eLife Episode 53: Insect Farmers and oxytocin

29 January 2019
Presented by Chris Smith.

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An ant

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This month in the eLife Podcast, how scientists got oestrogen signalling all wrong in breast cancer, fungus-farming ants and their microbial helpers, how smells influence memory, the tension between Pacific mineral riches and deep-sea species, and how oxytocin boosts bravery...

In this episode

Oestrogen response in breast cancer cells is not cyclical, as previously thought.

00:35 - Oestrogens and breast cancer

Oestrogen response in breast cancer cells is not cyclical, as previously thought.

Oestrogens and breast cancer
with Andrew Holding, Cambridge Institute, Cancer Research UK

Arguably one of the most important discoveries so far in the field of breast cancer is the finding that many of these tumours are sensitive to oestrogens; indeed, the subsequent use of hormone therapy has had a remarkable impact on breast cancer outcomes. But when scientists first looked at how tumour cells respond to oestrogens there appeared to be a very specific and conserved pattern to the response, suggesting that it must be critical to the tumour cells. But, as Andrew Holding explains to Chris Smith, when he tried to reproduce the results in order to understand them at the level of the whole genome, he began to think maybe he should reevaluate his career aspirations as a scientist…

Andrew - So I was hired five years ago to look at how the oestrogen receptor drives breast cancer. So in 70 per cent of breast cancer cases, which is the most common form of cancer, the hormone oestrogen drives the growth and proliferation of tumours. We have this body of literature that said that when you actually supply the hormone to the tumour, the way the tumour turns sort of turns on in pulses, in 45 minute pulses, so these are a bit like daily rhythms - circadian rhythms - but happening on a 45 minute interval. So really kind of rapid response, and we thought this would be a really interesting thing to model and if we could try throwing lots of things at the system and see how it changed those timings, mybe this could have a really big impact on how we develop therapeutics for breast cancer patients.

Chris - Now when you say it comes in cycles, literally the hormone goes to the cell; goes inside the cell - because the way the steroid hormones work is that they physically engage with the genome and turn on and off different segments of the genome - and you're saying that the literature had counselled us that this happens with these funny pulses: it goes on for 45 minutes of activity, then it goes off again. That sounds a bit extraordinary! Why did people draw that conclusion?

Andrew - Yes. So when it first came out, this was extraordinary because, as you mentioned, these receptors - oestrogen receptors - they actually bind onto the genes they turn on. And what someone showed, was that one particular gene, that was studied before we had all these genome-wide technologies, was pulsing on and off; and this everyone was astounded by. And then there've been several papers since where people said "look, we see the same thing!" And this is a really tightly controlled mechanism, and it was sort of seen as a dogma of the field that this is how the signaling works.

Chris - And, clearly, if oestrogen plays such a big role in cancer, and it's got this very rigidly-controlled cyclical activity, that must be important; so, therefore, it might be an important therapeutic avenue - is that your thinking?

Andrew - Exactly. And when we came to approach this, genome-wide technologies had happend. So instead of looking at one gene, we thought we could look at all 20,000 places in the genome where the oestrogen receptor turns on genes.

Chris - So you are hired five years ago; you're going to try and unpick what's going on. How did you approach the problem. How were you trying to study it.

Andrew - So the first thing I did was try and approach it repeating those original results, so looking at that single gene using these techniques which shows whether the receptors engaged at that gene and activating it. And what I found was on some days or weeks I got something similar and other days I found it was very different. And I kind of assumed it was me and I took it very personally that I was failing to reproduce this work because I wasn't as good in the lab as I kind of hoped I was.

Chris - Oh, ouch! So in other words this whole grand scheme of unpicking this cyclical activity didn't look like it was going to pan out?

Andrew - No; it looked like we had a really big challenge on our hands. And originally, you don't go around assuming that everyone else is wrong; and the other challenge was the methods we used didn't have very good controls; and there were steps the process that you didn't know whether the engagement on the gene wasn't there because you did the experiment wrong, or because it wasn't there. So I had to start thinking about whether it's me getting it wrong or actually the oestrogen receptor isn't doing what we think it's doing.

Chris - So how did you build in the right sorts of controls that would enable you to to unpick this problem and work out whether there really was this on off cyclical activity, or whether - as you put it - the field had got it wrong?

Andrew - So the technique we developed we actually decided to look for something else in the genome that was engaged at positions on the DNA that we could use as a control that we thought would always be there. And the thing we decide to pick on was this protein called CTCF. CTCF is one of the most stable things you can find in the genome. So we then went and checked that this was true in breast cancer. So we had a really robust solid sort of marker saying had we done the experiment right.

Chris - And this means that you can ask, well if I go in and if that control marker is not there some of the time, with a similar sort of frequency that we keep seeing the oestrogen signal going on and off apparently, maybe what's actually happening is that our system doesn't work very well. And in fact people were being misled before?

Andrew - Yes. So the idea was that we'd have this sort of benchmark to know what's going on. The other thing we did was we decided right, we know that people are going to be slightly concerned that we've gone and used a whole new technique, so what we did was we decided previously people would use one - maybe two - replicates in their studies, only doing it once or twice before publishing. We went, well we have the resources here to try and do this six times at 10 different time points. So we're talking about 60 genome-wide experiments and these are big experiments. And the idea of that was we had also the reproducibility to show that whatever you got was consistent every time we did it.

Chris - And what is the bottom line; does this cycle in the way that the field had suggested, or does it not?

Andrew - So the answer seems to be that, if you put oestrogen as a hormone onto these breast cancer cells they turn on and stay on.

Chris - So this is completely different to what people had said. The whole kind of there is this interesting cycle going on, which might give us a new therapeutic avenue, that's just not true?

Andrew - No! it seems to be that, actually, the simple answer is the right one. The only sort of caveat we had to apply to that, when we looked at our control, that was really really nice and stable; when we looked to the oestrogen receptor binding after 10 minutes, so we had a zero - nothing happened; then, at 10 minutes, we found it was really noisy. The signal had quite a lot of variability in it; some replicates there would be a lot of binding and other replicates there wouldn't be very much. But it wasn't tightly controlled. And when you averaged that out across all the genes and across all the time points, you found it was pretty static.

Chris - So does this mean then that what people were seeing and interpreting as these cyclical changes was the noise in the system; it's just random and they were interpreting that as this is this this cyclical binding activity?

Andrew - So there are a thousand papers that cite the original paper, and I went through all 1000 of them, found the studies that did exactly the same conditions - which turned out to be only four - some of them have bar graphs where I read off with a ruler, because the original data - I mean these are 20 year old papers, people didn't put the raw data out then - or they had pictures of these representing this activity and I was measuring how dark the image was using image analysis software, and we reanalyzed this data and what we found was exactly that. And that was just the noise in the system: the variability in how it responds.

An ant

07:27 - Fungus farming leaf-cutter ants

Mollicutes bacteria help leafcutter ants to become better fungus farmers.

Fungus farming leaf-cutter ants
with Koos Boomsma, University of Copenhagen

We depend upon our microbiomes, the populations of bacteria that live all over us, to keep us healthy. They assist us in digesting our dinner; they keep out other disease-causing microbes; and they even manufacture molecules that we can’t and which play an important role in many organs in our bodies, including even the brain. Some insects have gone further and developed an even closer relationship with their microbial passengers, as the University of Copenhagen’s Koos Boomsma explains to Chris Smith...

Koos - Well the research is about attine fungus-growing ants; and they're very special: they farm their own food in underground gardens, and that is almost everything they eat. These ants have been around for a very long time. They emerged shortly after the dinosaurs went extinct. So what we set out to do is actually look at the bacteria that live in their guts. We focused on a group that is called mollicutes: tiny bacteria without a cell wall. They're usually considered to be pathogens, but that didn't make sense to us because there were often millions inside a single ant that never looked sick. So we decided to get two of those genomes sequenced, because if you have that, you can usually infer a lot about what the functions.

Chris - So you can begin to ask questions about what these bugs are and where they might have come from?

Koos - Yes. So we had two sources of background material. One is that the Internet actually has lots of sequenced genomes of similar bacteria that just live inside other insects. So once you have genomes you can start making these comparisons. The other opportunity to that offered is actually to try and see what their closest relatives are, which gave us some very interesting pointers at where they may come from. And it turned out the two bacteria that we did end up sequencing had very different origins, even though they're in the same group of bacteria; and that one of them is basically findable throughout all the fungus-farming ants, whereas the other is exclusively found in the leaf cutter ants. And it quite intriguingly might have a close ancestor that is actually a symbiont that lives inside the leaves of plants, which is very interesting given that leaf cutter ants actually cut leaves to manure their fungus gardens.

Chris - So your hypothesis then would be that, way back in history when these ants first evolved, they were preying on plants - or interacting with plants - and they acquired these or very similar members of this bacterial family via that route, and they've since incorporated them into their microbiome?

Koos - Yes that is what it looks like. And they actually dominating the microbiome. One thing that we found these bacteria have special abilities to decompose chitin, which is very common in the cell walls of fungi and that is what these ants eat. Two other major things that we found is that both of the symbionts process a single amino acid: arginine. And, finally, that there was an important function of decomposing citrate.

Chris - Tell us about the arginine first; why is that important, and where's all the arginine coming from?

Koos - Well arginine is the amino acid that has most nitrogen and nitrogen is always important because that's what you need for making protein. So nitrogen is often a substance that limits growth. And a hallmark of this symbiosis,  when the ends became completely dependent on farming fungi for food, basically the hallmark of that is that the ants lost the ability to synthesise argenine, because the fungus was providing plenty. So the only kind of challenge that such a clever symbiotic swap may imply is that you later may sometimes get too much and you can't just give a complex amino acid back to your fungus garden when you defaecate on that - because that's what the ants do, they manure the fungus gardens with their own faeces - it is actually very clever if he can first return that to ammonia; and that is exactly what these bacteria - these molecutes - seem to be providing to the ants.

Chris - And what about the other two functions?

Koos - Well the fact that chitin is decomposed seemed obvious, because if you only eat fungus a lot of that will be relatively hard to digest fungal cell wall material. So if you have a bacterial symbiont in your gut that does that for you, that seems to be quite a clever acquisition. The final thing, citrate, is a function only found in the leaf cutting ant symbiont, not in the other one that is general for all the fungus growers. And citrate is something that you typically find in juices that you get when you start cutting fresh leaves, and the leaf cutter ants basically were ingesting - and which they probably couldn't really utilise - until they had a bacterial symbiont helping them to do that. The evolutionary less advanced fungus-growers don't cut fresh leaves - they live off dead plant material which they put on that fungus gardens - so they wouldn't necessarily have any use of having a bacterial symbiont that could handle citrate.

Chris - And do the ants acquire the symbiont when they are larvae? So when they're being fed and nurtured by workers is that when they pick it up?

Koos - Yes, as far as we've been able to reconstruct, when queens found new colonies they will obviously have some of these molecutes with them, and then any new ants that hatches from the pupa in the colony will be fed by her older sisters and acquire her complement of molecutes inoculation, which will then basically mean she in her own body can manage that symbiont as far as is required to be an optimal farmer of the fungus gardens...

Scent sticks

14:26 - Smells boost long-term memory

How do smells influence memory consolidation during sleep?

Smells boost long-term memory
with Laura Shanahan, Northwestern University

A key question in neuroscience is how are memories “locked in”, or consolidated, so that they last in the long term? Speaking with Chris Smith, Laura Shanahan, at Northwestern University, has been asking volunteers inside a brain scanner to memorise things that she pairs with different smells...

Laura - We wanted to understand this process of memory consolidation, and how it can be influenced by sensory stimuli like odours and sounds during sleep. I think the best way to explain this process is to talk about the first reactivation experiment that happened about 10 years ago. So, in this experiment, human participants learned a visual spatial memory task while they were smelling an odour. And in this case it was a rose odour. The idea being that, if the scientists delivered the same rose odour later on while they were sleeping, it might help to improve their memory. When they woke up and they did find this was the case actually. So when participants woke up from sleep they were better able to recall those memories that were linked to that rose odour.

Chris - So you show people something you want them to remember; you present that thing alongside the smell of a rose. And then when they're off sleeping you represent the rose odour and that seems to reinforce the memory recall - their ability to get the memory back - somehow?

Laura - Right. That's exactly right.

Chris - So what was the difference between what was done then and this set of experiments you're publishing now?

Laura - Well, in our experiment we are really focused on the brain mechanism. So how do these stimuli, like odours, influence consolidation during sleep. We used MRI, which is a technique to image brain activity. And the first thing that participants did was go into the MRI scanner and they saw pictures from four categories appear on a four by four grid: animals buildings faces and tools. And the idea here was they were supposed to try to remember where those pictures appeared on the grid.

Chris - So they might see, for example, a picture of a cow and it might be in the bottom left?

Laura - Right. Exactly. So this part of the experiment served two purposes: first, the participants started to learn these object locations. And, second, we could use the MRI data to look at the patterns of brain activity for each subject in response to the different category images. So your brain activity looks different depending on whether you're looking at animals, buildings, faces or tools.

Chris - And then what happened?

Laura - So, next, participants came out of the scanner and they learned to associate objects from those categories with different odours. So, for instance, we might pair a banana odour with animal images; and maybe a cedar odour could be paired with building images, for instance. Next we did a variety of memory tests to see how well subjects remembered those original object locations. So those grid spaces that they had learned previously in the scanner. And then finally we fitted subjects with an EEG cap so an EEG cap is another way to measure brain activity and in sleep research it's often used to tell how deeply someone is sleeping. So we're able to wait until they fell asleep and then we could deliver two of the four category specific odours right to their noses, while they were sleeping in the scanner.

Chris - And the critical point about by using two of the four, you then had the other two as a sort of control, didn't you; the two you hadn't presented versus the two you had you could compare the relative performance of the recall of one so the categories against the other sort of categories?

Laura - That's right. So our hypothesis was that participants would perform better when they woke up for those objects that had been cued. That is if we delivered the banana odour during sleep then they would be better able to remember those paired animal images when they woke up.

Chris - And is that what you found?

Laura - So yeah, in fact what we did see is that participants perform better for those cued object locations compared to the non-queued object locations. And what we're even more interested in was to see what was happening in the brain during this time; and specifically we were looking for those same patterns of brain activity associated with the four picture categories to reemerge in response to those odours. So, for instance, if we presented a banana odour to a sleeping participant, we wanted to see whether the animal pattern of brain activity would reemerge at that time.

Chris - And is that what happened?

Laura - We did see a link between the reemergence of these category patterns and behaviour, specifically in a brain region called the ventromedial prefrontal cortex; and this part of the brain is near the front and it's important for many things; among those is recalling remote memories. So what we saw, essentially, is that the more these category patterns were reactivated in this part of the brain, called the ventromedial prefrontal cortex, the better that participants later remembered the associated material.

Chris - So what do you think is actually underpinning this effect, because obviously we haven't evolved to learn by people presenting cues to us when we sleep at the right time in order to reinforce our memories. So this must be pointing at some other fundamental process that underpins how memory works. So what do you think's going on? What is this telling you?

Laura - Yeah. So I think that the fundamental idea here is that memory replay - the idea that the same neurons or brain areas are active during learning are active again later on during sleep in order to reinforce our memories - this is happening all the time. And when we do this specific reactivation technique, trying to use these sensory cues in order to influence memory consolidation, we're kind of hacking into that natural replay phenomenon that already happens; we're taking advantage of that and using it to direct memory consolidation in a way that we choose in our experiments.

Chris - So normally your brain would naturally be replaying experiences to consolidate the ones it wants to keep and reinforce them. But by pairing the thing with the smell first, what you basically do is make the brain present that replay phenomenon more, so you represent the thing that the smells are associated with more often so it gets consolidated better and possibly faster?

Laura - Exactly. Our research supports that theory by showing a specific area of the brain where this phenomenon of memory reactivation is correlated with behaviour.

Chris - Now why is sleep so critical? Because, obviously, we can remember stuff during the day when we want to. Is it just that the brain's having a noisy a time when we're awake, so it's harder to get the result you're looking for?

Laura - Yeah that's definitely one theory. Sleep has been shown for decades to be a particularly important time window for memory consolidation; and specifically deeper sleep is a time period that's really important. And so in these reactivation experiments we specifically target slow wave sleep delivering odours while subjects are very deeply asleep. And this seems to have the particular impact on memory. In our experiment we never delivered odours during wake; but in previous experiments of this kind it's been shown that delivering these sensory cues during wake don't really cause the same memory effects. So we think there's something unique about the brain and its environment during sleep that allows us to do this...

Deep sea creatures from the Pacific seafloor

21:41 - Mining minerals from Pacific seafloor

Taxonomy could help ensure that the resources in our oceans are managed in a sustainable manner.

Mining minerals from Pacific seafloor
with Adrian Glover, Natural History Museum, London

In the latter half of the 20th Century, researchers discovered an abundance of mineral riches literally sitting on the Pacific seafloor. But at up to 5 kilometres down, they’re not easy to access, which is why they’ve remained largely untouched. But as the price of raw materials rises globally, these deeper deposits look increasingly more tempting to exploit. Apart from the depth though, another problem is that these deposits are sitting amongst an incredibly rich animal ecosystem and it’s one that we know almost nothing about, mainly for the same reason that we’ve left the minerals untouched. But before the gold rush begins, speaking to Chris Smith, Adrian Glover wants to see some basic science being done…

Adrian - There's really a remarkable story which is the story of the first attempts to explore the oceans, in particular the high seas, for mineral resources for metals such as cobalt, copper, nickel, which have always been of high value but now have even more value. We live in a time now where companies and contractors, industry are interested in exploring our high seas, collecting these minerals. It started in the mid 1960s, when John Mero, who was a geologist, published a remarkable book, which was really a call to arms in some ways for industry to start exploring particularly a place in the Central Pacific where these small potato-sized mineral accretions - manganese nodules - were; and it was really from the beginning a geological enterprise: can we extract and bring these minerals up and use them to provide an alternative source from terrestrial mining. And now it's major exploration activity and potentially a major environmental issue.

Chris - Why is it a major environmental issue?

Adrian - One of the sort of unique features of our deep oceans is that they are rich in biodiversity. The deep sea's are a remarkable environment. Of course it's very cold and very dark, very deep, separated from the surface oceans - we're talking about mineral extraction here in areas of depths of 4000 to 5000 metres. But the diversity is remarkably high. We don't actually know why. We know that it rivals, for example, actually tropical shelf environments in some cases, but, tragically, the problem that we really have is the lack of actual descriptions of what those animals are. Remarkably, this is really slowing down the process of actually making assessments of environmental impact.

Chris - The cynic in me is wondering whether there is this extraordinary biodiversity there because we haven't got there to mess it up yet?

Adrian - That's true to some extent this is an amazing wilderness area. Our deep ocean abyssal plains are almost half the surface of the planet. If you took away the water, the average depth of the oceans is three thousand eight hundred metres roughly. And humans have essentially not touched. There are some fundamental processes. I don't want to say it's the absence of human impact, but there are some fundamental and remarkable processes which maintain that diversity that we still don't really understand. But this is an environment which is unique and we are trying to understand that, and key to that understanding is actually taxon specific information. What I mean is, what animal is there. What does it look like. What's it most closely related to? What's its evolutionary origin? What kind of ecological role does it play in environment? We're talking about invertebrates mostly; there are vertebrates - fish - down in these environments as well. Nothing is known about them.

Chris - So are you advocating then that before we allow further exploitation of this area that we should advocate strongly that we go and study it properly so that we know what applecart we might be upsetting but equally how to minimise our impact?

Adrian - I think it's fair to say that everyone has really been advocating that, and I mean that from the point of view of the regulator, the high seas the International Seabed Authority, the contractors involved, governments involved. I haven't really met anyone in this day and age that says we should just go in guns blazing and ignore the environmental consequences. What I'm advocating is that we've missed a rather important step in the process, which is the taxonomic work to describe what that biodiversity is in those environments. It's a big challenge. We're looking at a large number of animals - there's no plants down there in a dark environment - all of which are undescribed and we need to know something about them. I don't believe that it's impossible task. I think in a 5 years timescale you could probably describe a thousand new species from an environment such as the central Pacific Mining-contracted areas. The problem has been gaining traction with the regulators and the contractors and the governments involved to fund that research one way or the other...

Chris - Who should fund it Adrian? Do you think this should be added on as a sort of surcharge? "If you seek to exploit this environment, the first thing that's got to happen before you're allowed to do it is you have to fund a research expedition to go and catalog and taxonomise what's in the area you're seeking to explore,"?

Adrian - To be fair to the regulator and the government's support the regulator they do state that at the moment so the regulations are such that only exploration activities are allowed. There is baseline data is to be collected. The costs are very very high and I think it is beholden on governments to help, you know, if they genuinely want to see industry move forward in a sustainable way. They also need to help that research and particularly at the very fundamental level.

Chris - Have you had conversations with those various stakeholders industry governments those people you are advocating to in order to see how receptive they are to this argument?

Adrian - I think they are receptive, and I think that that has been changing. I think what I've tried to make as argument in the piece is a sort of slightly more nuanced argument than we just need to know more things before we go there, which everyone has been saying from almost every side of the argument for decades - to here is some very specific recommendations, which is an achievable goal. And the interesting thing about the taxonomic work is you don't actually need to do it over and over. Once you've described the fauna and have a reasonable handle on that, the job is done and then we can move on! The work can move on to those which are expert in, for example, monitoring of sites over time; you know and people like me and the groups that work on the very fundamental biodiversity of the system we can move on to something else. I think that has been missed in the arguments, and that's one of the reasons I wanted to publish this. And it was very well-received by colleagues at the Seabed Author, by the regulator. This is exactly the kind of recommendations they need to move forward in this argument, from the sort of arm waving scientific argument that we need to know everything before we can do anything to hear some very specific recommendations on how you can solve this particular biodiversity impasse.

Young rats

28:24 - Oxytocin boosts confidence and lengthens telomeres

Oxytocin makes rats more adventurous and protects their cells from ageing...

Oxytocin boosts confidence and lengthens telomeres
with Gerlinde Metz, University of Lethbridge, Canada

Ironically, as the Internet shrinks the globe and the world becomes increasingly better connected, record numbers of people are admitting to being lonely. And, as she explains to Chris Smith, Gerlinde Metz has been discovering that this could have significant impacts on the way our brains work, how healthy we are and even how well we age; the hormone oxytocin is a key player...

Gerlinde - We're very interested in novelty seeking and we were actually using a rat model - rats - that were housed either in a social condition housing with 10 or 11 individuals per cage, or a two or three individuals per cage as a more smaller group setting; and then we testing their behaviour in terms of a field, which has like a corridor on the outside and an open space on the inside; and usually rats try to be on the safe side when they explore a novel environment, so they try to hide in the corners or close to the walls, and what we were interested in was how much time do those rats that had social experiences - over the control conditions of only two or three animals per cage - how much time would they spend in the centre of the field, which is the more open space and potentially a more dangerous space in nature...

Chris - And what makes you think that oxytocin has a role to play in that, and how did you measure that?

Gerlinde - So oxytocin is a hormone which is classically linked to the birth process, and also pair bonding, helping each other, sharing and generosity actions. And we wanted to see if oxytocin is also linked to behavioral changes and this is what we've actually observed: that the female rats especially responded very well to the social housing conditions - so they were actually more brave in exploring - and they were also investigating novel objects that we gave them. We also saw this effect in the male animals, but it was a little bit weaker than in the females overall.

Chris - So you can show that when you put these animals into this socialised environment they respond with an elevation in the baseline of oxytocin in their brains. So you can say that effect is happening and you can see behaviorally they spend more time being adventurous, and you're saying that one is is linked to the other?

Gerlinde - That's right. We've wanted to do a causal study here so we gave these animals an antagonist that is a chemical that blocked the effect of oxytocin. So these animals acted as if they had no oxytocin in their system. So if oxytocin was involved in the behavioral phenomenon that we were seeing, this should have blocked this effect in novelty seeking and adventurous behaviour. And that's exactly what we saw, so these animals that before were investigating more dangerous spaces more often now were hiding away closer to the wall spaces and in the corners when they had this antagonist chemical.

Chris - Why do you think oxytocin does this, and why do you think it does it more to the females than the males?

Gerlinde - So this is a really interesting question. The females showed a really astounding significant difference here, which, I think, might have an evolutionary background. First of all there's a biological phenomenon in that the females are more sensitive to oxytocin. They have more receptors for that in their brains, so certain brain areas are more receptive to the effects of this, but also evolutionarily there might be a benefit for actually the males not paying so much attention to the oxytocin in a biological way, because when they go out hunting or they're attacking invaders they have to fight them. They have to be a bit more aggressive and this would be very difficult if they were acting under high oxytocin levels all the time because this helps social bonding and being generous and sharing resources.

Chris - If one thinks about a woman who's recently given birth though we know that the birth process produces a very big surge in oxytocin, both during the birth and the suckling reflex that happens. Would not the safest thing for that person to do to be to retreat and and stay away from danger with the newborn so that there was less risk of predation? So isn't that sort of slightly counter intuitive? Because the oxytocin you're saying should make her much more daring.

Gerlinde - Well that is definitely a really good question you're bringing up. So as you point out, which is correct, the social bonding is mediated by oxytocin after the birth, also helps milk production and so on. And of course I mean the mother should rather stay safe at home. But also what we see is that with the children in tow we basically venture out a lot as mums! Being a mum myself I took my my daughter out on walks a lot and showed her the world. So maybe there could be a benefit to that: we seek social support. We attend child care groups. We meet with other mothers; we meet with family members. So I think that's a great benefit of having this oxytocin linkage in bringing us out and about and sharing our experiences, which also would reduce stress because oxytocin is kind of the candlelight dinner hormone: it down-regulates the stress response and I think it might make a mum a bit more relaxed!

Chris - It's nice sort of confirmation and corroboration of what we thought was going on, so it's nice that you've come at this from a novel angle and been able to provide additional weight. But why does this actually matter this research?

Gerlinde - So we also had another measurement in our study, which is measuring telomere length. Telomere length is a biological marker of age. Biological age as a really interesting measurement because it can actually predict longevity and successful ageing; and what we did here, we measured telomere length, which is like the plastic tip on a shoelace: it protects the end of a chromosome, and with each cell division the telomere length will shrink. So a shorter telomere length would be indicative of a more advanced biological age. And so we looked at telomere length and we found telomere length was larger in animals that were exposed to the social housing condition. So here we have a really nice correlation between successful ageing and social experiences throughout a lifetime. And I think this has a lot of implications also in understanding what can do about having healthy life trajectories, helping our ageing population to do successfully and protect brain health as well!

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