TheCellularScale

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The Cellular Scale
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  • May 27, 2014
  • 08:16 PM
  • 286 views

Sex alters DNA in the brain

by TheCellularScale in The Cellular Scale

It's already known that sex causes the neurotransmitters dopamine and oxytocin to be released in the brain. But a recent study has shown that sex can epigenetically modify the DNA in the brain in a way that facilitates pair bonding. The Cellular Scale has an article over at The Toast today telling you all about it.Check it out: The Virgin BrainWang H, Duclot F, Liu Y, Wang Z, & Kabbaj M (2013). Histone deacetylase inhibitors facilitate partner preference formation in female prairie voles. Nature neuroscience, 16 (7), 919-24 PMID: 23727821© TheCellularScale ... Read more »

  • February 15, 2014
  • 12:59 PM
  • 439 views

A Hop, Skip, and a pre-synaptic Patch

by TheCellularScale in The Cellular Scale

This new technique is just too cool not to blog about.  Novak et al. 2013 Figure 1A pre-synaptic patch clampThe synapse is the connection between two neurons. The pre-synaptic part is from the neuron sending a signal and the post-synaptic part is from the neuron receiving the signal. If you want to learn about the connection between the two neurons, you want to know what is happening on both sides of the synapse. It's relatively easy to record signals from the post-synaptic side using patch clamp or sharp electrode recording, but it is much much harder (basically impossible until now) to record from the pre-synaptic side.There is a gigantic synapse called the Calyx of Held where the pre-synaptic side is huge and envelops the post-synaptic side like a baseball glove holding a baseball.Calyx of Held (a schematic diagram) source The calyx of held is relatively easy to record from because it is so huge. So it is essentially where all the information about pre-synaptic terminals comes from. But Novak et al. have published a paper using this 'electrode hopping' technique to find and patch normal sized pre-synaptic terminals. A computer controlled nanopipette (which is essentially a micropipette) goes up comes back down across a layer of cells. It 'senses' cell membrane by an increase in resistance and stops before it hits the cell. Then it raises up again and moves over a little bit and comes back down. After a bazillion hops, the whole surface of an area of cell can be mapped. You can see a video of this in their very nice video abstract. After they have mapped an area, they find a pre-synaptic terminal (called a bouton) and they use the same pipette that was just used to map the area to patch the bouton (They have to make the opening of the pipette bigger first, so they just smash it into the glass near the tissue until it breaks...!!.. .but apparently that works). They patch the pre-synaptic bouton and record the calcium channels that help the pre-syanptic cell send its signal to the post-synaptic cell. © TheCellularScaleNovak P, Gorelik J, Vivekananda U, Shevchuk AI, Ermolyuk YS, Bailey RJ, Bushby AJ, Moss GW, Rusakov DA, Klenerman D, Kullmann DM, Volynski KE, & Korchev YE (2013). Nanoscale-targeted patch-clamp recordings of functional presynaptic ion channels. Neuron, 79 (6), 1067-77 PMID: 24050398... Read more »

Novak P, Gorelik J, Vivekananda U, Shevchuk AI, Ermolyuk YS, Bailey RJ, Bushby AJ, Moss GW, Rusakov DA, Klenerman D.... (2013) Nanoscale-targeted patch-clamp recordings of functional presynaptic ion channels. Neuron, 79(6), 1067-77. PMID: 24050398  

  • September 12, 2013
  • 05:57 PM
  • 609 views

Use Imposter Syndrome to become an excellent grad student

by TheCellularScale in The Cellular Scale

Let's talk about Aristotle for a minute.School of Athens Aristotle is the one in blue.Many people mis-attribute this quote to him:"We are what we repeatedly do. Excellence therefore is not an act, but a habit." -Will DurantBut really this quote is from someone summarizing Aristotle. It's a great summary and it seems to say what Aristotle means, just more concisely. Aristotle does say:"For these reasons the virtues are not capacities either; for we are neither called good nor called bad, nor are we praised or blamed, insofar as we are simply capable of feelings. Further, while we have capacities by nature, we do not become good or bad by nature." Nicomachean Ethics Book II 5.5Ok, so what does this have to do with grad school?Well lots of people are starting grad school right now with lots of potential. Tons of potential probably, it's what got them into grad school in the first place.But here's the thing, your potential doesn't mean anything unless you live up to it (or at least come close). Basically Aristotle says that your feelings and intentions and capabilities do not make you excellent, your actions do.The real lesson here is that you ARE what you DO. if you want to be a good person think 'what would a good person do in this situation?' and then do that thing. Simple really. So in grad school this translates to: Make Imposter Syndrome work in your favor.Imposter Syndrome is when someone thinks 'I'm not good enough to be where I am, and I'm just minutes away from the moment my colleagues find out' and it is apparently a plague of many grad students and there are plenty of blog posts around on how to combat it. But guess what? Playing dress up can make you smarter. People wearing a white coat called a lab coat did better on focus tasks that people wearing the same white coat called an painter's coat (Adam and Galinsky 2012). These are the same people who did the perspective taking experiments showing that when you pretend to be something you become more like it. (See item number 4 on this post.)Pretending to be what you want to be is actually a completely valid and useful way to become what you want to be. This doesn't mean go into class and pretend you are the professor (that's not a good idea). It means go into class and pretend you are the BEST student in that class.  So go put on those 'smart person clothes' and make believe that you are the best student that school has ever seen. If you run into a dilemma think to yourself 'what would an excellent grad student do in this situation?' or better yet think 'what would an excellent scientist do in this situation?' and then do that thing.© TheCellularScaleAdam and Galinsky (2012). Enclothed Cognition Journal of experimental social psychology DOI: 10.1016/j.jesp.2012.02.008... Read more »

Adam and Galinsky. (2012) Enclothed Cognition. Journal of experimental social psychology. DOI: 10.1016/j.jesp.2012.02.008  

  • July 7, 2013
  • 09:23 AM
  • 562 views

Male DNA in the Female Brain

by TheCellularScale in The Cellular Scale

When you are pregnant, people like to tell you all sorts of things about yourself.probably the most complimentary thing I have been compared to."you are going to have a boy/girl""you are carrying high/low""you look like an olive on a toothpick/beached whale""you probably have some of your husband's DNA/baby's cells in your brain now."huh?That last one requires a little more explanation. How could new external foreign cells get into my brain? First of all there is the blood-brain barrier which prevents your own blood cells from getting mixed in with your neurons, and second of all there is the placental barrier that prevents your blood from mixing with the baby's blood.Neither of these barriers are perfect. Certain drugs and chemicals can cross the blood-brain barrier, and drugs and chemicals that a pregnant woman ingests can cross the placental barrier to get to the baby. But are these barriers so leaky that whole cells can get through?Apparently they are. Dawe et al., 2007 explains possible ways that this can happen. The placenta, up close. (Dawe et al,. 2007 Figure 1)The placenta develops with the fetus, and so it is a hotbed of new growing cells early in pregnancy. It is made up of a combination of cells that contain the mother's DNA and cells that contain the new baby's DNA. However it is not clear exactly how baby cells get transferred to the mom. In the author's words:"The mechanism by which cells are exchanged across the placental barrier is unclear. Possible explanations include deportation of trophoblasts, microtraumatic rupture of the placental blood channels or that specific cell types are capable of adhesion to the trophoblasts of the walls of the fetal blood channels and migration through the placental barrier created by the trophoblasts." (Dawe et al., 2007)It is also not clear how these baby cells, once in the mother, could cross the blood-brain barrier. In fact, it is not perfectly clear (as of this 2007 paper) that these cells do get into the mother's brain in humans, though studies have shown fetal DNA-containing cells in the brains of mice. So in conclusion, if you have ever been pregnant, you probably still have some of that baby's DNA (and consequently some of the baby's father's DNA) in your body. If you were pregnant with a boy, then you probably have Y chromosomes in some of your cells! It even seems that mothers can transfer cells from previous babies into future babies. This means that if you have an older brother or sister, you might have some of their DNA in your body as well.The next question is: Do these foreign DNA cells have a meaningful impact on your body? © TheCellularScaleDawe GS, Tan XW, & Xiao ZC (2007). Cell migration from baby to mother. Cell adhesion & migration, 1 (1), 19-27 PMID: 19262088... Read more »

Dawe GS, Tan XW, & Xiao ZC. (2007) Cell migration from baby to mother. Cell adhesion , 1(1), 19-27. PMID: 19262088  

  • May 18, 2013
  • 09:21 AM
  • 537 views

Homeostatic platsicity in a thorny situation

by TheCellularScale in The Cellular Scale

Synapses, the connections between neurons can strengthen and weaken depending on the specific activity at that synapse. This is called synaptic plasticity, and we've talked about it a lot on this blog (here, here, here and here).the strengthening and weakening of synaptic connections corresponds to the spine growing or shrinking (Matsuzaki 2007)However, there is another kind of plasticity that can occur at synapses. This is called homeostatic plasticity. And instead of the synapse strengthening or weakening depending on the specific activity at that synapse, the synapses strengthen and weaken in homeostatic plasticity depending on the activity of the whole cell. To drastically simplify, each cell 'wants' to fire about a certain amount, if it suddenly starts to fire a lot less, it will take steps to strengthen its connections or make itself more 'excitable' so it can get back to its preferred amount of firing. Similarly if the cell starts to fire a lot more than normal, it will take steps to make itself less excitable and to weaken its connections until it reaches the right amount of firing.  Thorny Excrescences from Lee et al., (2013)A recent paper from the Pak lab explains how in some specific neurons in the hippocampus (CA3 pyramidal cells), the activity of the whole cell is strongly controlled by a some very peculiar synapses. These synapses are close to the cell body, and are on these HUGE weirdly shaped spines (see above) called "Thorny Excrescences". For comparison 'normal' spines look more like this:Spines from Lee et al. (2013)The Thorny Excrescences (TEs) are massive spines that contain many separate synapses on them, but connect to the dendrite through 1 neck. 'Normal' spines, on the other hand, usually have 1 synapse at the spine head, and connect to the dendrite through 1 neck.The size of the TEs, and their proximity to the soma makes them an extremely powerful way to control the signals that the soma receives. Lee et al (2013) shows that when you drastically reduce activity by blocking action potentials (using TTX), you get massive growth of these TEs, but the normal spines further away from the soma stay the same.They test 3 things to determine whether the TEs have undergone homeostatic plasticity. They look at the morphology (they are bigger), the activity (the electrical signals from them are bigger) and the molecular signatures (the molecules indicative of new synapses are more plentiful). The paper is a really nice complete story showing that these TEs have a lot of control over the general activity of the cell.It also solves an important problem with homeostatic plasticity. That is, how can the general activity of the cell be modulated without the specific differences between synapses being erased, and consequently the memories or pieces of information they encode? If homeostatic plasticity occurs at spines dedicated to it, then the other spines can still encode specific signals while the activity of the cell as a whole changes. © TheCellularScaleLee KJ, Queenan BN, Rozeboom AM, Bellmore R, Lim ST, Vicini S, & Pak DT (2013). Mossy fiber-CA3 synapses mediate homeostatic plasticity in mature hippocampal neurons. Neuron, 77 (1), 99-114 PMID: 23312519 ... Read more »

  • May 12, 2013
  • 08:00 PM
  • 457 views

The Inadvertent Psychological Experiment

by TheCellularScale in The Cellular Scale

Escape from Camp 14 is deeply disturbing, and I highly recommend it. Escape from Camp 14 by Blaine HardenEscape from Camp 14 is a chilling tale of Shin Dong-hyuk's escape from a North Korean prison camp. What is so interesting about Shin Dong-hyuk's story as written by Blaine Harden is that he was born inside this North Korean prison camp. Apparently they allow breeding between prisoners as a reward for 'good behavior.'Escape from Camp 14 reveals the obscene violations of human rights that occur in North Korean prison camps, and was especially poignant because I am a similar age to Shin Dong-hyuk and could directly compare my memories during the specified years to his. For example he escapes on January 2nd, 2005 and I couldn't help but think of the New Years party I was at that year and how absurdly different my life has been from his.This book struck me in a way that reading about the horrors of the Holocaust never could. Those atrocities happened long before I was born. But the atrocities in North Korea are happening right now. I mean right this minute in a prison camp, a child is likely being beaten, a woman is likely being raped by a guard (later to be killed if she happens to become pregnant), someone may be picking undigested corn kernels from cow dung to ease hir starving belly, and maybe two lucky prisoners are getting to have 'reward breeding' time. Right now. This minute. That is just nuts.The other thing that struck me about this whole situation is that having children born into a hostile prison environment is an inadvertent psychological experiment. These children are raised without love and without trust. One of the sharpest points in the book is the reveal that Shin Dong-hyuk turned his own mother and brother in to the guards for planning an escape. He watched his mother's execution shortly thereafter and felt nothing but anger at her for planning an escape.When he finally escaped, it was shocking to him to see people talking and laughing together without guards coming over to (violently) stop it. In Camp 14, gathering of more than 2 people was forbidden. These prison children are being raised on fear of the guards and suspicion of each other. One of the easiest ways to be rewarded is to tattle on another prisoner for something (stealing food, for example), and the children learn this quickly.If something drastic happens and North Korea dissolves, these children raised in prison camps will have a near impossible time trying to adjust to a life of freedom and will have a difficult time forming attachments and trusting others (as seen in Shin Dong-hyuk and other refugees from North Korea). Their personalities and psychological profiles could be fundamentally different from any other group on earth. These atrocities should be stopped and these people should be studied and rehabilitated. © TheCellularScaleLee YM, Shin OJ, & Lim MH (2012). The psychological problems of north korean adolescent refugees living in South Korea. Psychiatry investigation, 9 (3), 217-22 PMID: 22993519... Read more »

  • May 2, 2013
  • 12:51 PM
  • 604 views

a STORM inside a cell

by TheCellularScale in The Cellular Scale

We've been talking about some of the most cutting edge intracellular visualization techniques lately. Array tomography and Serial block-face electron microscopy have been featured. Today we'll talk about STORM imaging. STORM imaging (Xu et al., 2013)STORM stands for Stochastic Optical Reconstruction Microscopy. While Array tomography and Serial block-face EM are both revolutionary in that they can combine very high resolution imaging with relatively large volumes of tissue, STORM is an advancement that lets you see tiny tiny little molecules within the cell. The problem with 'normal' imaging is that molecules are smaller than the diffraction of light. Example of the STORM resolution (from Zhuang lab's webpage)In the figure above, imaging some tiny molecules next to each other is impossible with traditional fluorescence microscopy, but with STORM, you can resolve 10s of nanometers (nm).To do this, STORM uses photoswitchable dyes, which means that the dye can be turned on or off. This allows researchers to turn on tiny little areas and then turn them off. If all the dye is turned on all at once, the image will look like a big mess because the signals will all overlap each other. But turning on only a few at a time allows you to estimate where the actual protein or molecule is."The imaging process consists of many cycles during which fluorophores are activated, imaged, and deactivated. In each cycle only a subset of the fluorescent labels are switched on, such that each of the active fluorophores is optically resolvable from the rest. This allows the position of these fluorophores to be determined with nanometer precision." -Zhuang lab webpage So what amazing things can they do with this STORM?A recent paper by Xu et al. (2013) found that the actin which plays a huge role in the intracellular structure of a neuron, has a specific ring-like structure along the axons.Xu et al., 2013 Figure 4FThis is the kind of research that will immediately go into neuroscience and cell biology textbooks. Xu et al. discovered how actin was structured along the axon simply by being able to 'see it'. Not only did they discover the structure of actin and spectrin (magenta above) in the axon, but they also found some other interesting molecular patterns that appear to relate to the actin ring structure. The sodium channels, which control action potential propagation down the axon, are concentrated about half way between the ends of the spectrin tetramers. The potential for super-resolution microscopy like STORM is huge. The location of molecules with relation to one another probably plays a huge role in the function of cells and now we have the tools to map them.© TheCellularScaleXu K, Zhong G, & Zhuang X (2013). Actin, spectrin, and associated proteins form a periodic cytoskeletal structure in axons. Science (New York, N.Y.), 339 (6118), 452-6 PMID: 23239625... Read more »

  • April 22, 2013
  • 08:20 PM
  • 710 views

Connecting Form and Function: Serial Block-face EM

by TheCellularScale in The Cellular Scale

The retina is a beautiful and wondrous structure, and it has some really weird cells. Retina by Cajal (source)Retinal Ganglion Cells (RGC) have all sorts of differentiating characteristics. Some are directly sensitive to brightness (like rods and cones), while some are sensitive to the specific direction that a bar is traveling. I am discussing really amazing new techniques to see inside cells this month, and have already posted about the magic that is Array Tomography. Today we'll look at another amazing new technique that (like array tomography) combines nano-scale detail with a scale large enough to see many neurons at once. This technique is called Serial Block-face Electron Microscopy (SBEM), and was recently used to investigate how starburst amacrine cells control the direction-sensitivity of  retinal ganglion cells.Serial Block-face EM (source)SBEM images are acquired by embedding a piece of tissue (like a retina) in some firm substance and slicing it superthin (like 10s of nanometers thick) with a diamond blade. The whole slicing apparatus is set up directly under a scanning electron microscope, so as soon as the blade cuts, an image is taken of the surface remaining. Then another thin slice is shaved off and the next image is taken, and so on.Using this technique, Briggman et al. (2011) are able to trace individual neurons and their connections for a (relatively) large section of retina. What is so great about this paper is that before they sliced up the retina, they moved bars around in front of it and measured the directional selectivity of a bunch of neurons. Then, using blood vessels and landmarks to orient themselves, they were able to find the exact same cells in the SBEM data and trace them.Briggman et al. (2011) Fig1C: Landmark blood vesselsThe colored circles above represent the cell bodies and the black 'tree' shape are the blood vessel landmarks. Once they found the cell bodies, the could trace the cells through the stacks of SBEM data. What is really neat is that you can try your hand at this yourself. This exact data set has been turned into a game called EYEWIRE by the Seung lab at MIT. Reconstructing the cells, they could not only tell which cells connected to which other cells, but they could also see exactly where on the dendrites the cells connected. This is the really amazing part. They found that specific dendritic areas made synapses with specific cells.Briggman et al. (2011) Fig4: dendrites as the computational unitThis starburst amacrine cell overlaps with many retinal ganglion cells (dotted lines represent the dendritic spread of individual RGCs)...BUT its specific dendrites (left, right, up down etc) synapse selectively onto RGCs sensitive to a particular direction. Each color represents synapses onto a specific direction-sensitivity. e.g. yellow dots are synapses from the amacrine cell onto RGCs which are sensitive to downward motion.This suggests that each individual dendritic area of these starburst amacrine cells inhibits (probably) a specific type of RGC, and that these dendrites act relatively independently of one another. "The specificity of each SAC dendritic branch for selecting a postsynaptic target goes well beyond the notion that neuron A selectively wires to neuron B, which is all that electrophysiological measurements can test. Instead the dendrite angle has an additional, perhaps dominant, role, which is consistent with SAC dendrites acting as independent computational units."  -Briggman et al (2011)(discussion)These cells are weird for so many reasons, but the ability of the dendrites to act so independently of one another is a new and exciting development that I hope to see more research on soon. © TheCellularScaleBriggman KL, Helmstaedter M, & Denk W (2011). Wiring specificity in the direction-selectivity circuit of the retina. Nature, 471 (7337), 183-8 PMID: 21390125... Read more »

  • April 17, 2013
  • 05:34 PM
  • 557 views

Van Gogh was afraid of the moon and other lies

by TheCellularScale in The Cellular Scale

I remember the first time I realized just how easily false information gets spread about.A terrifying starry nightI was in French class in high school. Our homework had been to find out 1 interesting fact about Van Gogh and tell it to the class. When it was my turn, I said some boring small fact that I no longer remember. My friend sitting behind me, however, had a fascinating fact: When Van Gogh was a young child, he was actually afraid of the moon.The teacher and the class were all quite impressed and thought about how interesting that was and how that fact might be reflected in the way that he paints the Starry Night. Though this fact was new to everyone, including the teacher, no one even thought to question its truth. In fact, the teacher was so enthralled by this idea that she passed the information on to all the other French classes that day.When talking to my friend later that day, he admitted that he had not done the assignment, and just made the 'fact' up. I was completely surprised, not only that someone had not done their homework *gasp*, but that I hadn't even thought to question whether this was true or not.  The best lies have an element of truth (source) Misinformation like this spreads like wildfire and is exceptionally difficult to undo. The more things you can link this piece of information to in your brain, the more true you might think it and even after your learn that it's not true, you still might inadvertently believe it or fit new ideas into the context it creates. Myths like the corpus callosum is bigger in women than in men is just one of those things that is easy to believe.An interesting paper by Lewandowsky et al. (2012) explains how this kind of persistent misinformation is detrimental to individuals and to society with the example of vaccines causing autism. This particular piece of misinformation is widely believed to be true despite numerous attempts to publicize the correct information and the most recent scientific findings showing no evidence for a link between the two.  The authors of this paper give some recommendations for making the truth more vivid and effectively replacing the misinformation with new, true information. For example:"Providing an alternative causal explanation of the event can fill the gap left behind by retracting misinformation. Studies have shown that the continued influence of misinformation can be eliminated through the provision of an alternative account that explains why the information was incorrect." Lewandowsky et al. (2012)Misinformation can be replaced with information, but it takes more work to replace a 'false fact' than to just have the truth out there in the first place. It is much better when misinformation is not spread around in the first place, than when it is retroactively corrected. This paper is also covered over at The Jury Room. © TheCellularScaleLewandowsky, S., Ecker, U., Seifert, C., Schwarz, N., & Cook, J. (2012). Misinformation and Its Correction: Continued Influence and Successful Debiasing Psychological Science in the Public Interest, 13 (3), 106-131 DOI: 10.1177/1529100612451018... Read more »

Lewandowsky, S., Ecker, U., Seifert, C., Schwarz, N., & Cook, J. (2012) Misinformation and Its Correction: Continued Influence and Successful Debiasing. Psychological Science in the Public Interest, 13(3), 106-131. DOI: 10.1177/1529100612451018  

  • April 13, 2013
  • 10:54 AM
  • 653 views

Seeing Inside Cells: Array Tomography

by TheCellularScale in The Cellular Scale

I wrote a lot about dopamine and its complicated nature last month after coming back from the IBAGs conference, so for a change of pace, I'll talk about some truly amazing new techniques that allow us to see inside cells with unprecedented resolution and at unprecedented volumes.I've previously discussed some traditional techniques for visualizing specific details in neurons, and this month I'm going to talk about some of the newest fanciest ways to look at cellular scale information.  First off, Array Tomography!  Micheva et al. 2010 Figure 1 Array TomographyArray Tomography combines the enhanced location information of the electron microscopy with the scale and context of immunohistochemistry or in situ hybridization. Not only that, but Array Tomography is done in such a way that the same preparation can be stained for 100s of different proteins.  This is a priceless gift to those who want to study protein co-localization.  Do certain receptors 'flock together', and if so does a mutation, or drug treatment alter their abundance or proximity to one another?Micheva et al. 2010 Figure 4 spine head and neck locations of specific proteinsAnd just how do they accomplish this feat?The trick is in the slicing. Using an ultramicrotome these guys can slice a section of brain 70 nm thin. That's 70 NANOmeters, which is really really thin. (Compare it to 'thick section staining' which works on sections 350,000 nanometers thin). The smallest cellular features, the necks of spines can be as thin as 50-100nm, so 70nm can really capture a lot of detail.Here is a 'fly through' video of the cortical layers in a cortical column. The red dots are identified synapses, and around 2:11 of the video you get to the pyramidal cell bodies (green) which is pretty stunning. While "Array Tomography" doesn't quite capture the public imagination like "neurons activated by light", it is huge leap forward in the domain of cellular neuroscience. With array tomography, it becomes possible to investigate co-localization of many proteins in a relatively large section of brain tissue.  © TheCellularScaleMicheva KD, Busse B, Weiler NC, O'Rourke N, & Smith SJ (2010). Single-synapse analysis of a diverse synapse population: proteomic imaging methods and markers. Neuron, 68 (4), 639-53 PMID: 21092855... Read more »

  • April 4, 2013
  • 11:26 AM
  • 609 views

Neurons and New Newt Legs

by TheCellularScale in The Cellular Scale

Salamanders are amazing and mystical creatures. Salamanders and their amazing leg-growing superpower (source)Not because they can survive in fire (they can't), but because they can regrow amputated limbs.A paper in 2007 investigates exactly what neural signals are required for this amazing superpower. Newt Amputee (Kumar et al., 2007)This paper brings together two interesting things about salamander (newt) leg growth.1. The salamander arm 'knows' where it was cut. If it is cut at the wrist it only grows a hand (paw?...foot?), if it is cut at the shoulder, it grows the whole leg/arm. So one question is HOW does the arm know?The answer is surprisingly simple: there is a small protein called Prod 1 that is highly concentrated at the shoulder and progressively decreases along the arm. This protein could tell the new bud of growing cells where it is, and what it should grow into.and2. To regenerate, the arm needs intact nerve endings at the point of the cut. That is, the nerve fiber that goes down the arm has to be attached to the nervous system. If the nerve is cut further up than the arm cut, the arm will not regenerate.Kumar et al., 2007 Author Summary FigureKumar et al. (2007) found a molecule that ties these two interesting things together, completing the newt leg regeneration story. They find a molecule, nAG (n for newt and AG for anterior gradient) which binds to Prod 1, and is secreted by the nerve sheath (the Schwann cells that surrounds nerve fibers).They show that when they cut the nerve further up the arm (denervation), they don't get nAG expression and they don't get limb regeneration. But, when they artificially supply nAG, (see D and E above), the amputated and denervated limb starts to grow.  This is a really neat 'rescue experiment' suggesting that the reason the nerve is necessary for regeneration is because it triggers nAG release which binds to Prod 1 and says "GROW".One thing that they don't do (because genetically manipulating salamanders is not really a thing yet) is remove nAG, but keep the nerve intact. This would show that the only important thing the nerve fiber is doing is triggering nAG.This study is also a small step towards limb regeneration in humans, not because injecting nAG into an amputated human limb could regenerate it (It couldn't), but because the more we understand about how the system works, the more likely we can figure out a way to engineer a similar system in humans.  © TheCellularScaleKumar A, Godwin JW, Gates PB, Garza-Garcia AA, & Brockes JP (2007). Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate. Science (New York, N.Y.), 318 (5851), 772-7 PMID: 17975060... Read more »

Kumar A, Godwin JW, Gates PB, Garza-Garcia AA, & Brockes JP. (2007) Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate. Science (New York, N.Y.), 318(5851), 772-7. PMID: 17975060  

  • March 26, 2013
  • 06:42 PM
  • 736 views

Advice vs Victim-blaming: a proposed study on #safetytipsforladies

by TheCellularScale in The Cellular Scale

So there has been a lot of noise about whether giving women 'safety tips' to avoid being raped is a form of 'victim blaming'.Don't get Raped (source)This culminated in a great hashtag (as many things do). Follow #safetytipsforladies to see some lovely tips for avoiding rape.For example:Don't be anywhere. 100% of rapes happen in places and locations. #safetytipsforladies— Conna Stevenson (@1000DaysOfRain) March 25, 2013Others suggest simply not being a woman, not ever drinking anything, not ever wearing anything (but not being naked either), not ever leaving the house (or since many rapes happen inside the house, not ever being home). And so forth.The main point is that it's absurd to tell women to not get raped. Rape by definition is NOT under the victim's control.Yet people still tend to blame the victim in rape cases. An interesting study was published in 2011 showing that people were more likely to blame the victim in a rape case than in a robbery case. The authors gave people short vignettes describing either a rape or a robbery, and had these participants fill out a perpetrator blame scale and a victim blame scale.Bienek and Krahe 2011 Figure 4 Interestingly, but maybe not surprisingly, rape always had more victim blame and less perpetrator blame than robbery and this difference increased with how close the victim and perpetrator were to each other (stranger, acquaintance, ex-partner).  Now some people say 'hey, I'm just trying to keep women safe by telling them to avoid dark places, and not take drinks from strangers.' But here's the thing, maybe the mere suggestion that women can do something to avoid being raped is enough to subtly nudge one's opinion toward thinking that if a woman got raped, she should have done something to avoid it and is therefore somewhat to blame.So I propose the following study:Have one group of people read a short article on tips for women to avoid being raped (a serious and well meaning one), and one group of people read some unrelated article. Then have both groups read rape vignettes similar to the ones described in the Bienek and Krahe study and fill out the victim and perpetrator blame scales. They would also fill out a scale for how much punishment the perpetrator should get in a court of law. I hypothesize that simply reading a list of well meant tips for how women can avoid being raped would increase victim blame and would make people more lenient in their prescribed punishment for the perpetrator.Somebody please do this experiment!© TheCellularScale Bieneck S, & Krahé B (2011). Blaming the victim and exonerating the perpetrator in cases of rape and robbery: is there a double standard? Journal of interpersonal violence, 26 (9), 1785-97 PMID: 20587449... Read more »

  • March 25, 2013
  • 08:38 AM
  • 713 views

Guest Post: AMPA Receptors are not Necessary for long term potentiation

by TheCellularScale in The Cellular Scale

Today's post is brought to you by @BabyAttachMode, who is an electrophysiologist and blogger. Today we are blog swapping! I have a post over at her blog and her post about AMPA receptors and LTP is here. So enjoy, and when you're done reading about the newest advances in synaptic plasticity here, you can head over to InBabyAttachMode and read about my personal life. AMPA Receptors are not Necessary for long term potentiationScience is most interesting to me when you’re testing a hypothesis, and not only do you prove the hypothesis to be false, but you discover something unexpected. I think that happened to Granger et al. They were trying to find which part of the AMPA receptor is necessary for long-term potentiation(LTP), the process that strengthens the connection between two brain cells when that connection is used often. Indeed they find that AMPA receptors are not necessary at all for LTP, which is very surprising given the large body of literature describing how the GluA1 subunits of the AMPA receptor, through interactions with other synaptic molecules that bind to the intracellular C-tail (the end of the receptor that is located inside the cell), are inserted into the synapse to induce LTP. LTP (source)The authors made an inducible triple knock-out, which means that they could switch off the genes for the three different AMPA receptor subunits GluA1, GluA2 and GluA3. This way, they ended up with mice that had no AMPA receptors at all. The authors were then able to selectively put back one of the AMPA receptors, either the entire receptor or a mutated receptor. By inserting mutated receptors, for example a receptor that lacks its intracellular C-tail that was thought to be important for insertion of the AMPA receptor into the synapse, they could then study whether this mutated receptor was still sufficient for induction of LTP.Surprisingly, they found that deleting the C-tail of the GluA1 subunit does not change the cell’s ability to induce LTP. Even more so, they showed that you don’t even need any AMPA receptor to still be able to induce LTP; the kainate receptor (another type of glutamate receptor that has never been implicated in LTP) can take over its job too.Figure 6C from Granger et al. (2013). Kainate receptor overexpression can lead to LTP expression, without the presence of AMPA receptors.About this surprising discovery the authors say the following:"These results demonstrate the synapse's remarkable flexibility to potentiate with a variety of glutamate receptor subtypes, requiring a fundamental change in our thinking with regard to the core molecular events underlying synaptic plasticity."Of course if you say something like that, the main players in the LTP field will have something to say about it, and they did. Three giants in the field of synaptic physiology commented in the journal Nature, but their opinions differed. Morgan Shang called it "a step forward", whereas Roberto Malinow and Richard Huganir called it "two steps back", saying that LTP without AMPA receptors can only happen in the artificial system that the authors of the paper use to study this. They expect that cells lacking all three AMPA receptors will look so different from the normal cells that the results are difficult to interpret.Either way, this paper opens new views and questions to how LTP works, and whether AMPA receptors are as important as we thought. Granger AJ, Shi Y, Lu W, Cerpas M, & Nicoll RA (2013). LTP requires a reserve pool of glutamate receptors independent of subunit type. Nature, 493 (7433), 495-500 PMID: 23235828 Sheng M, Malinow R, & Huganir R (2013). Neuroscience: Strength in numbers. Nature, 493 (7433), 482-3 PMID: 23344353 ... Read more »

Sheng M, Malinow R, & Huganir R. (2013) Neuroscience: Strength in numbers. Nature, 493(7433), 482-3. PMID: 23344353  

  • March 19, 2013
  • 04:41 PM
  • 509 views

What is up with the "Dopamine Project"?

by TheCellularScale in The Cellular Scale

Someone is trying to make me eat my words.yum. (source)That someone is the Dopamine Project. I am on record as saying "It is better for the public to learn simplified bite-size science morsels than to learn nothing at all." And my specific example was that it's better for people to know that 'dopamine is a reward molecule' than to not even know the term dopamine.But sometimes things just go too far. The "Dopamine Project" is a website run by Charles Lyell with a stated 'self-help' purpose: "The Dopamine Project was founded to foster positive change by encouraging open-minded individuals to share readily available research into the connections between dopamine and a growing list of addictive behaviors." -About TabDoesn't sound too terrible, right? Share research about dopamine? sign me up! .... However, I don't see ANY research, or even references to research, on this website. In fact it's quite wootastic. Going through the posts, you get some gems like"A Message from you Dopamine Angel"and"Keeping a Dopamine Diary: Wrestling with Dopamine-Induced Ignorance"It's all about how 'good dopamine' makes you want things you should want (food) and 'bad dopamine' makes you want things that will hurt you later (addictive drugs for example). Basically the website's message is a self-help, self-control one with the word dopamine sprinkled all over it.The worst part is that not only does the website not include a single citation to a research paper, it actively rails against science. "The future depends on how long it takes scientists to discover what they haven’t been interested in discovering so far. Rather than wait for the mainstream scientists and media to get started, we’re reaching out to anyone interested in fostering positive change by raising dopamine awareness." -Welcome to the Dopamine Project Trust me, scientists want to understand dopamine. At the IBAGS conference half the talks related to dopamine, and there is a conference completely devoted to dopamine coming up in May. The specific action of dopamine is really really complex, and scientists are working really really hard to unravel its intricacies. This Charles Lyell guy is pulling out a typical woo card, implying that he knows what scientists don't want you to know. "If the thought of fostering positive change through dopamine awareness triggers a shot of dopamine that brings a smile to your face, this might be your chance to be among the top .001% who go on record as the first to understand and apply what we know about dopamine to make a difference."  -Welcome to the Dopamine Project  He also seems to feel personally attacked by Steven Poole's New Statesman article on Neurobollocks. Is the 'Dopamine Project' ridiculous and unscientific? Absolutely.Is it harmful and dangerous to people? ... Honestly, I'm not sure. Reading it certainly makes me want to throw up, but there are worse things for pseudoscience to encourage than self-control. I'm not sure if I should devour my earlier words quite yet. © TheCellularScaleTo read more on the confusing line between science and pseudoscience, see Michael Shermer's Scientific American article: Shermer M (2011). What is pseudoscience? Scientific American, 305 (3) PMID: 21870452... Read more »

Shermer M. (2011) What is pseudoscience?. Scientific American, 305(3), 92. PMID: 21870452  

  • March 15, 2013
  • 01:26 PM
  • 567 views

Is it 'Important' or is it 'valuable'?

by TheCellularScale in The Cellular Scale

We've recently discussed dopamine as a reward prediction signal. But that is really just the start of the complicated dopamine story. Dopamine's role in reward and punishment (by the hiking artist)Some research groups have also found that dopamine neurons respond to aversive stimuli, like an air puff to the face or an electric shock. This finding seems to be be completely incompatible with the idea that dopamine is a signal for reward. Luckily some scientists took the time to try to resolve this discrepancy. Bromberg-Martin, Matsumoto, and Hikosaka (2010) have written an excellent review paper explaining that some dopamine neurons do code for value (reward), but other dopamine neurons code for salience (importance). Differential Dopamine Coding (Bromberg-Martin et al., 2010 Fig 4)When researchers are recording from a value coding dopamine neuron, it looks like the neuron responds to reward and actually reduces its response to the air puff. This makes sense as a 'dopamine = good' signal.However, when a researcher is recording from a salience coding dopamine neuron, it looks like the neuron is responding equally to the good thing (reward) and the bad thing (air puff). This is confusing if you think 'dopamine = good', but makes sense if you think 'dopamine = important'. When the cue comes on (a light or a tone that signifies a reward is coming next or an air puff is coming next), these dopamine neurons fire if that cue means something. Instead of just being confused about why sometimes dopamine would code for value and sometimes it would code for salience, Hikosaka's group showed that these two types of neurons are actually separate populations, and even seem separated in space. (Bromberg-Martin et al., 2010 Fig 7B)The value dopamine neurons are more ventral in the (monkey) brain, while the salience dopamine neurons are more dorsal-lateral. Importantly these two populations of neurons go to slightly different parts of the striatum and receive signals from different parts of the brain. The review paper suggests that the salience coding neurons receive their input from the central nucleus of the amygdala, while the value coding neurons receive their input from the lateral habenula-RMTg pathway. The important thing here is that dopamine does not do just one thing to the brain. It doesn't just tell the rest of the brain 'yay, you won!' or 'you want that' etc... It says different things depending on different specific conditions. Dopamine doesn't 'mean' anything, the cell it comes from and the cell it goes to are what determine what it does. It certainly can't be classified as the 'love molecule' © TheCellularScaleBromberg-Martin ES, Matsumoto M, & Hikosaka O (2010). Dopamine in motivational control: rewarding, aversive, and alerting. Neuron, 68 (5), 815-34 PMID: 21144997... Read more »

  • March 9, 2013
  • 04:07 PM
  • 730 views

Dopamine and Reward Prediction Error

by TheCellularScale in The Cellular Scale

I am back from the IBAGS conference and full of new information! I plan to blog about tons of amazing things over the next month or so, but today we'll start with some foundation building.Dopamine nails (source)The IBAGS (international basal ganglia society) meeting is all about the basal ganglia (which includes the striatum), and as you may know, dopamine is a super important molecule for the proper function of the striatum (it is the dopamine cells that die in Parkinson's Disease).There were many fantastic talks during the IBAGS meeting and almost a third of them showed the exact same figure on one of their slides. So much so that everyone would start to laugh when someone showed it. And as you may have guessed, it is about dopamine. Here it is:Schultz 1998 Figure 2This figure is the basis for the belief that dopamine represents a 'reward prediction error'.  Let me explain. The scattered dots on the lower half of each panel represent action potentials from individual dopaminergic neurons. The x axis it time in seconds. The black columns above them are a histogram showing how much firing is going on at each point in time. When the black columns are tall, there was more dopamine neuron firing. You can see that the height of the black columns matches up with the density of the scattered dots below them.During 'reward learning', an animal is trained to associate a stimulus (like a tone or a flash of light) with getting a reward (like a drop of water or juice). These three panels show how dopamine responds to this whole process. The first panel shows that when there is no stimulus (CS) and the reward is a surprise, the dopamine neurons respond very strongly to it. The second panel shows that when there is a stimulus that tells the animal that a reward is soon to come, the dopamine neurons respond to the stimulus, but not to the reward. Finally the third panel shows that when there is a stimulus the dopamine neurons respond to it, but if the reward (R) never comes, the dopamine neurons actually stop firing when the reward should have happened. What is so fascinating about this is that it shows dopamine neurons do not just fire in response to reward, they encode the actual reward with respect to the expected reward. In the author's words:"Dopamine neurons report rewards relative to their prediction rather than signaling primary rewards unconditionally (Fig. 2). The dopamine response is positive (activation) when primary rewards occur without being predicted. The response is nil when rewards occur as predicted. The response is negative (depression) when predicted rewards are omitted. Thus dopamine neurons report primary rewards according to the difference between the occurrence and the prediction of reward, which can be termed an error in the prediction of reward..." Schultz 1998 This finding is so important to researchers now because it shows that dopamine neurons can encode learning rules. Dopamine neurons constantly and dynamically tell the rest of the brain which stimuli lead to reward, and which stimuli don't. The implications here for pathological learning are huge as well. Mis-signalling in dopamine neurons could lead to an inability to tell what is rewarding and what is not. © TheCellularScaleSchultz W (1998). Predictive reward signal of dopamine neurons. Journal of neurophysiology, 80 (1), 1-27 PMID: 9658025... Read more »

Schultz W. (1998) Predictive reward signal of dopamine neurons. Journal of neurophysiology, 80(1), 1-27. PMID: 9658025  

  • February 27, 2013
  • 09:48 AM
  • 736 views

GABA, how exciting!

by TheCellularScale in The Cellular Scale

I would like to thank my good friend Anonymous for asking me a great question on a previous post. Anonymous asks: "Are there any known transmitters in the NS that activate both inhibitory receptor subtypes AND excitatory receptor subtypes? Or does every known transmitter activate EITHER a bunch of excitatory subtypes OR a bunch of inhibitory subtypes?" (btw. This doesn't qualify as a LMAYQ post because it's a real true question that someone directly asked, not a search term)While I don't know of any instances of glutamate (excitatory) activating GABA (inhibitory) receptors or of GABA activating glutamate receptors, there is an interesting little way that GABA can activate an inhibitory receptor, but actually help excite the cell.  GABA receptor (source) Here's how that works: GABA(A) receptors are permeable to chloride ions, and as the picture above shows, chloride ions (Cl-) are negatively charged. When GABA binds to the receptor, the receptor opens and chloride ions rush in, bringing their negative charge with them. This hyperpolarizes the cell, meaning it brings it lower and lower in total charge (membrane potential), which brings it further and further away from the threshold where it will fire an action potential.BUT.... if there is a lot of chloride inside the cell already (or if the cell is resting more negatively than the chloride reversal potential), chloride will actually flow out of the cell, bringing its negative charge with it. Negative ions flowing out of the cell will depolarize the neuron increasing its total charge (membrane potential), which brings it closer and closer to the threshold where it will fire an action potential.GABA reversing at -62mV (source)A paper published last year in the Journal of Neuroscience shows that in a model of a hippocampal neuron, when a strong excitatory (glutamate) stimulation happens right after a GABA stimulation close by on the dendrite, the cell is actually more likely to fire than when the glutamate stimulation occurs on its own. This effect is dependent on the location of the GABA stimulation along the dendrite.Chiang et al., 2012 Figure 4E (GPSP in the dendrite)This figure shows that a GABA stimuation (first dotted line, blue trace) can push the glutamate (excitatory) stimulation (second dotted line, red trace) up to the point of firing an action potential (green trace). This paper also showed that GABA can still inhibit the action potential in these cells, it just has to be at the soma and almost the same time as the glutamatergic input.Chiang et al., 2012 Figure 4G (GPSP in the soma) So there you have it, GABA enhancing the likelihood of an action potential and acting excitatory sometimes, and acting inhibitory other times.   © TheCellularScaleChiang PH, Wu PY, Kuo TW, Liu YC, Chan CF, Chien TC, Cheng JK, Huang YY, Chiu CD, & Lien CC (2012). GABA is depolarizing in hippocampal dentate granule cells of the adolescent and adult rats. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32 (1), 62-7 PMID: 22219270... Read more »

Chiang PH, Wu PY, Kuo TW, Liu YC, Chan CF, Chien TC, Cheng JK, Huang YY, Chiu CD, & Lien CC. (2012) GABA is depolarizing in hippocampal dentate granule cells of the adolescent and adult rats. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(1), 62-7. PMID: 22219270  

  • February 24, 2013
  • 01:00 PM
  • 646 views

Scientizing Art

by TheCellularScale in The Cellular Scale

I've always been fascinated with the way the eye moves around a piece of art. Andrew Wyeth's "Christina's World" (or as I looked up "that painting of a girl in a field looking at a house")This piece by Andrew Wyeth is an obvious example of an artist completely controlling your gaze. There are pretty much no options here. You look at the girl and then you follow her gaze to the house. You probably then take a quick glance at that other house/barn to the left, and then maybe follow the edge of the light circle around the houses. (It's my opinion that that is how the eye should go on this painting, but I have no eye tracking data to support it.)A paper last year in PLoS One really tries to "scientize' this process by testing what factors determine the eye movements, and the 'clusters' where the eye tended to fall. Massaro et al., (2012) compare dynamic and static images and images that contain human subjects or nature subjects. Their cluster analysis overlaying classic paintings makes for quite interesting images: The next installment at MoMAThis one is a dynamic human image. Each patch of color shows where the parts of the painting where the eye lingers (face, hands, ....crotch...). The authors do all sorts of interesting analysis on this and other paintings, having participants rate the painting for 'movement' or for 'aesthetic value' and since the paper is open access, it is free to people who may not have university access to journal publications. Anyone can read the whole thing here. One interesting thing that the authors find is that pictures containing humans have fewer clusters than pictures of nature. I expect this is because certain aspects of humans (faces, hands ...crotches...) are so salient and the brain focuses directly on them, while all the branches of a tree for example have about equal 'meaning' for a person.science creates modern art Another great image from this paper. The authors show how much gazing was done at different parts of a painting through a heat map. This one is a human static image. The end result is actually quite haunting because the place that you want to look is blanked out (sort of like a Magritte painting). So here are my questions: If someone looks at a blank page, where does their eye naturally go? Is there some sort of common pattern that most people use just to scan an area? Do chimpanzees use a similar pattern to scan a blank page? Does everyone have their own unique scanning pattern? Or is it just pretty much random?  And here's an idea for artists: Buy yourself an eye tracker and have customers come use it and stare at a blank page. Trace their eye movements and then create a dynamic painting (or T-shirt, or napkin drawing) that follows the person's natural scanning patterns. This would be the ultimate in commissioned custom art! (Then give me one for free, because I think this sounds like fun.)© TheCellularScale Massaro D, Savazzi F, Di Dio C, Freedberg D, Gallese V, Gilli G, & Marchetti A (2012). When art moves the eyes: a behavioral and eye-tracking study. PloS one, 7 (5) PMID: 22624007... Read more »

Massaro D, Savazzi F, Di Dio C, Freedberg D, Gallese V, Gilli G, & Marchetti A. (2012) When art moves the eyes: a behavioral and eye-tracking study. PloS one, 7(5). PMID: 22624007  

  • February 21, 2013
  • 06:37 PM
  • 885 views

Birthing new neurons at night

by TheCellularScale in The Cellular Scale

By now it's well established that adults can grow new neurons.Growing Neurons (source)But how, when and why these neurons grow is currently under investigation. A 2008 paper attempts to answer the 'when' of neurogenesis. They labeled (PH3) cells in the mouse hippocampus (dentate gyrus to be specific), and counted how many cells were currently going through mitosis at different times of day. They found that during the dark phase, more cells were PH3-positive, indicating that more cells were growing at night.They also tested whether neurogenesis was modulated by exercise. And it was. Mice who had access to a running wheel in their cage grew about the same number of cells during the night, but grew more cells during the day. So much so that the difference between night and day disappeared. Tamai et al.,, 2008 Figs 1B and 2DThis figure shows the light-dark cycle (Zeitgeber time) and the number of 'growing' cells. B shows the pattern for control mice, and D shows the pattern for the running mice. Notice that the y axes are scaled differently.So exercise helped new cells grow, but without exercise more cells grew during the night time. Now all this use of the phrase 'night time' might make you think that this neural growth is happening during sleep.After a long night of wheel running, Jasper succumbs to a restful days sleep. (source)But it's not. Mice are nocturnal. They sleep during the day and are wide awake at night. The paper shows that almost all the running that occurs on the running wheel happens at night. So the enhanced cell growth is happening when the mice are active. Why exercising at night causes cells to grow during the day is interesting, but the authors offer no mechanism for why that might be happening.© TheCellularScaleTamai S, Sanada K, & Fukada Y (2008). Time-of-day-dependent enhancement of adult neurogenesis in the hippocampus. PloS one, 3 (12) PMID: 19048107... Read more »

  • February 14, 2013
  • 10:38 AM
  • 779 views

It's not you, it's my birth control

by TheCellularScale in The Cellular Scale

So, Valentine's Day, what better time to question the foundations of your relationship?It's my brain that loves you (source)Well, part of your relationship may be based on your Major Histocompatibility Complex (MHC) compatibility. The MHC is a cluster of genes that define which antigens get expressed on white blood cells. It is thought to control the ability of the body to recognize pathogens as 'other.' It is also thought that the more varied the genes in your MHC are, the more resistant to pathogens or parasites you are.So what does the MHC have to do with your love life?Well the most popular theory goes as such: If you want to have a healthy baby, you want to give it a varied MHC, therefore you want to find a man who has an MHC that is very different from your own. And... Maybe you can detect whether a man has a MHC that is the same or different from yours through smell (maybe vision too). In 2005, a paper came out explaining that the Major Histocompatibility Complex (MHC) can be detected through smell, and (importantly) that women prefer the smell of men who have an MHC that is different from their own. (However another paper in 2008, did not replicate this preference)Possible new fragrance? Now here's the real kicker: Taking oral contraceptives (birth control pills) might mess this preference up. Roberts et al., 2008 show that in an armpit sweat test (like this one), women on birth control showed more of a preference for the MHC similar men than the women not on birth control. If true, this could have implications for women starting relationships when they are either on or not on birth control. To take this to the greatest sensationalist extreme, you might pick the WRONG GUY because you were on birth control. However, just like I don't believe in destined, fated true love, I don't believe you need to have opposite MHCs to have a good relationship or healthy children.Roberts et al. 2008 Figure 2C: Odor desirability ratings.And not only that, I have somewhat of a problem with this graph and their data. As far as I can tell (I found the description to be pretty confusing), the white bars represent 'session 1' in which NO ONE was on the pill and then the gray bars represent 'session 2' when the women labeled 'pill' were actually on the pill, but the women labeled 'non-pill'  were still not on the pill. (following this?)  AND, 0 means that they liked the similar MHC and the dissimilar MHC guys equally, negative means the like the similar guys more and positive means they like the dissimilar guys more... (I told you this was confusing).So my question is, why are the non-pill and pill users so different to begin with? Unless I am completely misunderstanding this graph, I would think the white bars should be similar, as they represent 'women who are not on birth control.' The huge difference between groups before the 'experimental treatment' should be a red flag: Something is already different between these women.However, the pill session 1 (white) and pill session 2 (gray) bars are indeed different, and that is their 'main result.' Basically, women on the pill had an overall slight odor preference for MHC similar men, and the same women not on the pill had an odor preference for MHC dissimilar men.So should you worry this Valentine's Day? Should you break up with your boyfriend because you were on birth control when you met? Should you spend a lot of time smelling your boyfriend's worn shirts analyzing how 'desirable' a scent the give off?Probably not (unless you really like smelling sweaty shirts). There is more to relationship compatibility than histocompatibility, and making life-changing decisions based on possible olfactory disruptions due to birth control is just not a good idea.Though if you are worried, you can read more about it at:Context and Variation "will the pill mess up my ability to detect my one true love?"andFirst Nerve "pill goggles"© TheCellularScaleRoberts SC, Gosling LM, Carter V, & Petrie M (2008). MHC-correlated odour preferences in humans and the use of oral contraceptives. Proceedings. Biological sciences / The Royal Society, 275 (1652), 2715-22 PMID: 18700206... Read more »

Roberts SC, Gosling LM, Carter V, & Petrie M. (2008) MHC-correlated odour preferences in humans and the use of oral contraceptives. Proceedings. Biological sciences / The Royal Society, 275(1652), 2715-22. PMID: 18700206  

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