This is the fourth and final post is a series focusing on exercise and the brain. In the first post, I reviewed research documenting the brain's role in exercise fatigue. The second post examined the hypothesis that aerobic physical activity had a key evolutionary role in the growth of brain size in humans. The third post focused on animal study research supporting a role for exercise in reducing vulnerability to anxiety by changes in the 5-HT2C serotonin receptor.In this post, I will review a provocative study suggesting that physical fitness and it's effect on brain vascular health, may limit the brain damage produced by stroke.Dunn and colleagues at the University of Calgary in Canada conducted an experiment in rats that has recently been published in the journal PLOS ONE. They noted that in the mammalian brain a chemical called hypoxia inducible factor, or HIF-1alpha, exists that improves "the capacity of tissue to survive low oxygen conditions". They hypothesized that manipulation of environmental factors that increase HIF-1alpha may serve as a potential mechanism to reduce the brain damage associated with hypoxic events.In their study, rather than exercise, they exposed rats to hypoxia by placing them in a 1/2 atmosphere environment for three weeks. This results in brain changes that can also be seen with aerobic exercise including:Increase in capillary density by up to 30%Increase in brain oxygen partial pressure by up to 40%The hypoxia-exposed experimental rat group was then compared to a group of control rats following stroke simulation by occlusion of the middle cerebral artery for one hour. They then compared the stroke outcome of the case and control groups and noted the following key findings:Case rats had an increase in total hemoglobin, total hematocrit, capillary density and brain tissue oxygen level prior to the stroke simulationAbsolute brain volume of stroke damage assessed by magnetic resonance imaging was reduced by 52% in the case group compared to controlsCase rats showed no motor behavioral deficits 48 hours after the stroke simulation while control rats showed continued motor deficitsCase rats showed a reduction in brain inflammation post stroke simulation measured by levels of lymphocyte infiltration and number of macrophagesThe authors note in their discussion, that one clinical implication from their study relates to humans living in high altitudes under chronic acclimation to hypoxia. They note there is limited study of stroke in these populations. There is some human research showing that chronic high-altitude hypoxia with increased hemoglobin and hematocrit might actually lead to a higher incidence of stroke. However, individuals living at high-altitude might be expected to have a better stroke outcome due to other adaptive brain mechanisms associated with acclimation to hypoxia.The authors also note their study supports additional research in humans for ways to increase brain neuroplasticity through stimulation of HIF-1alpha. This might be accomplished by a high baseline rate of aerobic exercise or use of pharmacological agents such as desferoxamine.Such interventions in high-risk stroke populations (i.e. those who have had a transient ischemic attack) may lead to reduction in brain damage related to future stroke events. For the general population, this study suggests one benefit of aerobic exercise might include reduction in both the risk for stroke and a better outcome if one occurs.For free access to this study, select the PMID link from the reference below. Photo of blue jay is from the author's files.Dunn JF, Wu Y, Zhao Z, Srinivasan S, & Natah SS (2012). Training the brain to survive stroke. PloS one, 7 (9) PMID: 23028788... Read more »
Smells can bring back great memories, but they can also predict the future. Neuro researcher Marijn van Wingerden tells us all about it.... Read more »
van Wingerden, M., Vinck, M., Tijms, V., Ferreira, I., Jonker, A., & Pennartz, C. (2012) NMDA Receptors Control Cue-Outcome Selectivity and Plasticity of Orbitofrontal Firing Patterns during Associative Stimulus-Reward Learning. Neuron, 76(4), 813-825. DOI: 10.1016/j.neuron.2012.09.039
Aerobic exercise appears to have significant therapeutic benefits in the treatment of anxiety and depression. This effect has been demonstrated in animal models as well as in humans. However, there has been limited study of the potential brain mechanisms that produce an anti-anxiety or an anti-depressant effect.Brain serotonin neurotransmitter receptors have been implicated in anxiety and depressive disorders. Additionally, selective serotonin reuptake inhibitor drugs such as fluoxetine (Prozac) play a key clinical role in the pharmacologic treatment of anxiety and depression. These associations suggest that the therapeutic effect of exercise may involve a adaptation of brain serotonin receptors.Greenwood and colleagues at the University of Colorado recently published a study of the effect of exercise on the 5-HT2C (serotonin 2C) receptor in a rat model of anxiety and depression in the journal PLOS ONE. The key elements of their study design included:Male rats were exposed to either six weeks of voluntary exercise in a cage with running wheels (cases) or six weeks in a cage without running wheels (controls)Case and control rats received a brain injection of an anxiogenic drug into brain amygdala or striatumCase and control rats completed behavioral tasks (shock-elicited fear and shuttle box escape learning) that assess anxiety behaviorsLevels of 5-HT2C messenger RNA (mRNA) in the brain amygdala and striatum regions were measured in both rat groupsThe principal findings of the study included:The voluntary running rats showed reduced anxiety behaviors when injected with the drug known to activate the 5-HT2C receptorThe voluntary running rats showed reduced 5-HT2C mRNA levels in the amygdala and striatum suggesting a down regulation of this anxiety-related receptorThe authors the conclude their results "extend previous work identifying the 5-HT2C receptor as a relevant target for pharmacologic discovery, as well as shed light on the potential mechanisms which underlie the anxiolytic effects of physical activity".This study supports a direct role for exercise in modifying a key brain anxiety-related serotonin receptor. Clinicians should consider recommending the addition of aerobic exercise to pharmacological and psychological treatment options for anxiety disorders.Photo of anhinga from the author's files.Greenwood BN, Strong PV, Loughridge AB, Day HE, Clark PJ, Mika A, Hellwinkel JE, Spence KG, & Fleshner M (2012). 5-HT(2C) Receptors in the Basolateral Amygdala and Dorsal Striatum Are a Novel Target for the Anxiolytic and Antidepressant Effects of Exercise. PloS one, 7 (9) PMID: 23049953... Read more »
Greenwood BN, Strong PV, Loughridge AB, Day HE, Clark PJ, Mika A, Hellwinkel JE, Spence KG, & Fleshner M. (2012) 5-HT(2C) Receptors in the Basolateral Amygdala and Dorsal Striatum Are a Novel Target for the Anxiolytic and Antidepressant Effects of Exercise. PloS one, 7(9). PMID: 23049953
To celebrate the dawn of December, a month of intense introspection and widespread brooding, Sick Papes brings you an exclusive soul-wrenching interview with neuroscientist and celebrity theoretician, Dr. Shaul Druckmann. Shaul’s recent pape (w/ Mitya Chklovskii) suggests a fresh answer to a beguiling question- how does the brain maintain persistent representations despite the fact that neuronal activity is constantly changing?
Personal experience tells us that the brain can maintain stable representations of images, numbers, and ideas for seconds and minutes. However, the activity of neurons in brain regions thought to be involved in working memory, such as prefrontal cortex, varies on a much faster time scale, (~10-50 milliseconds). Shaul’s pape proposes a network model, called FEVER, which can maintain persistent representations even as the activity of individual neurons varies. It turns out that this network model has many features in common with the organization of real cortical networks.
SP: If I’ve got my mules in order, your model network is constructed such that the receptive field of each neuron is equivalent to a weighted sum of the receptive fields of all other neurons in the network, and the weights in this weighted sum are the strength of synaptic connections between neurons. This allows the activity of individual neurons to vary, while the output of the network remains constant. This structure seems precarious. If I were to go into your brain and cut one single synaptic connection, how would this affect stable representations in a dense FEVER network? In other words, how robust is this network to wanton destruction?
SD: Yup, your mules are definitely in order and marching. As you say, destroying synaptic connections will momentarily throw the network off balance. However, since the representation is highly overlapping and there are many ways to represent each stimulus there would be no problem readjusting the network so as to ignore the destroyed part of the network. Given the high degree of overcompleteness that we suspect exists in cortex, there is a lot of room to recover from damage.
SP: In his Tractatus, Wittgenstein proposes that, “A logical picture of facts is a thought”; in other words, that thoughts must adhere to the same logical form as things in the real world. Agree or disagree?
SD: Wittgenstein huh? I am not sure I can even properly pronounce his name, much less understand his writings. The end of my serious reading of philosophical literature timeline is more or less with Kant… Regardless, I am not sure I read the sentence the same way you do. “A logical picture of facts is a thought”. First, I like the stress on the term “picture of facts” which for me relates the thought to the many aspects of taking a picture: we select what to put in our frame and what to keep out, the lighting we throw on the objects matters a lot as well as the angle and ultimately it needs to be developed to become a real thing (okay maybe the last one was a stretch). Regarding what thoughts must adhere to, I am not sure thoughts are under control, so lets read “thoughts” as “theories”. I strongly believe that theories must first and foremost have a sound logical structure. In one interpretation that is pretty straightforward since it just means that the math needs to check out. However, I believe that, somewhat related to that sentence, one of the most interesting things about theories is that they rearrange facts that we thought we previously knew into a new order. If that new order makes more “sense” and teaches you (the experts) new things about the facts then the theory is actually valuable. Anyhow, this sounds like something better talked about over a beer…
SP: Your pape addresses how a brain might hold onto specific representations for periods of seconds, even as the activity of individual neurons varies wildly during this period. A slightly different problem is how human thought and perception seems to occur on the time-scale of seconds, despite the fact that neural activity varies on the order of milliseconds. Do you think this is simply a matter of perception, or do evolving network dynamics across longer time scales matter?
SD: Actually our first draft discussed that briefly, but reviewers hated it since it was too speculative. I think there are two possibilities, one is that representation is constantly changing, but there is a little leprechaun working really hard in our brain all the time to make sure our conscious perception is smooth (this may sounds crazy, but think change-detection blindness). The other is that the networks themselves bridge the gap between the time scale of neural activity (milliseconds) and the time scale of the world (seconds say) by mechanisms such as the one we describe in order to allow downstream circuits a smooth readout of the representation and the leprechaun to have a much more relaxed life. Which is true? I really don’t know.
SP: When you are building a model, do you start with the acronym first and work backward? Or do you build the model first and then tweak it until it fits with a catchy acronym?
SD: Given the allowed artistic freedom of basically picking any random word and letter within it for an acronym it is pretty easy to find one once the work is done. But what you suggests sounds fun, randomly thinking up an acronym, finding the most reasonable sentence you can attach to it and seeing whether that inspires and idea worth working through.
SP: Do you think the phrase “persistent representation” accurately describes what is happening in the brain during working memory? For example, remembering a phone number requires a certain amount of active rehearsal, and is susceptible to distraction. Why must prefrontal cortex maintain a representation within itself, rather than relying on repeated structured inputs from other sensory networks?
SD: In the delayed-match-to-sample working memory task design as much as possible is done to eliminate the possibility of input driven memory (turning stimulus on only transiently, long delay periods). Therefore, that is less of an option in my opinion. More generally though, if it is an input driven memory then one has to answer the question how does whatever circuit that provides the input keep its ability to provide an input for such a long time despite the transient stimulus. Then all our explanations would need to be shifted to that area. I don’t think it has been worked out in an airtight manner that this isn’t a possibility, but I think it is less likely.
SP: In Borges’ story, ”Funes the Memorious”, a young boy falls off a horse and loses his ability to forget. His life is haunted by the banal details of every moment he has ever experienced, including all the associated physical and emotional sensations. Are there certain conditions under which a FEVER network architecture could result in such a condition?
SD: Good point! In fact the way we develop the math in the first section leads to a network with an infinite integration, which is exactly Borges’ idea, sans the horse. That’s why we later add the scaling factor to the equation that allows you to have a very long, but not infinite, time constant. Otherwise, with an infinite time constant one would run into all kinds of problems such as saturation due to the integration of all the (banal) past stimuli ever encountered.
SP: One method to test the relevance of the FEVER network is to compare the synaptic structure of a cortical network to the range of eigenvalues predicted by the model. Are there any unexpected features of the eigenspectrum that you could look for in real cortical networks? You mention a few in the paper that support your model (e.g., prevalence of reciprocal connections), but are there others that would be worth looking for?
SD: In terms of synaptic reconstruction, I think the neat thing to do is to try to map the receptive field of neurons and then do EM reconstruction a la Denk. Then one option is trace down the axon of a single cell, find all the post-synaptic cells, sum up their receptive fields and see if you come up with the original neuron’s own receptive field (I guess you could do it with trans-synaptic vir... Read more »
Druckmann, S., & Chklovskii, D. (2012) Neuronal Circuits Underlying Persistent Representations Despite Time Varying Activity. Current Biology, 22(22), 2095-2103. DOI: 10.1016/j.cub.2012.08.058
The prefrontal cortex can select a rule to deploy in a particular situation. How is this done? The group of neurons that deploy a rule oscillate in synchrony when that rule is to be used. This synchrony explanation is becoming quite common. Synchrony is what produces functioning groups of neurons. Buschman at al have looked [...]... Read more »
Jensen, O., & Bonnefond, M. (2012) Prefrontal alpha- and beta-band oscillations are involved in rule selection. Trends in Cognitive Sciences. DOI: 10.1016/j.tics.2012.11.002
Buschman TJ, Denovellis EL, Diogo C, Bullock D, & Miller EK. (2012) Synchronous oscillatory neural ensembles for rules in the prefrontal cortex. Neuron, 76(4), 838-46. PMID: 23177967
In a series of posts, I am examining recent research related to exercise and the brain. In the first post in this series, I summarized some evidence of the role of the brain in exercise-related fatigue.In this post, I will review a hypothesis that aerobic physical activity (APA) played a key role in the evolution and growth of the human brain.Raichlen and Polk have recently published a review on this topic in the journal Proceedings of the Royal Society.This review begins by noting the recent research supporting a role for aerobic physical activity in the formation and growth of neurons. Human studies show a link between level of aerobic fitness and brain hippocampal volume, cognitive function including performance on memory tasks and the rate of cognitive decline with age.The authors note that aerobic physical activity may influence brain health through several mechanisms:Increased levels of brain neurotrophins including brain-derived neurotrophin factor (BDNF)Increased levels of two growth factors: insulin-like growth factor I (IGF-1) and vascular endothelial growth factor (VEGF)Peripheral metabolic pathway benefits of these neurotrophins through vascular and muscle growth, repair and enhanced oxygen deliveryThese mechanisms linking aerobic physical activity and brain health and growth support the possibility of an evolutionary model. In this model, the authors propose that evolutionary selection for athletic fitness brings with a selection for "increased brain growth during ontogeny in species adapted for endurance activities".The authors note this is model represents a testable hypothesis requiring additional research for confirmation. However, there is some support already for this hypothesis in studies of rodents, other mammals and in humans. Addtionally, this hypothesis is supported in some artificial selection experiments in mice and rats.This review then summarizes some anthropological data showing that the evolution of endurance running in hominids tracks with overall brain size and growth. Obviously, these types of studies are limited to indirect and somewhat imprecise measures of brain size such as size of the semicircular canal.The authors conclude that their model of selection for aerobic physical activity leading to human brain growth evolution requires additional research support. However their review "suggests that humans' evolutionary story may ultimately be more complex than the traditional view of brains over brawn". This is an interesting review that readers can access in full through the link below. In upcoming posts, I will look at some recent research involving the benefits of exercise during pregnancy on fetal cognition and potential role of fitness on limiting the brain damage associated with stroke.Photo of yellow-crowned night heron from the author's files.Raichlen DA, & Polk JD (2013). Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings. Biological sciences / The Royal Society, 280 (1750) PMID: 23173208... Read more »
Raichlen DA, & Polk JD. (2013) Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings. Biological sciences / The Royal Society, 280(1750), 20122250. PMID: 23173208
Neurons don't grow in a vacuum. They have white fibers, other neurons, blood vessels and all sorts of other obstacles to grow around.Some NeuroArt (source)A recent paper from France details the making of a 3D environment that can facilitate 'realistic' neural growth. Labour et al. (2012) created a collagen biomimetic matrix which contains neural growth factor (NGF). Labour et al., (2012) Figure 3These scanning electron microscope images show the porous fibril texture of the collagen matrix. Most of the paper is spent explaining the methods for making this biomimetic matrix, but they also actually grow some pseudo-neurons (PC-12 cells) on the matrix. They show that when cultured on top of this collagen surface, the cells extend neurons in three dimensions into the matrices and are affected by the NGF. (when there is no NGF, the neurites don't grow and the cells die.) This paper is mostly about the methods, but I like the new possibilities that growing 3D cells opens up. With these biomimetic collagen matrices, the factors that cause specific dendritic arborizations in three dimensions can be analyzed. The environment can be completely controlled and the neurons easily visualized during growth. The authors suggest using these matrices to study neurodegeneration as well.Another interesting thing this paper introduced me to is the 'graphical abstract.' I didn't know that that was a thing, but it seems like a good idea. However, trying to summarize an entire paper in one figure seems pretty difficult. Here is their attempt:Labour et al. (2012) graphical abstractI think it does actually get the feel of the paper across pretty well, though it's not really informative without the actual abstract next to it. © TheCellularScaleLabour MN, Banc A, Tourrette A, Cunin F, Verdier JM, Devoisselle JM, Marcilhac A, & Belamie E (2012). Thick collagen-based 3D matrices including growth factors to induce neurite outgrowth. Acta biomaterialia, 8 (9), 3302-12 PMID: 22617741... Read more »
Labour MN, Banc A, Tourrette A, Cunin F, Verdier JM, Devoisselle JM, Marcilhac A, & Belamie E. (2012) Thick collagen-based 3D matrices including growth factors to induce neurite outgrowth. Acta biomaterialia, 8(9), 3302-12. PMID: 22617741
There's been lots of interest in the idea that ADHD meds reduce crime rates.No doubt that, even as we speak, worried pundits are writing of how this is a worrying Orwellian scenario and yadda yadda. But what's really going on?The research is from Sweden and published in the New England Journal of Medicine: Medication for Attention Deficit–Hyperactivity Disorder and Criminality. The first thing to note is that the study is not about giving medication in order to prevent crime; it was purely looking at what happened to people given ADHD treatment for their ADHD.In a nutshell, the authors found that people diagnosed with ADHD were about 10% less likely to be convicted of a crime during periods when they were on medication for the disorder. This was true of both men and women, and the effect was greater for the more serious offences.It was a huge study with over 25,000 ADHD patients and the data comprise pretty much everyone in Sweden over the relevant period so in that respect it's a very good study - although speaking of Orwellian, these studies are only possible because of the Scandinavian tendency to make national registers of everything.Now the big criticism here is that it's just a correlation, it doesn't prove that the meds were what prevented crime. It might be that ADHD meds have no effect on crime, but that people are less likely to commit crimes at periods when they have their lives sorted out (when they're 'on the rails'), one marker of which is that they're seeking treatment for their ADHD.However, the authors found that periods of use of SSRI antidepressants were not associated with changes in conviction rates. This is quite good evidence against the 'on the rails' critique, assuming that being prescribed SSRIs is as much a marker of being on the rails as being prescribed Ritalin is.So, in my view, this is pretty good work, as good as any observational non-randomized study. However, remember: this is just about treating ADHD. Not drugging criminals to stop crime.Lichtenstein P, Halldner L, Zetterqvist J, Sjölander A, Serlachius E, Fazel S, Långström N, and Larsson H (2012). Medication for attention deficit-hyperactivity disorder and criminality. The New England journal of medicine, 367 (21), 2006-14 PMID: 23171097... Read more »
Lichtenstein P, Halldner L, Zetterqvist J, Sjölander A, Serlachius E, Fazel S, Långström N, & Larsson H. (2012) Medication for attention deficit-hyperactivity disorder and criminality. The New England journal of medicine, 367(21), 2006-14. PMID: 23171097
Aerobic exercise results in improved cardiovascular and muscular health. However, the benefits of exercise on the brain are only now beginning to be understood. In the next series of posts, I will review some recent research addressing the effects of exercise on the brain. One area of research on this topic is understanding the biological mechanism for exercise fatigue and this effect contributes to athletic performance.Historically, the brain was felt to have no significant contribution to the perception of fatigue. Exercise fatigue was felt to be primarily a peripheral phenomenon regulated by muscle fatigue, development of anaerobic mitochondrial metabolism and the production of peripheral lactic acid accumulation.Timothy Noakes from South Africa recently summarized research into the brain's contribution to fatigue in the journal Frontiers in Physiology. In this review he summarizes a central nervous system model of fatigue that helps in the "protection of whole body homeostasis".Noakes notes the peripheral model of fatigue fails to account for a variety of central nervous system moderators of fatigue and exercise performance including:CNS stimulants such as amphetamines, caffeine, pseudoephedrine and modafanilExercise after a full night of sleep (no sleep deprivation)CNS pain drugs such as acetaminophen and naloxoneOther CNS drugs and inflammatory compounds such as the dopamine and norepinephrine re-uptake inhibitor bupropion and CNS cytokine levels of IL-6 and IL-18The presence of psychological motivating factors such as presence of competitors and the possibility of a monetary reward in the exercise taskRecent research supports both a physical and brain contribution to the perception of exercise fatigue. Brain imaging research indicates a key role for the brain insula region in regulating subjective fatigue and in making a decision to discontinue exercise. Highly trained athletes show an ability to attenuate the brain right insula activation found in untrained athletes with extreme exertion. The figure labeled 3D Brain View highlights the brain insular cortex region in a teal color. In a previous post, I looked at the growing understanding of the role of the insular cortex in a variety of cognitive tasks. It appears that the insula additionally plays a key role in central fatigue via CNS connections to the brain primary motor cortex and the limbic emotional regulation network.Noakes suggests that the highest performing athletes have an ability to train their brains to moderate central fatigue signaling. This might allowing for final bursts of speed necessary for winning performances. Photo of a wood duck from Busch Gardens in Tampa, Florida is from the author's files. Brain insula figure is a screen shot from the iPad app Brain Tutor.Noakes TD (2012). Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis. Frontiers in physiology, 3 PMID: 22514538... Read more »
Noakes TD. (2012) Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis. Frontiers in physiology, 82. PMID: 22514538
There are maps of your body in your brain. Some maps represent the control over your muscles. Other maps show the input coming in from your senses. One of the best known sensory maps is the one for touch.
But we might think of everything we feel with our skin as one sense – touch – these are several separate sense. We feel pressure. We feel changes in temperature, and and different neurons handle warmth and chills.
And we feel pain.
While Wilder Penfield published the famous maps of the somatosensory cortex over 60 years ago, it hasn’t been clear if the neurons that we use to pick up pain from tissue damage, nociceptors, make maps in the brain the way other sense do. There are fewer nociceptors in the skin than other sensory neurons.
A new paper by Mancini and colleagues set out to test this. They gave their volunteers either innocuous little puffs of air on their hands, or...
They shot their volunteers with frikkin’ laser beams.
This hurt. Not much, but enough to set off the nociceptors in the volunteers’s fingers. The authors describe it as “pinprick.”
While they were doing this to the hands, Mancini and company were taking brain scans using functional magnetic resonance imaging (fMRI).
If you look at your hand, the middle finger is well, in the middle, flanked on either side by the ring and index fingers.
If there’s a map of nociceptors in the cortex, you should find that same order in the parts of the brain that respond to being shot with lasers. Using the colour scheme above, the blue should always be flanked by red on the one side and green on the other.
And that’s what you see. Check the area surrounded by the dotted white line in the picture:
The team also shows that the responses for the control puffs of air also map out in the same way.
Strictly speaking, the authors only show that there’s a map of the nociceptors of the fingers. Now, to assert that this means there is a full map of the sort that gets shown in textbooks is sort of like saying that because you have a decent map of the Mediterranean, you also have a decent map of Australia. That’s plausible, though strictly speaking, they haven’t mapped the entire nociceptive globe, so to speak.
It’s a nice demonstration that these neurons follow some of the same patterns of organization as other sensory systems. Which does lead to a bigger question: why does the nervous system tend to make these maps instead of some other form of organization?
Mancini F, Haggard P, Iannetti GD, Longo MR, Sereno MI. 2012. Fine-grained nociceptive maps in primary somatosensory cortex. The Journal of Neuroscience 32(48): 17155-17162. DOI: 10.1523/JNEUROSCI.3059-12.2012
Classic graphics #3: The somatosensory cortex
... Read more »
Mancini F., Haggard P., Iannetti G. D., Longo M. R., & Sereno M. I. (2012) Fine-Grained Nociceptive Maps in Primary Somatosensory Cortex. Journal of Neuroscience, 32(48), 17155-17162. DOI: 10.1523/JNEUROSCI.3059-12.2012
I hope you had a Happy Thanksgiving Julie!(source)I’m not exactly sure what that means, as we don’t celebrate it in Australia, but I hope you had a great time with your family and friends all the same!Thanks for all those fantastic resources you included in your last blog post. It was also great to see some extras posted by readers in the comments section. (source)Last time I looked at ‘The Good’ of some the science surrounding children and dogs. This post, it’s time to cover some of the ‘The Bad’. What can possibly be bad about children and dogs? Well, dogs don’t live as long as us, for one.When dogs die(source)Having established last time that dogs can benefit kids’ confidence, self-belief, trust, respect and heaps of other positive attitudes and behaviours, I was left wondering how losing a pet dog impacts children. Loss of a companion animal can be a devastating event for people of any age.Humans don’t all experience grief equally.Our understanding of death is linked to our developmental state, but young children can still feel pain at the loss of a family dog. For many children, the death of a pet dog will be their first experience with this kind of loss and grief. Pet dogs can be almost-constant companions for children, and have been assigned a role in reflected appraisal similar to that of a best friend.Psychologists encourage parents/guardians to explain death to kids sensitively and with honesty. Adults should answer questions simply, using clear and accurate information and avoid the desire to ‘protect’ children from death by hiding the truth of a pet’s illness or euthanasia. This is because children with active imaginations may create scenarios about the death that are far worse than reality. Adults should allow children to express their grief (through verbal, artistic or written expression; reading stories about the death of pets, etc.), acknowledging the importance of the relationship lost (rather than trivializing the death or running to buy a new puppy) and helping children to understand that grief is a normal and natural emotion that helps us cope with death. ... Read more »
Gerwolls Marilyn K., & Labott Susan M. (1994) Adjustment to the Death of a Companion Animal. Anthrozoos: A Multidisciplinary Journal of The Interactions of People , 7(3), 172-187. DOI: 10.2752/089279394787001826
SERPELL JAMES A. (1981) CHILDHOOD PETS AND THEIR INFLUENCE ON ADULTS' ATTITUDES. Psychological Reports, 49(2), 651-654. DOI: 10.2466/pr0.19220.127.116.111
Davis Janet Haggerty. (1987) Preadolescent Self-Concept Development and Pet Ownership. Anthrozoos: A Multidisciplinary Journal of The Interactions of People , 1(2), 90-94. DOI: 10.2752/089279388787058614
Van Houtte Beth A., & Jarvis Patricia A. (1995) The role of pets in preadolescent psychosocial development. Journal of Applied Developmental Psychology, 16(3), 463-479. DOI: 10.1016/0193-3973(95)90030-6
Bryant Brenda K. (1990) The Richness of the Child-Pet Relationship: A Consideration of Both Benefits and Costs of Pets to Children. Anthrozoos: A Multidisciplinary Journal of The Interactions of People , 3(4), 253-261. DOI: 10.2752/089279390787057469
Bonanno George A. (2004) Loss, Trauma, and Human Resilience: Have We Underestimated the Human Capacity to Thrive After Extremely Aversive Events?. American Psychologist, 59(1), 20-28. DOI: 10.1037/0003-066X.59.1.20
Bingham Glenda M., Budke Christine M., & Slater Margaret R. (2010) Knowledge and perceptions of dog-associated zoonoses: Brazos County, Texas, USA. Preventive Veterinary Medicine, 93(2-3), 211-221. DOI: 10.1016/j.prevetmed.2009.09.019
PANIC.As much as I enjoy silly people, I really dislike jumping on the silly person bandwagon here but I feel compelled to counter nonsense with real sense.As Vaughan Bell over at mindhacks has repeatedly noted, Baroness Greenfield of Oxford likes to turn to the press to talk about how video games, the internet, and other generally fun things are ruining the brains of our children.In response, Ben Goldacre has made a simple request of the Baroness: publish your findings in a peer-reviewed study.This has yet to happen.Over the years many reasonable, intelligent, knowledgeable, practicing scientists like Vaughan, Ben, Dorothy Bishop, NeuroSkeptic, Dean Burnett, and others have tried to counter the Baroness's claims through appeal, humor, sarcasm, etc.But the Baroness keeps making public claims to the media such, "Several scientific studies have suggested that playing an excessive number of computer games or spending too much time surfing the internet can have a physical impact on the brain," with the implication that this change is bad.But truth is better than fear, and neuroscientist Daphne Bavelier recounts almost a decade of her research regarding the effects of action video games on the brain and cognition in her recent TED talk.The reality? Action video games, such as first-person shooters, improve attention, visual perception, cognitive control, and a host of other executive functions. This research began with a accidental finding by C. Shawn Green that he and his video-game playing friends were performing much better on attention talks than their controls. This culminated in their 2004 Nature paper, "Action video game modifies visual selective attention". Since then their research has progressed quite well.This is a fantastic talk, and one I'm adding to my now-growing list of good neuroscience TED talks. So here's the real evidence on the effects of video games on the brain. I'd love to know what evidence the Baroness's has to counter.Green, C., & Bavelier, D. (2003). Action video game modifies visual selective attention Nature, 423 (6939), 534-537 DOI: 10.1038/nature01647... Read more »
Green, C., & Bavelier, D. (2003) Action video game modifies visual selective attention. Nature, 423(6939), 534-537. DOI: 10.1038/nature01647
The Ketogenic Diet is a very low carbohydrate, high fat, "adequate protein" diet. Ketogenic diets have proven helpful to people with uncontrolled epilepsy and may be of benefit to epileptics in general, to victims of stroke and other forms of brain injury and possibly cancer. It has become somewhat popular among CrossFit-ters and followers of he paleo-type diet.
They come with other effects that may not be worth the discomfort or unintended risks to healthy people. This includes kidney stones and, in women and girls, amenorrhea. Amenorrhea is associated with bone loss, increasing risk of osteoporosis, and indicates problems in hormone balance. Supplementation with calcium may help with this, but then again, it might not. Physiology can be quite complex, and consumption does not necessarily indicate absorption is occurring. It is quite possible that something that causes hormonal imbalance in women may also cause hormonal imbalance in men. Playing with one’s physiology, when we don’t know the unintended outcomes of such play, may be inadvisable, especially long-term.
What is the optimal diet? Is the Paleo Diet the Optimal Diet?
It is very hard to say what is the optimal diet. Vegetarians, as described in some current diet books, are weak and "skinny-fat". However, one can be a vegetarian and have excellent bone density, low blood pressure, low resting heart rate, low fasting blood sugar, excellent blood lipid profile and great strength to body weight ratio .I will leave it at this: The "optimal diet" for one person may not be the "optimal diet" for another, nor the optimal diet for all conditions. Humans are omnivores and physiologically polymorphic and adaptable. This has given us tremendous flexibility and enabled us to survive in wildly different climes and environments. It has made us resilient. It is also quite possible, that our individual resilience allows our bodies to adjust to dietary and environmental change. Gut microbiota populations, after all, change as diet changes.
The current state of research indicates no harm though, from short-term ketogenic diets. There has been little, if any, research on the risks and benefits of long-term ketogenic diets in healthy adults.
Brinkworth GD, Buckley JD, Noakes M, Clifton PM, & Wilson CJ (2009). Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of internal medicine, 169 (20), 1873-80 PMID: 19901139
Kossoff, E., Zupec-Kania, B., & Rho, J. (2009). Ketogenic Diets: An Update for Child NeurologistsJournal of Child Neurology, 24 (8), 979-988 DOI: 10.1177/0883073809337162
Bergqvist AG, Chee CM, Lutchka L, Rychik J, & Stallings VA (2003). Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Epilepsia, 44 (4), 618-20 PMID: 12681013
... Read more »
Brinkworth GD, Buckley JD, Noakes M, Clifton PM, & Wilson CJ. (2009) Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of internal medicine, 169(20), 1873-80. PMID: 19901139
Bergqvist AG, Chee CM, Lutchka L, Rychik J, & Stallings VA. (2003) Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Epilepsia, 44(4), 618-20. PMID: 12681013
What is a ketogenic diet? Ketogenic Diet is a very low carbohydrate, high fat, "adequate protein" diet. Ketogenic diets have proven helpful to people with uncontrolled epilepsy and may be of benefit to epileptics in general, to victims of stroke and other forms of brain injury and possibly cancer. It has become somewhat popular among CrossFit-ters and followers of the paleo diet.They come with other effects that may not be worth the discomfort or unintended risks to healthy people. This includes kidney stones and, in women and girls, amenorrhea. Amenorrhea is associated with bone loss, increasing risk of osteoporosis, and indicates problems in hormone balance. Supplementation with calcium may help with this, but then again, it might not. Physiology can be quite complex, and consumption does not necessarily indicate absorption is occurring. It is quite possible that something that causes hormonal imbalance in women may also cause hormonal imbalance in men. Playing with one’s physiology, when we don’t know the unintended outcomes of such play, may be inadvisable, especially long-term. What is the optimal diet? Is the Paleo Diet a ketogenic diet?It is very hard to say what is the optimal diet. Vegetarians, as described in some current diet books, are weak and "skinny-fat". However, one can be a vegetarian and have excellent bone density, low blood pressure, low resting heart rate, low fasting blood sugar, excellent blood lipid profile and great strength to body weight ratio .I will leave it at this: The "optimal diet" for one person may not be the "optimal diet" for another, nor the optimal diet for all conditions. Humans are omnivores and physiologically polymorphic and adaptable. This has given us tremendous flexibility and enabled us to survive in wildly different climes and environments. It has made us resilient. It is also quite possible, that our individual resilience allows our bodies to adjust to dietary and environmental change. Gut microbiota populations, after all, change as diet changes. That said, the paleo diet is not necessarily ketogenic. But you follow a paleo diet and choose to make it ketogenic if you wanted to. The current state of research indicates no harm though, from short-term ketogenic diets. There has been little, if any, research on the risks and benefits of long-term ketogenic diets in healthy adults.Brinkworth GD, Buckley JD, Noakes M, Clifton PM, & Wilson CJ (2009). Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of internal medicine, 169 (20), 1873-80 PMID: 19901139Kossoff, E., Zupec-Kania, B., & Rho, J. (2009). Ketogenic Diets: An Update for Child NeurologistsJournal of Child Neurology, 24 (8), 979-988 DOI: 10.1177/0883073809337162Bergqvist AG, Chee CM, Lutchka L, Rychik J, & Stallings VA (2003). Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Epilepsia, 44 (4), 618-20 PMID: 12681013... Read more »
Brinkworth GD, Buckley JD, Noakes M, Clifton PM, & Wilson CJ. (2009) Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of internal medicine, 169(20), 1873-80. PMID: 19901139
Bergqvist AG, Chee CM, Lutchka L, Rychik J, & Stallings VA. (2003) Selenium deficiency associated with cardiomyopathy: a complication of the ketogenic diet. Epilepsia, 44(4), 618-20. PMID: 12681013
Quick! Introduce yourself to this guy before his baby-high wears off! Photo by David Castillo Dominici at FreeDigitalPhotos.net. What happens if you take a wrestler or action star and force him to babysit obnoxious but lovable kids? Well, if you’ve seen movies like The Pacifier with Vin Diesel, The Tooth Fairy with Dwayne ‘The Rock’ Johnson, Kindergarten Cop with Arnold Schwarzenegger, or The Spy Next Door with Jackie Chan, you know that he will fall madly in love both with his young charges and with the closest available woman. Hollywood is so sure of this phenomenon that they have based a whole genre of family movies on it. Now, scientists are finding that Hollywood may be on to something. Prairie voles are one of the only 3-5% of mammals that are monogamous and in which both parents help take care of young. In females, maternal care is regulated in part by the hormones associated with pregnancy, birth and lactation. The fact that males don’t do those things and they still provide paternal care is curious. The fact that male prairie voles will often provide care to offspring that aren’t even their own is even more curious. Will Kenkel, Jim Paredes, Jason Yee, Hossein Pournajafi-Nazarloo, Karen Bales, and Sue Carter at the University of Illinois at Chicago recently explored what happens to male prairie voles when they are exposed to unfamiliar vole pups. Male voles without any experience with females or pups were placed in a new clean cage. Then the researchers put either a pup (that was not related to the male), a dowel rod (an unfamiliar object), or nothing into the cage with them for 10 minutes. Afterwards, they measured oxytocin (a hormone associated with bonding between mothers and their offspring) and corticosterone (a stress hormone) in the males’ blood at different time points. In another study, they also looked at the activity of brain neurons associated with the production of these hormones. A male prairie vole is startled to find a baby in his cage... But then he takes care of it. Video by Will Kenkel. Both adult and juvenile males exposed to a pup for 10 minutes had higher oxytocin and lower corticosterone compared to the males not exposed to a pup. But this effect was short-lived, as male hormone levels quickly evened out again. Most of these males that were exposed to a pup showed alloparental care (care of a baby that is not their own), like approaching the pup, cuddling with it and grooming it. Males with higher oxytocin and lower corticosterone levels were more attentive towards the pups. Additionally, alloparental males exposed to pups had more activity of oxytocin-producing neurons and less activity of neurons associated with corticosterone-production in a specific brain region called the paraventricular nucleus (or PVN for short). Oxytocin is strongly associated with pair bonding in prairie voles, particularly in females, and corticosterone affects pair bonding too (generally increasing pair bonding in males and preventing it in females). If exposure to a pup affects these hormones, maybe it affects how the male would interact with adult females. To test this, the researchers put male voles in a new clean cage and put a pup, a dowel rod, or nothing into the cage with them for 20 minutes. Then they put the males with an unfamiliar adult female for 30 minutes. After getting acquainted with the female, the males were put in a “partner preference apparatus”, which has three connected chambers: a neutral center chamber, a connected chamber with the familiar female tethered into it, and a connected chamber with an unfamiliar female tethered into it. The researchers measured how much time the males spent in each of the three chambers and with each of the two females over the next 3 hours. A prairie vole pair snuggles. Photo from Young, Gobrogge, Liu and Wang paper in Frontiers in Neuroendocrinology (2011) Males that were exposed to a dowel rod or to nothing before they were introduced to a female spent equal amounts of time with each of the two females. But males that were exposed to a pup before they were introduced to a female spent nearly 4 times as much time with that female than with the unfamiliar one. In other words, hanging out with a random pup acted like Love Potion #9 on these bachelor males and made them fall for the next female they encountered! Interestingly, this effect was true not only for the males that acted in an alloparental way towards the pups, but it was also true of males that attacked the pups (The researchers quickly rescued the pups if this occurred). Perhaps, males that were alloparental with the pups had increased oxytocin and males that were aggressive with the pups had increased corticosterone, either of which would make it more likely for them to form a preference for the female they were with. Hmm… Got your eye on a special someone? Try volunteering him to babysit before your next date. Want to know more? Check this out:... Read more »
Kenkel, W., Paredes, J., Yee, J., Pournajafi-Nazarloo, H., Bales, K., & Carter, C. (2012) Neuroendocrine and Behavioural Responses to Exposure to an Infant in Male Prairie Voles. Journal of Neuroendocrinology, 24(6), 874-886. DOI: 10.1111/j.1365-2826.2012.02301.x
Honeybees are clever wee beasties. If you give a honeybee a scent, then give her food, she can quickly learn to extend her mouthparts when she smells the scent alone. And they can remember this for at least a whole 24 hour day. This is a classic learning test made famous by Pavlov’s dogs. So honeybees are at least as smart as dogs, for this test anyway.
What’s going on in that tiny little head as they learn that some arbitrary smell means food? Usually, neurons need to make new “stuff” to form a memory. Making proteins, for instance, is usually needed for long term memory, but not short term memory.
Actin is a protein that is best known as half of the machinery that powers muscles (myosin in the other), but actin is also a more general component of a cell’s skeleton. In rats and mice and other furry mammals, you need to make actin to get long-term potentiation (LTP), which is a strengthening of the connections between two neurons.
Ganeshina and colleagues injected honeybees with chemicals that blocked the making of actin. You would expect that this would mess up the poor little honeybee’s memory.
But expectations were dashed. These actin-inhibiting drugs made the honeybees remember better, not worse.
The authors’ aren’t sure what’s going on here, but they have a guess.
The parts of the honeybee’s nervous system that learns smell are called the mushroom bodies. These mushroom bodies grow a little as the honeybee gets older, adding in new connections between neurons all the time, regardless of whether the honeybee learns anything or not. These new connections, because they aren’t related to anything the bee learns, would mostly add noise to the neural pathway. And that could drown out some of connections between neurons that are formed or strengthened as the honeybee learns.
The authors seem to think that knocking out the actin production prevents “random” new connections that would form just during normal aging. As a result, the honeybee gets more memory signal and less noise.
This is a story of diversity. This paper reminds us that even when animals can learn the same kinds of tasks, they may not be learning them in the same ways.
Ganeshina O, Erdmann J, Tiberi S, Vorobyev M, Menzel R. 2012. Depolymerization of actin facilitates memory formation in an insect. Biology Letters 8(6): 1023-1027. DOI: 10.1098/rsbl.2012.0784
Photo by BugMan50 on Flickr; used under a Creative Commons license.... Read more »
Ganeshina O., Erdmann J., Tiberi S., Vorobyev M., & Menzel R. (2012) Depolymerization of actin facilitates memory formation in an insect. Biology Letters, 8(6), 1023-1027. DOI: 10.1098/rsbl.2012.0784
Studies have shown that men's testosterone levels increase after sexual stimulation. However, other research shows that merely briefly chatting to a woman also causes testosterone release, making it unclear whether sex, per se, is associated with testosterone changes.So an intrepid band of researchers decided to find out using a unique methodology. Their paper's called Salivary Testosterone Levels in Men at a U.S. Sex Club and it's about... that.They first set the scene: Subjects were recruited from an internationally known "adult social club" in Las Vegas, Nevada, also referred to as a "sex club"... patrons pay a membership fee (akin to an entrance fee) to enter the 18,000 square foot, 2-story club. The first floor is open to all paying customers. The second VIP floor is available for an additional fee and includes a variety of rooms, including fetish rooms...All are not created equal in this Garden of Eden, however: Personal observation and communication with staff and members revealed to the investigators that there is a semi-structured hierarchy of patrons in the club. Single men (also referred to as ‘‘sharks’’) are easily identified by an orange wristband. Single women also wear an orange wrist band. Couples are identified by a green colored wristband. Single men are often considered to be a nuisance, as reported by many patrons, and are avoided in certain circumstances. Single women, moderately rare, do not share the stigma.Anyway, the authors went there and recruited 44 men, of whom 18 ended up having sex, while 26 only looked at other patrons doing so. Saliva samples were taken before and afterwards, and levels of testosterone were measured. The results showed that testosterone increases were much larger in the do-ers than the watchers (see above).This is an important result, the authors say, becauseit runs against the grain of previous human testosterone and sexual stimuli studies in which testosterone increases in response to erotic videos and "courtship"’ behavioral interactions appeared more reliably induced than those related to active sexual behavior... We suggest that the reason for our findings, in contrast to the overarching pattern of previous work, is that lab-based paradigms may quell men’s testosterone responses... engaging in sexual behavior while wired up to machines in a sterile lab may put a damper on men’s arousal and physiological responses.A good point.In general, lab studies can be misleading when the behaviors under investigation are the kind of thing you can't really do in a lab. For research on fairly 'basic' memory, perception and cognitive tasks, a lab is probably as good an environment as any but for more complex behaviours it may be systematically misleading. And if a lab is bad, an MRI scanner is even less realistic.Now, I thought the neuroscientists who threw a cocktail party on their grant money had it good, but these authors really hit a home run by using theirs to get into a sex club. It would be hard to top that but I note that surprisingly little is known about the, er, physiological correlates of lying on a beach in the Bahamas atop a pile of gold bars and bottles of Dom Pérignon. Someone needs to find out and I for one would be willing to undertake this challenge. Escasa, M., Casey, J., and Gray, P. (2010). Salivary Testosterone Levels in Men at a U.S. Sex Club Archives of Sexual Behavior, 40 (5), 921-926 DOI: 10.1007/s10508-010-9711-3... Read more »
Escasa, M., Casey, J., & Gray, P. (2010) Salivary Testosterone Levels in Men at a U.S. Sex Club. Archives of Sexual Behavior, 40(5), 921-926. DOI: 10.1007/s10508-010-9711-3
How would the brain process a truly 'ageless' face? Moraine, an ageless Aes Sedai (source)I am sure this question has plagued many Wheel of Time fans, but only now has an experiment been designed to test it. Just 4 days ago, Homola et al. (2012) published a paper in PLoS ONE in which they have people guess ages of people in pictures and scan their brains. Homola et al. (2012) Figure 1A. (Which one looks most Aes Sedai to you?)The first interesting thing that they found was that the older the person in the picture (either a real picture of a real person, or a hybrid 'morphed' picture like the ones above), the harder it was to tell how old they were. This isn't really that surprising, as the range of ages that can 'look' a certain age gets wider over the years. Homola et al., (2012) Figure 2B.Here they plot the standard deviation in years for people's guesses as to the age. The authors showed videos of the faces morphing from one age to another to volunteers while they were in the fMRI machine.As a side note: they found that there was no difference between male and female volunteers. If they had I think a big deal would have been made about it. but since they didn't it's just a tiny sentence in a long paper. Ok, back to the processing of age. They threw out the results from people who were really really bad at rating age because they 'weren't motivating' and weren't really trying apparently. (This could be a bit of cherry picking or data massaging) Then they compared the areas of the brain that were active for people who were really really good at guess age, and people who were only average.Homola et al., (2012) Figure 4DThe basic finding was that the posterior angular gyrus area (pANG) on the left hemisphere was 5 times more active for the expert age guessers than it was for average. Conclusion: pANG is important for age-processing. This on its own is good to know, but not amazingly interesting. What I think is cool is the idea that the authors present as a follow up experiment in their discussion:"Even though our study highlights pANG as one key component for age processing, its precise role in this context is still speculative and needs further investigation. Our model, illustrated in Figure 7, gives rise to interesting hypotheses: One testable prediction would be that disruption of left pANG activity using transcranial magnetic stimulation (TMS), for example, should impair numerical age but not gender judgements, and that brain lesion-symptom mapping can eventually dissociate the two. " Homola et al., (2012)So now we know, the Aes Sedai must have some magic that transcranially impairs pANG in everyone around them so they can't guess their age. That is how to stay truly ageless.© TheCellularScaleHomola GA, Jbabdi S, Beckmann CF, & Bartsch AJ (2012). A Brain Network Processing the Age of Faces PLoS One DOI: 10.1371... Read more »
This paper (citation below) starts with the assumption (call the modal view) that, “It is not surprising then that the modal view holds that the semantic processing of multiple-word expressions and performing of abstract mathematical computations require consciousness (reason: they are human skills). In more general terms, sequential rule-following manipulations of abstract symbols [...]... Read more »
The response of the human brain to light harks back to Cro-Magnon times, when sunrise signalled the earliest opportunity to leave your cave to get your breakfast without being pounced on by a carnivorous beast lurking in the shadows. In … Continue reading →... Read more »
LeGates TA, Altimus CM, Wang H, Lee HK, Yang S, Zhao H, Kirkwood A, Weber ET, & Hattar S. (2012) Aberrant light directly impairs mood and learning through melanopsin-expressing neurons. Nature, 491(7425), 594-8. PMID: 23151476
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