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  1. What can you show with one minute and one slide? It turns out, quite a lot! For the past 21 years, the NIH National Center on Sleep Disorders Research has hosted a DataBlitz at the annual SFN meeting, challenging 20 speakers to present their work in only 60 seconds, and with only a single slide. The night is then capped-off with a plenary speaker, respectifully given two slides and two whole minutes. When I received the email inviting me to present my sleep research at this year’s DataBlitz, having never previously attended I naively assumed this would be a formal evaluation of my data, and I agonized over how to pare down my data into its most salient puncta. Well, talk about missing the mark… The Sleep and Circadian Biology DataBlitz is anything but formal. Dr.'s Chris Leonard and Michael Twery introduced the concept to everybody with drinks in hand, and encouraged the audience to cheer wildly for the good speakers, but to boo vociferously at anyone who dared pass the 60 second mark. With that warning ringing in my ears, he passed the mike to the MC of the evening, Dr. Lisa Lyons, and we began our rapid fire dive into the cutting edge of circadian research. I learned there are a number of unique approaches to communicating your entire paper in only one minute. The first is just to speak faster… Rebecca Northeast from University of Manchester walked us all the way through the brainstem’s involvement in circadian timekeeping and demonstrated single-cell cycling rhythmicity between the the area postrema and the nucleus of the solitary tract. Kevin Zhang explained the importance of peripheral light sensing for mice and humans alike, and pretty clearly walked through their new deep-brain photoreceptor Opn3. Others, myself included, applied a whittling-down approach, and painfully distilled the past several years of our lives into a couple key figures. William Todd for example showed the circuit controlling time-dependent aggression propensity in mice, and explained its possible relevance to “sundowning” in Alzheimer’s patients. I could show only my most striking behavioral phenotype, and had to hand-wave through the rest of the model, and I still barely made it off the stage with 2 seconds left on the big clock. Several talks really embodied brevity as the soul of wit, and turned their research story into short poems. Nadir Balba explained how light therapy can improve sleep quality in veterans with traumatic brain injuries using only four rhyming lines. Carolyn Jones needed only a limerick to tell the sad tale of a prairie vole who couldn’t form long-term social bonds due to cortical disruptions brought on by early-life sleep disruptions. Our plenary speaker Dr. Luis de Lecea also chose the poetic route, and although he did run over his two minutes of alloted time, his verses and videos told the graphic story of hypocretin-positive neurons and their influence on sex drive in mice. Even though I was only a first-timer, I was not alone in calling the 2018 DataBlitz a rousing success. Out of 615 sleep/circadian relevant abstracts at the SFN meeting, 21 presenters powered through a minute of rapid fire information presented to ~3-400 audience members. In under 30 minutes, 100 cumulative years of research on at least 7 model organisms was rushed, sang, and rhymed (with only 2 presenters running long and earning boos!) until the data overload could be washed down with sliders, wine, and beer. I’ve only just gotten home and I’m already excited for DataBlitz 2019. Benjamin Bell PhD Candidate, Johns Hopkins School of Medicine Sleep and Circadian Rhythms, Mark Wu Lab
  2. Light and Mood: From retina to brain Although we don’t photosynthesize our food, animals including humans are as reliant as plants on the nurturing light emanating from our sun rhythmically for hours each day. This light sets our circadian rhythm and times all of the important physiological functions that rise and fall over the course of the day. But light has other powerful effects on our minds, and when light availability is disrupted either naturally or by our busy lifestyles, our moods and cognitive function suffer greatly. In order for our brain to receive this vitally important light, it must pass first through the photoreceptor cells in our retinas. Most of us are familiar with these ‘rods’ and ‘cones,’ which perceive dim, black and white light or rich colors and motion, respectively. But there is another type of photorecipient cell, called the intrinsically photosensitive Retinal Ganglion Cell, (ipRGC) which express the light sensitive protein melanopsin and transmits light information directly to the brain enclosed in its dark skull. These cells directly synapse onto the suprachiasmatic nucleus, the master circadian pacemaker in mammals, and research into their role has largely been limited to the clock. Previously, Samer Hattar’s lab has shown that ablation of these cells fully disables the circadian clock’s ability to entrain to light cues. But in addition to this loss of internal timekeeping, light’s affect on mood and learning was also lost. Diego Fernandez took this to mean the ipRGC’s were responsible for mediating this effect, and at his talk on Day 1 of SFN, explained his delineation of two Retina-Brain pathways which enable light to modulate both learning and mood in mice. (Fernandez et. al. Cell, 2018) While the talk was excellent, the paper is even better, and I highly recommend giving it a read to fully appreciate their beautiful experiment construction and all of the supporting information. I recognize this post must sell their work short, but here are the quick points highlighted in Diego’s talk Mice kept in a disturbed light cycle called T7 (3.5 hours of light then 3.5 hours of dark) perform worse on assays of memory and learning, such as the Novel Object test and Morris Water Maze. This light-based effect on learning and memory requires the ipRGC - to - SCN connected cells. The T7 light cycle also causes mood deficits in mice, as measured by sucrose preference and Forced Swim tests. However, this deficit is lost when the ipRGC - to - SCN cells are genetically and specifically ablated. So if not the SCN, then where does light have its mood-affective impact? They traced ipRGC projections to the perihabenular nucleus, and showed that this poorly described region was both strongly light-activated, and projected to other mood-related areas, such as the vmPFC. In short, the non-SCN directed ipRGC’s were connected to mood areas by only two synapses, and this thalamic relay circuit is responsible for light’s direct affect on mood regulation, at least in mice. It will be very interesting to see if these findings shape the direction of neuropsychiatric treatments in the future. We all suffer more now than ever before from a preponderance of light at night, and maybe that’s having a non-negligible effect on dramatically rising depression rates in the US, and across the developed world. Disclaimer: this is only my speculation and hand-waving, but I’m very curious to see how this bears out into the future. Benjamin Bell PhD Candidate, Johns Hopkins School of Medicine Sleep and Circadian Rhythms, Mark Wu Lab
  3. The Ventral Tegmental Area - Reward and Arousal During this afternoon, one of my favorite poster sessions took place (Sleep systems, and sleep regulators). Here, a poster that grabbed my attention was titled “GABA and glutamate networks in the VTA regulate sleep and wakefulness” from Xiao Yu, a member of William Wisden’s lab at Imperial College London. gaba and dopamine vta.jpg1327×910 666 KB Dopamine (green) and GABA (red) expressing neurons in the mouse ventral tegmental area (VTA; outlined) studies by Xiao Yu and colleagues demonstrates that these neurons bidirectionally regulate sleep and wakefulness (Credit: Jeremy C Borniger, PhD; Stanford University) The ventral tegmental area (VTA) is largely known as the seat of the brain’s ‘reward’ system. This is because neurons in this area are the primary source of all the brain’s dopamine, a ‘feel good molecule’ that is responsible for the rewarding effects of drugs, sex, and all things fun. Neurons in this area signal reward by calculating the so called ‘reward prediction error’. This is the difference between an expected and unexpected reward. For example, if you expect to get one piece of candy from your mom, but then she gives you 100 pieces of your favorite treat, neurons in the VTA calculate the difference, fire, and release a large surge of dopamine proportional to the reward ‘error’. This signal acts to reinforce the behaviors that led to the unexpected reward. A ‘good’ error like this is a called a ‘positive prediction error’ while the opposite, where a reward is omitted when it is expected, is called a ‘negative prediction error’. Negative prediction errors result in less dopamine release, and therefore aversion to the behaviors that led to this unexpected ‘disappointment’. As you may well predict, drugs of abuse like cocaine, alcohol, heroin, and others elicit a strong positive prediction error, resulting in a lot of dopamine release and reinforcement of drug seeking behavior. In addition to dopamine neurons in the VTA, there exists two other primary populations, one that expresses the inhibitory neurotransmitter GABA, and another that produce primarily glutamate, an excitatory neurotransmitter. Recent research has demonstrated that in addition to their roles in reward signaling, VTA-dopamine neurons strongly promote wakefulness, likely through their projections to the nucleus accumbens (NAc) (see image below). How other VTA populations relate to wake/sleep states remains unknown. vta da wakefulness ada.jpg696×476 200 KB Activation of VTA-dopamine neurons (TH-positive) strongly promotes wakefulness. You can see that when these neurons are stimulated (by light sensitive ChR2 activation), the mice rapidly wake up (panels c,d,e) (Credit: Eban-Rothschild et al., 2016; Nature Neuroscience) To investigate these other populations, Xiao Yu and colleagues used optogenetics, chemogenetics, fiber photometry (Ca2+), and neuropharmacology to untangle the roles GABA and glutamate neurons in the VTA play in sleep/wake states. First, they identified that most glutamate neurons in the VTA also express NOS1 (nitric oxide synthase 1), and therefore used NOS1 and vglut2-cre mice to specifically target these neurons for manipulation. VGLUT2 stands for ‘vesicular glutamate transporter 2’, and is expressed on virtually all subcortical neurons that signal via glutamate. Using viral vectors to specifically express the stimulatory (hM3Dq) or inhibitory (hM4Di) DREADDs, they demonstrated that stimulation of VTA-glutamate neurons strongly promotes wakefulness while inhibition of this population strongly promotes sleep. To investigate how these neurons promoted arousal, they stimulated their projections in different brain regions using optogenetics. They focused on two primary output regions, the lateral hypothalamus (which contains many sleep-related neural populations) ,and the nucleus accumbens. Stimulation of glutamate nerve terminals arriving from the VTA to the lateral hypothalamus strongly promoted wakefulness, while stimulation of similar fibers arriving at the NAc had a less pronounced effect. This suggests that VTA-glutamate neurons likely promote wakefulness via dual projections to the lateral hypothalamus and NAc. Importantly, the natural activity of these neurons (examined via fiber photometry) was shown to be highest during wakefulness and REM sleep compared to NREM sleep. This suggests that they normally change their firing rates during distinct vigilance states. photometry example.jpg1393×229 82.8 KB Example of a fiber photometry trace showing the activity of GABA neurons across sleep-wake states. As you can see, these neurons are mostly active during wakefulness and REM sleep compared to NREM sleep (wake = white background, NREM = blue, REM = red) (Credit: Jeremy C Borniger, PhD, Stanford University) Similar experiments were done to examine the VTA-GABA population. Activation of these neurons (via DREADDs or optogenetics) strongly promoted sleep, while inhibition of this population powerfully promoted wakefulness. Activation of GABA nerve terminals from the VTA to the LH strongly promoted sleep, an opposite effect to that of glutamate stimulation in LH. This effect was partially inhibited when stimulations occurred in combination with a drug (gabazine) that inhibits GABA signaling. This suggests that it is GABA (and not other molecules) released by these neurons that is largely responsible for their effects of sleep/wake states. Finally, they hypothesized that this effect could be driven by GABA’s inhibitory influence over VTA-dopamine populations. By inhibiting VTA-GABA neurons in combination with dopamine blockade, they were able to (mostly) eliminate the effect of VTA-GABA silencing on wakefulness. This supports a model in which VTA-GABA neurons inhibit neighboring VTA-dopamine neurons in order to promote sleep. This is an exciting research area as a major problems for drug abuse victims are insomnia and chronic fatigue, which inevitably lead to the reinstatement of drug seeking behavior. Sleep drugs targeting the VTA could really help rectify general sleep problems and specifically those related to drug abuse. That’s it for now, I’ll post another sleep story later, as that’s sorta my field! Jeremy C Borniger, PhD Department of Psychiatry & Behavioral Sciences Stanford University SoM Twitter: @jborniger website: jeremyborniger.com
  4. Poster Highlights: Theme F (Integrative Physiology and Behavior) This morning I had the pleasure of exploring some posters for Theme F--Integrative Physiology and Behavior, specifically on the topics of Sexual Differentiation in Neuroendocrine Processes, as well as Stress Modulated Pathways (hypothalamus, amygdala, and BNST). The majority of the posters I observed today were from animal studies, which are less familiar to me as a clinical researcher. This is the benefit of SfN--you can both share your expertise in your own field, as well as learn applicable skills or advancements outside of your field all at the same conference. One poster that particularly stood out to me was TT15, which discussed the role of maternal buffering during fear conditioning. As our research team (STARC--Wayne State University) has identified a relationship between maternal stress and the psychological symptoms of her children in Syrian and Iraqi refugees, I was interested to hear more. Amanda White, from the University of Michigan, shared her work replicating findings that presence of the mother mouse during fear conditioned pups resulted in decreased freezing behavior when the pup was again exposed to the unconditioned stimulus (an odorant). She added that this effect was only observed for female offspring, and that male offspring did not seem to benefit from maternal buffering. In an attempt to identify neural networks involved, Ms. White also looked at c-Fos expression (a robust marker of neuronal activity) in selected regions of interest. I was most excited by the technique she used to do so--she applied the Brain Connectivity Toolbox, which is traditionally used for functional neuroimaging data, to her c-Fos expression data. I observed similar methodological advancements with posters T5 and VV14. At poster T5, Kristen Krolick from Miami University told me about how she used DAVID, an online opensource tool for conducting biological pathways analysis, to determine whether more genes were expressed than usual in particular brain regions--including the hypothalamus, hippocampus, and amygdala--due to restraint stress in adolescent rodents. I look forward to seeing how Kristen will assess between-sex differences given these data. At poster VV14, I got to see a successful example of using 7T MRI for the detection of subfields in the amygdala, including the basolateral amygdala and the central amygdala, which have previously been indistinguishable using 3T magnets. Throughout the poster session, I also learned how cortisol seems to buffer subjective emotional appraisal to negative stimuli in men but not women, and about Mycobacterium Vaccae as an anti-anxiolytic in animal models in the presence of a stress. The potential mechanism proposed was M. Vaccae's suppression of expression of corticotrophin releasing hormone particularly in the central amygdala (the region of the brain implicated in fear expression) and the bed nucleus of the stria terminalis (the region of the brain implicated in anxiety). One of the highlights of the session was meeting a former collaborator in person for the first time, after working together via Skype and email on a project regarding neuroaesthetics of art, music, and literature during my undergraduate years. I love that SfN brings together colleagues and friends, old and new! I cannot wait to learn more throughout the conference, and I especially look forward to running the Wayne State University Translational Neuroscience Program booth at the Graduate Fair tomorrow between 12:00pm and 2:00pm! Find me at booth 53 to hear more about our diverse faculty, research interests, and innovative approaches to trauma, psychiatry, and neuroimaging. Lana Grasser @lana.grasser
  5. Theme C and F Blogger: Lana Grasser Hello everyone! My name is Lana Ruvolo Grasser, and I am one of your 2018 Society for Neuroscience annual meeting bloggers. This is my second year in graduate school, and my first year at SfN! While I have attended our state’s region meetings before, I am happy to be in sunny San Diego, coming from cold and rainy Detroit. Despite the weather, I am loving my time as a graduate student at Wayne State University’s School of Medicine. Here, I am studying trauma and related disorders in a variety of ways, including functional neuroimaging, neuroinflammation, and efficacy of interventions. My work in particular focuses on dance/movement therapy, art therapy, and yoga for relieving symptoms of trauma in Syrian and Iraqi refugees. However here at SfN, I will be presenting work from my mentor’s study, which investigates the combinatorial effects of instruction and experience learning in fear conditioning and fear extinction using functional MRI. This is not my first experience with neuroimaging–during my undergraduate study at Michigan State University, where I received my Bachelors of Science in Neuroscience, I worked in a literary neuroscience lab directed by Dr. Natalie Phillips. I am excited to be sharing my experience at SfN, particularly regarding Themes C and F - Neurodegenerative Disorders and Injury, and Integrative Physiology and Behavior. I really hope that you enjoy my posts. Lana Grasser @lana.grasser
  6. Stress-induced depression and feeding circuits in the arcuate nuclei During the day 2 poster sessions, one that caught my eye was titled “Chronic unpredictable stress modulates neuronal activity of AgRP and POMC neurons in hypothalamic arcuate nucleus” presented by Xing Fang in the Xin-yun Lu lab at the Medical College of Georgia at Augusta University Agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) neurons in the arcuate nucleus strongly regulate feeding behavior and food intake. Broadly, AgRP neurons promote feeding (orexigenic), while POMC neurons work in a reciprocal manner to suppress feeding (anorexigenic). AgRP and POMC arcuate.jpg583×782 130 KB AgRP neurons in the arcuate promote food intake while POMC neurons inhibit food intake via their actions on downstream MC4R- expressing neurons in the paraventricular nucleus (Credit: Carol A. Rouzer, Vanderbilt University) Depression is characterized by aberrant responses to environmental stimuli. For example, chronic psychological stress can promote depression in humans and animal models. Stress-induced depression is characterized by anhedonia (not enjoying what you used to love), lethargy and despair, and changes in feeding behavior and appetite. How does stress cause these behaviors to come about? Using in vivo electrophysiology, behavioral assays, and DREADDs, Fang and colleagues investigated the role of hypothalamic AgRP and POMC neurons (two populations that powerfully control appetite) in mediating these behaviors. This work builds on previous studies by the group, long linking depressive-like behavior to alterations in feeding and satiety hormones such as leptin. To induce depression in mice, the researchers used a technique called ‘chronic unpredictable stress’ (CUS). This model strongly promotes a depression-like state after 10 days of unpredictable stress where mice go through a gamut of constant light exposure, tail pinches, restraint, and shock stimuli, among others. agrp and pomc anatomy.jpg666×547 191 KB Viral injections into the arcuate nucleus of POMC-Cre mice (left panels; projections in red) shows their wide axonal distribution throughout the brain. Similarly, injections into the arcuate nucleus of AgRP-cre mice demonstrate that they also project throughout the brain, although in a different pattern (right panels, projections in green) (Credit: Wang et al., 2015; Frontiers in Neuroanatomy) Through their electrophysiological recordings, the researchers demonstrated that CUS decreased the firing rate of AgRP neurons but increased the firing rate of POMC neurons. When they tested the role of AgRP neurons in depressive-like behavior using stimulatory (Gq) or inhibitory (Gi) DREADDs, they were able to elicit opposite responses. Stimulation of these neurons improved depressive-like behavior, while inhibition promoted it. Together, these studies suggest that AgRP and POMC neurons play an important role in stress-related adaptive behavior. Importantly, they provide a novel circuit related to depression which may be targetable for the treatment of the disease through pharmacological agents or lifestyle changes. Jeremy C Borniger, PhD Department of Psychiatry & Behavioral Sciences Stanford University SoM Twitter: @jborniger Website: www.jeremyborniger.com
  7. Circadian Surprises! Day and night, breakfast and dinner, winter and summer, wake and sleep…our lives are dominated by interacting rhythms in our environment and our behavior. Why is it that we sleep at night and not during the day? Why are heart attacks and strokes more common in the morning than the evening? How do animals adapt to winter and summer? Why do we get jet-lag, and what is it, exactly? All these questions revolve around a central subject in neuroscience: circadian clocks. During day 1 of the Society for Neuroscience annual meeting in San Diego, CA, I was treated to a nanosymposium (timely insights in circadian regulation) highlighting new and exciting research in this area. Chaired by Steven Brown and Alessandra Porcu, this session covered all aspects of circadian biology, from behavior to neuronal circuits, and from synapses to molecules. The suprachiasmatic nuclei (pictured above) serve as the master clocks controlling mammalian circadian rhythms (Credit: Jeremy C. Borniger, PhD; Stanford) Here, I highlight a few of the talks that I found the most interesting. Unfortunately, I am not able to cover everything, and some really cool stuff slipped through! That’s the downside of this immense conference…there’s never enough time to see everything! Two talks on the same protein (one in flies and the other in mammals) grabbed my attention. These talks were given by Masashi Tabuchi and Benjamin Bell, two researchers from Johns Hopkins University. During Masashi’s talk, he described a potential mechanism by which the protein Wide Awake (WAKE) regulates sleep/wake cycles in flies. Fly WAKE abstract.jpg557×557 127 KB WAKE regulates sleep quality through appropriate timing of neural firing codes (Credit: Tabuchi et al., 2018; Cell) He showed that irregular neural firing rates during the day (regulated by WAKE) promote arousal while regular firing patterns during the night promote sleep. Ben Bell followed up his talk by taking their findings in flies to mammals, describing a mammalian ortholog to the fly WAKE protein (called mWAKE). mWAKE is highly enriched in the master clock, the suprachiasmatic nucleus (SCN) suggesting it plays a role in circadian time keeping or regulation. Unlike in flies, knockout of mWAKE in mice only caused mild problems in sleep/wake states. However, through measuring locomotor activity, the researchers found that these mice were extremely hyperactive (>5 times more active than wild-type mice). Curiously, this trait (phenotype) only came about during the dark phase (mice are nocturnal, so active during the dark phase). To investigate this further, the researchers examined the firing rates of SCN neurons during the day and night. Normal mice have a large difference between the night and day in SCN firing rates, with peak neural activity occurring during the day. However, mWAKE knockout mice showed no difference between day and night, with firing rates remaining high all the time! Additionally, cells lacking mWAKE showed blunted responses to the inhibitory neurotransmitter GABA, and this lack of inhibition may explain the hyperactive profile mice lacking mWAKE had. Finally, they examined (using an mWAKE reporter mouse) where mWAKE expressing cells project to throughout the brain. They found that cell bodies were distributed throughout the brain, in all major arousal centers. Importantly, they seemed to be discrete from other neuromodulator systems present in these areas, like hypocretin/orexin neurons in the lateral hypothalamus, or histamine neurons in the tuberomammillary nucleus. Significant more research is required to fully understand the role this protein plays in sleep/wake states. Is it a ‘master regulator’ of arousal? Does it interact with every ‘arousal center’ differently or does it have a distributed ‘homogenous’ effect across the brain. When does mWAKE start to express during development? Does this coincide with changes to sleep-wake behavior during early age? I’m excited to follow this story going forward! That’s all for now, I’ll see you soon! Feel free to follow more updates on twitter @jborniger and on my website www.jeremyborniger.com Jeremy C Borniger, PhD Department of Psychiatry & Behavioral Sciences Stanford University SoM
  8. Techniques and Integrative Physiology and Behavior Highlights I am a neuroscientist funded by the NIH BRAIN Initiative currently working at Stanford University as a post-doc in Luis de Lecea’s Lab. My focus is understanding basic neurocircuitry that controls sleep and wakefulness using optogenetics, calcium imaging, chemogenetics, EEG/EMG, and other strategies. I am further interested in how the brain and periphery communicate, specifically in the context of cancer. I am using mass cytometry approaches to characterize the effects of brain stimulation on the peripheral immune response. 43O2QsVzTcWI2R9nPeF4vw_thumb_c1a.jpg602×1304 260 KB Jeremy C. Borniger, PhD Keep an eye out for my posts on the newest and coolest techniques in the field, as well as more general posts on sleep, circadian rhythms, neuroimmunology, and brain/body communication. Please visit my website for more detail, and follow me on twitter for real time updates during the meeting. I look forward to seeing everyone in San Diego! If you see me, feel free to say hi! Jeremy C Borniger, PhD BRAIN Initiative Postdoctoral Fellow de Lecea lab Department of Psychiatry & Behavioral Sciences Stanford University SoM Twitter: @jborniger NeurOnline: Jeremy_Borniger Website: http://www.jeremyborniger.com Email: jcbornig@stanford.edu
  9. Integrative Physiology and Behavior (Theme F) - Benjamin Bell Headshot.png368×537 209 KB Hi All, My name is Benjamin Bell, I’m a PhD candidate in Human Genetics at Johns Hopkins in Baltimore, and my main interest is sleep! Unfortunately, not my sleep, but the sleep of my mouse and fly models, which I use to characterize the role our circadian clock plays in maintaining timing of sleep and arousal. Over the course of SfN this year, I’ll be blogging about the various ways physiological changes affect behavior and cognition in animals, with a specific interest in psychoactive substances, from caffeine to LSD. If you’d like to learn more about sleep (or need a place to catch a few Z’s), come join me for my talk in the “Timely Insights in Circadian Regulation” symposium, Saturday Nov. 3 at 1 pm. See you all in San Diego! Benjamin Bell PhD Candidate Dr. Mark Wu Lab Johns Hopkins School of Medicine Neuronline: @ben.bell12 Email: Ben.bell12@gmail.com
  10. After a long and stimulating Day 1 of SfN, I fought against my circadian clock’s natural urge to sleep in and made it to the Convention Center early to catch Dr. Joseph Takahashi’s Special Lecture, titled “Molecular Architecture of the Circadian Clock in Mammals”. In mammals, daily rhythms of physiology and behavior are synchronized to the 24 hour light-dark (LD) cycle by the suprachiasmatic nucleus (SCN), the master circadian clock located in the hypothalamus. When people think of circadian rhythms, they typically think of sleep, and how the circadian system transmits timing information to other regions of the brain that induce rest or arousal. However, virtually every cell in the body contains its own autonomous circadian clock, the core of which is a transcriptional/translational feedback loop controlled by specific gene products. These single-cell oscillators interact to generate tissue-wide rhythms in organs from the lungs to the liver. While long-held wisdom says that the SCN is in charge of synchronizing these so-called “peripheral” clocks, we are now learning that they can be entrained by non-light cues independently of the SCN. In his lecture, Dr. Takahashi gave an overview of decades of pioneering work uncovering the molecular basis of the circadian clock, and offered new insights from his lab into how the circadian clock in the liver drives metabolism and affects the lifespan of mice. Doing my best this morning to spite my late chronotype during Dr. Takahashi’s talk. Dr. Takahashi’s claim to fame came in 1997, when his lab undertook a massive forward genetic screen in mice, chemically inducing mutations at random and screening individuals for abnormal circadian behavior. Their efforts paid off when they identified and cloned the first circadian rhythm gene in mammals, known as Clock. This opened the door for the discovery of other important clock genes including BMAL1 and Period, and provided circadian biologists and behavioral neuroscientists with an extremely powerful framework to explore how genes drive behavior. Circadian_clock_of_mammals.png760×502 27.5 KB A simplified schematic of the core mammalian circadian clockwork. In his current work, Dr. Takahashi continues to use innovative genetic approaches to characterize the circadian system. Dr. Takahashi described recent experiments using ChIP-sequencing technology to identify the binding sites of the core circadian transcription factor BMAL1 in the liver. Amazingly, his team found that BMAL1 has over 3,000 target genes in the mouse liver alone, allowing it to regulate virtually every basic metabolic pathway in a circadian fashion. Other work demonstrated that mice with brain-specific knockouts of BMAL1 were behaviorally arrhythmic. In these mice, the rhythms of the SCN and peripheral oscillators such as the liver were out of phase with each other under constant darkness conditions. However, time-restricting the availability of food in these mice re-synchronized circadian clocks in the liver and kidney. These studies provided important evidence that peripheral oscillators like the liver can be differentially affected by non-light cues, which can have important consequences for metabolism. Next, Dr. Takahashi described work by his collaborator Dr. Satchidananda Panda at the Salk Institute exploring how time-restricting feeding without restricting caloric intake affects metabolism in mice. In this set of experiments, mice were given a high-fat diet and given ad libitum access to food, or had their food access restricted to either day or night. Incredibly, mice that had their food restricted to the nighttime (when they are normally active) did not gain weight and were protected against metabolic diseases, unlike their counterparts with ad libitum or daytime-restricted food access. These results aligned nicely with classic work described by Richard Weindruch, which demonstrated that restricting caloric intake increased the lifespan of mice. Inspired, Dr. Takahashi reviewed this literature and realized that the feeding protocol described in these studies resulted in several potentially confounding effects such as mice being fed when they would normally be sleeping, and inadvertently being forced to fast for days at a time. This led him to ask the question - Is time restriction or caloric restriction the critical factor for increasing lifespan? To begin to answer this question, Dr. Takahashi’s team built an automatic feeding system that gave them full control of the timing, amount and duration of food availability. Using this system, the researchers used a combination of time (TR) and caloric (CR) food-restriction protocols in different groups of mice. While both day and night TR mice, as well as CR mice with day or night time restrictions ate less food than their counterparts with ad libitum food access, only the CR mice with nighttime food-restriction lost weight. Unexpectedly, these mice also self-imposed a 2-hour time restriction of food intake at the end of their active phase, which resulted in a brief increase in activity during their normal rest phase. These results suggested the relationship between feeding behavior and metabolism are more complicated than previously thought. Dr. Takahashi’s team is now embarking on a new study they hope will allow them to further separate the effects of time and caloric food restriction on metabolism and longevity, which they predict will take 4 years to complete. For now, it’s hard to say definitively whether time restriction, caloric intake, or some combination of both is most important for increasing lifespan - only time will tell. For more on sleep and circadian rhythms, be sure to head down to the posters today between 1 and 5, check out the Sleep: Key Advances Nanosymposium from 1-3, and keep an eye out for my write ups on these events later on!
  11. How could sleep, aging and myelin be related? Sometimes its good to get out of your wheelhouse. Neurone012-361x680.png361×680 Image source Two posters presented today explored myelin modifications at different life stages. In the first, the effect of chronic sleep loss during adolescence was found to decrease the thickness of myelin in the Corpus Callosum and the Lateral Olfactory Tract. Adolescence is a key time for myelin development which continues in the human brain until our late 20’s. This poster made me wonder what I did to my brain during those late nights I spent playing video games during my own adolescence? What is interesting about this finding on myelin in chronic sleep loss is that previous work showed sleep loss suppressed myelin-related genes. Suggesting at a molecular level an importance for sleep in myelin maintenance. Next steps should better characterize this relationship and how it may relate to adolescent development. 159835-full.jpg800×539 The second poster moved from me the young brain to the aged brain. This poster examined ERK1/2 activation in oligodendrocytes, which had previously been shown to enhance myelination. The role of ERK1/2 has been studied before at a molecular signaling level, so connecting this to cellular and behavioral function can help integrate our understanding of brain function. Further, as we age brain function decreases including affecting memory. Would sustained activation of ERK1/2 in oligodendrocytes affect cognitive decline? From a young age, mice had oligodendrocytes trigger sustained ERK1/2 signalling which persisted as long as the oligodendrocyte lived. Behaviorally this led to an increase in contextual fear memory in aged mice only. However, it remains unclear how to interpret this finding. Perhaps over time some oligodendrocytes die with aging, and it could be that those with sustained ERK1/2 activation survive longer. Therefore in old mice with their persisting ERK1/2 activation oligodendrocytes, these cells could help facilitate this behavior. This work is preliminary and needs additional experiments to explore this interpretation. Both these posters introduced me to new concepts on the shared topic of white matter in the brain. I can’t wait to see what new info tomorrow brings! Patrick E. Steadman, MSc PhD Candidate, Frankland Lab, The Hospital for Sick Children MD-PhD Student, University of Toronto Neuronline: @patrick.steadman Twitter: @pesteadman Blog: patricksteadman.ca/blog
  12. Dan_Vahaba

    Dan Vahaba, SfN 2017 Blogger

    Dan Vahaba, SfN 2017 Blogger Hi everyone My name is Dan Vahaba Quick science bio: I’m currently a PhD candidate at the University of Massachusetts Amherst, working in the lab of Dr. Luke Remage-Healey. My research explores how how baby songbirds learn to sing. In particular, I’m interested in how auditory processing develops over the critical period for vocal learning, how auditory memories are formed, and how locally synthesized brain estrogens modulate cortical sensory neurons. Some research themes/areas I’m interested include: Neuroethology Behavioral neuroendocrinology Vocal learning; animal communication Neurophysiology Critical peroid plasticity At #sfn17, I’ll be blogging about: Theme D: sensory systems, and Theme F: integrative physiology & behavior I’m also into science communication. This past year, I started writing quarterly for the Journal of Experimental Biology’s “Outside JEB” section. (Potentially) fun facts about me outside of science I have 2 adorable cats Peanut & Leon: IMG_20170723_141429.jpg959×719 232 KB I enjoy collecting Motown, soul, and funk records (esp. from Detroit), and like to DJ on occasion. Here’s one of my favorite tracks: https://www.youtube.com/embed/FmBs5HX3vwA I’m also really into road biking. I recently did my first bike tour by tandem with my partner IMG_20170916_141621.jpg959×719 288 KB If you see me among the masses at SfN, please say hello (I probably won’t look like a game show host there…)! I’m always eager to meet new people, especially ones I can nerd out with about brains/science. See you in DC! Cheers, Dan More ways to connect with me Twitter <-- I’ll be live tweeting throughout the conference #sfn17 Neuronline Google Scholar Personal Research Page LinkedIn
  13. My name is Dr. Rebecca Calisi Rodríguez, and I’m an Assistant Professor of Neurobiology, Physiology, and Behavior at the University of California, Davis. My lab studies how the brain regulates reproduction and sexual behavior. We also value outreach, undergraduate research opportunities, science communication, and supporting women and underrepresented minorities in science. I will be covering topics related to Integrative Physiology and Behavior, as well as issues related to Diversity and Social Justice in Neuroscience. Follow my blog posts here and on Twitter at @BeccaCalisi. See you in November!
  14. My name is Raymond Sanchez, and this year I’ll be one of the official meeting bloggers for the 2017 SfN meeting. I’m a PhD Candidate in Neuroscience at the University of Washington in the lab of Dr. Horacio de la Iglesia. My research focuses on sleep and circadian rhythm disturbances in Dravet syndrome, a severe form of epilepsy and autism-spectrum disorder, as well as how circadian rhythm disturbances like jet lag and shift work contribute to the etiology of mood disorders. I’ll be focusing primarily on Themes F (Integrative Physiology and Behavior) and G (Motivation and Emotion), with a special emphasis on sleep and circadian rhythms, their relationship to neurological and psychiatric disorders, and innovative approaches to solving big data problems in neuroscience. See you in D.C.! Raymond Sanchez PhD Candidate, University of Washington @raysan53 on Neuronline My personal blog @mangoraysan on Twitter
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