be-predator’s predators, thus giving the injured fish a chance to escape. Despite years of laboratory research, no hypothesis seems to be able to explain the presence of Schreckstoff. Furthermore, though some scientists have offered up potential compounds, what exactly Schreckstoff is has remained a mystery.
Chondroitin sulfate is a specialized chain of sugars that is a major component of fish skin, just like it’s a major component of our cartilage. Using zebrafish, a common laboratory organism, the research team found chondroitin from zebrafish tissues caused other fish to turn fin and run. They even took chondroitin from shark skin – the kind we take as supplements – and found that the zebrafish were terrified by it. The fish were also more afraid when the chondroitin was broken down by an enzyme first. The team hypothesized that when a fish is injured, enzymes released by the wounding break down chondroitin sulfate into smaller sugary chunks, and these bits and pieces, as well as the larger chondroitin molecules released by the wounded cells, are the smell that serves as a chemical alarm signal.
The best part of this discovery is that it solves evolutionary issue that scientists have had with the existence of Schreckstoff. The burden of producing a fear signal while dying doesn’t make sense unless that signal is something the fish already produced for other reasons which is only released in the case of injury – akin to some being afraid of the smell of blood. That way, the evolutionary impetus isn’t on the fish producing Schreckstoff to produce an alarm, it’s on other individuals to detect a sign of danger or death to save their own tails.
Here’s how it goes: once upon an evolutionary time, fish that were sensitive to Schreckstoff were the first to run in the face of danger, and thus were more likely to survive. Over time this would lead to an entire lineage of Schreckstoff-sensitive fish. Since chondroitin is a known component of fish skin for other reasons, but wouldn’t be released into the water unless that skin is ruptured, it perfectly fits this evolutionary scenario.
Because young zebrafish are see-through, researchers were also able to specifically examine what parts of the zebrafish brain are turned on by chondroitin fragments. They found that a specialized part of the brain called the mediodorsal posterior region was responsible for the fearful reaction. What is particularly interesting about this chunk of brain matter is that it is packed with a group of neurons called crypt cells which have no other known function. Scientists have been trying to uncover what these strange neurons do for awhile, and this new discovery may hold the key. Co-author Suresh Jesuthasan thinks that these cells are a part of a special brain circuit which mediates the fish’s innate fear response.
Together, the new findings, published in Current Biology, are the pieces to the Schreckstoff puzzle that scientists have been trying to fit for decades. There are still questions to be answered, of course – how do certain species only respond to injuries by their own species and not those of others, for example? – but this new study has provided valuable insight into fear responses in fish, and perhaps opened up new doors in our understanding of how fear originates and is processed in animal brains.
Article Link: Mathuru et al., Chondroitin Fragments Are Odorants that Trigger Fear Behavior in Fish, Current Biology (2012), doi:10.1016/j.cub.2012.01.06
Here’s the researchers’ video of the fear response:
153 years ago on November 24th a naturalist named Charles Darwin published a book with a rather long and cumbersome title. It was called On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (for its sixth edition in 1872, the title was cut short to simply The Origin of Species, which was found to be much more manageable to say in conversation). It was inspired by an almost five year journey around the world on a ship named for a small, floppy eared canine during which Darwin did his best to catalog and understand geology and the diversity of life he found.
It’s incomprehensible, now, to think of someone writing a single volume that could equally change science as we know it. The two simple ideas that Darwin fleshed out in his first publication were earth shattering at the time. He has since been called both a genius and a heretic for these two theories – both titles equally deserved. But whatever you call him, his vision has changed the world irrevocably. Today, on what would have been his 203 birthday, we celebrate the life and scientific contributions of this man. In honor of the occasion, I am reposting my first Darwin Day post ever, from way back in 2009. Enjoy!
If I ask you what group of organisms is an exhibition of evolution at its finest, what would you say? Most people, I think, would say human beings, or at least apex predators. After all, we have staggering intellect compared to our prey items and clearly dominate the planet, eat what we will, etc. Not only that, we’re insanely complex. Ask some scientists, and they might give you any number of answers. Cockroaches are likely to exist long after we do, as are rodents, so maybe they get the title. Or, being scientists, they might be biased to whatever organism they study. Maybe algae and plants, as the sustenance for all other life. But all of you, in my humble opinion, are wrong. That is, unless you choose parasites.
It’s ok if you don’t believe me yet. Darwin wouldn’t have, either. He and his contemporaries viewed parasites as degenerates who, at best, violated the progressive nature of evolution. Even in The Origin of Species, Darwin refers to parasites as regressive instead of progressive. But truly, no group of species is a better choice for evolution’s finest.
An ant being attacked by a parasitoid phorid fly. Photo Credit: Bernardo Segura
First off, let’s talk numbers. Parasitism is the most popular lifestyle on earth – over 40% of all known species are parasitic, and the number of parasitic species rises daily1. Sure, you might say, but they tend to be small. In that case, let’s talk biomass – weight, just to be clear. One group of parasites, the flukes, have been found to be equal in weight to fish in estuarine habitats, and three to nine times the weight of the top predators, the birds – estimates which are thought to be conservative for the earth as a whole2. Though they’re largely ignored when we study food webs, they’ve been estimated to be involved in over 75% of inter-species interactions1. Clearly, by the numbers, they are the most prolific and successful organisms on earth.
But even that is not why I would argue they are evolution’s finest. They, more than any other group out there, both exhibit extreme evolutionary adaptations and spur them onward in other species.
No matter how complex or how impressive any other species may be, it has parasites. We do – lots, actually. Every species we might hold as a masterpiece of evolutionary complexity cannot out maneuver their parasites. Not one. Even parasites, marvelous as some are, have parasites – like a crazy russian doll. They have evolved amazing abilities to survive host defense systems, manipulate host behavior and boost heir own reproductive success. They’ve even been implicated in major cultural differences in people. It turns out that a rat parasite, Toxoplasma gondii, needs to be eaten by a cat to complete its lifestyle. Somehow it developed a trick to make rats unafraid of cat smells. When it accidentally ends up in people, it does the same kind of mind-altering, making people more guilty and insecure, even more frugal, mild-tempered, and complacent3. Other parasites do far more intricate manipulations of behavior, turning males into females, creating walking zombies, even forcing suicide. If parasites can not only break into and survive the most complex assortments of systems available, even with modern medicine fighting against them, and manipulate those complex organisms to slave to their bidding, how can we not credit them as masters at what they do?
A malaria-infected blood cell. Image Credit: NIAID
But even more impressively, I would argue, is that no other group has so dramatically impacted how other species have evolved. They don’t just affect their hosts immune systems, either. If you read much into evolutionary theory, you realize it’s riddled with parasites. Why are some birds very colorful? Oh, because if they’ve got a lot of parasites they can’t be, so it’s a signal of a healthy male4. Why are we attracted to certain people? Because their immune genes are different from ours, giving our children the best chance to fight off the next generation of parasites. Almost everywhere you look, evolutionary changes are spurred on by parasites. It’s even suggested that sex itself evolved as a response to parasites. It’s a way of better shuffling our genes so that we have better odds at fighting off parasites.
Even we, as “ideal” or “complex” as we are, owe much to parasites. Some even argue that we are worse off without them. The argument, as it goes, is that our immune system evolved in the presence of unkillable parasites, particularly the parasitic worms. These worms, or Helminths as they are called as a group, were too costly to try and eradicate. Attacking foreign invaders, after all, is energetically expensive, and always runs the risk of over-activating our immune system, leading to self-inflicted injuries and diseases. So the best strategy, instead, was to have an immune system that functioned optimally against other issues, like the fatal viruses or bacteria, despite the mostly benign worm infections5. Since worms secrete anti-inflammatory compounds to fight off our defenses, we were better off with systems that overcompensated for that. Now, since we have drugs which kill them off, our immune system is out of balance. Many cite the rising rates of auto-immune and inflammatory diseases like allergies, arthritis, irritable bowel, type 1 diabetes, and even cancer in developed nations as evidence that ridding ourselves of helminths has damaged our health6. They’re backed up with multiple studies that show unexpected results, like that mice genetically predisposed to diabetes never develop it if infected with flukes at an early enough age.7
Parasites are uniquely capable of out-evolving their hosts and adapting to whatever changes go on in them. Simply put, they evolve better. They change their genes faster and keep up with a barrage of host defense systems, often like it’s effortless, spurring onward dramatic changes in other species. If Darwin had only known how amazingly complex the barriers these creatures have to overcome and the extent to which they have affected the species he’d encountered on his travels, he would not have labeled them “degenerates”.
As far as evolution is concerned, no group of species demonstrates it, causes it, and is so capable of it as the parasites. While disgusting or even cruel, they are truly evolutionary masterpieces. So while you may find them vile or detestable, you have to admit they’re good at it. Can you really argue that some other group is more deserving of the title of Evolution’s Finest?
Cited: 1. A. Dobson, K. D. Lafferty, A. M. Kuris, R. F. Hechinger, W. Jetz (2008). Colloquium Paper: Homage to Linnaeus: How many parasites? How many hosts? Proceedings of the National Academy of Sciences, 105 (Supplement_1), 11482-11489 DOI: 10.1073/pnas.0803232105
2. Armand M. Kuris, Ryan F. Hechinger, Jenny C. Shaw, Kathleen L. Whitney, Leopoldina Aguirre-Macedo, Charlie A. Boch, Andrew P. Dobson, Eleca J. Dunham, Brian L. Fredensborg, Todd C. Huspeni, Julio Lorda, Luzviminda Mababa, Frank T. Mancini, Adrienne B. Mora, Maria Pickering, Nadia L. Talhouk, Mark E. Torchin, Kevin D. Lafferty (2008). Ecosystem energetic implications of parasite and free-living biomass in three estuaries Nature, 454 (7203), 515-518 DOI: 10.1038/nature06970
3. Kevin D. Lafferty (2006). Can the common brain parasite, Toxoplasma gondii, influence human culture? Proceedings of the Royal Society B: Biological Sciences, 273 (1602), 2749-2755 DOI: 10.1098/rspb.2006.3641
4. Jesús Martínez-Padilla, François Mougeot, Lorenzo Pérez-Rodríguez, Gary R. Bortolotti (2007). Nematode parasites reduce carotenoid-based signalling in male red grouse Biology Letters, 3 (2), 161-164 DOI: 10.1098/rsbl.2006.0593
5. Joseph A. Jackson, Ida M. Friberg, Susan Little, Janette E. Bradley (2009). Review series on helminths, immune modulation and the hygiene hypothesis: Immunity against helminths and immunological phenomena in modern human populations: coevolutionary legacies? Immunology, 126 (1), 18-27 DOI: 10.1111/j.1365-2567.2008.03010.x
6. Joel V. Weinstock, David E. Elliott (2009). Helminths and the IBD hygiene hypothesis Inflammatory Bowel Diseases, 15 (1), 128-133 DOI: 10.1002/ibd.20633
7. Anne Cooke (2009). Review series on helminths, immune modulation and the hygiene hypothesis: How might infection modulate the onset of type 1 diabetes? Immunology, 126 (1), 12-17 DOI: 10.1111/j.1365-2567.2008.03009.x
I stare hard into his hazel eyes. Those damned eyes. I blink, and I’m bombarded with flashes of those eyes through lenses of love, trust, fear and anger. My blood is pumping with passion, sped on by norepinephrine and vasopressin. The neurons in a round structure at the base of my forebrain are firing like crazy, a cacophony of neural activity. I glance down at his lips. Half of me wants to kiss him – half of me wants to break his jaw.
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