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  1. Neurohistory Cartoons: A scientific outreach project combining the history of neuroscience and cartoon imagery While preparing for a microteaching class on neuroscience I stumbled upon notes on a poster I attended at #SfN18 about “Neurohistory Cartoons”. To be honest this (History of Neuroscience) is one of the topics I found harder to digest when I took my first neuroscience class and I’m confident that others felt the same. As an instructor and as a learner I have seen the effectiveness of using cartoons as a tool for teaching/learning. The effectiveness of cartoons in teaching can also be found in the literature and it is used in many fields including economics, social and physical sciences [1,2]. Ok, I’ll get to the point. Neurohistory Cartoons are an online tool developed by the Neuroscience Graduate Students’ Association (GSA) at the University of British Columbia (UBC) in Vancouver, Canada. While at the poster I learned from Samantha Baglot, the lead project organizer, that this project aims to share the history of neuroscience through cartoon imagery and the content is freely accessible. One of their goals for the future is to share information about scientists whose discoveries may not be as well-known and have paved the way for current research questions. Neurohistory Cartoons are shared in the form of a timeline (shown above and at the Neurohistory Cartoons website) and once you click on the image it gives you the information from the scientist highlighted in the picture (below). There are currently ten scientists listed and the list will continue to grow as the team has recently been awarded funds for the expansion of this project. I think this is a great resource for teaching about “Neurohistory” and think it should be widely shared. All of the content can be downloaded through their website. Finally, the creators are open to ideas and collaborations. If interested feel free to contact them through this form or Twitter @neurohistoons. References Van Wyk MM. (2017). The Use of Cartoons as a Teaching Tool to Enhance Student Learning in Economics Education. JSS. 117-130. Shurkin J. (2015). Science and Culture: Cartoons to Better Communicate Science. PNAS. 112 (38): 11741–11742. Alexandra Colón-Rodríguez, Ph.D. Postdoctoral scholar Genome Center University of California Davis Twitter: @alexcr_1
  2. Low-cost neuroanatomy learning tools for visually impaired and blind students Did you know that approximately 1.3 billion people live with some form of vision impairment?[1] Well if you didn’t I don’t feel as bad because this was one of the first things I learned when I visited Giovanne Diniz and Dr. Luciane Sita’s poster on “Development of low-cost tactile neuroanatomy learning tools for blind and visually impaired students”. I always try to stay updated on new tools used for inclusive instruction. That is how I learned about Giovanne and Dr. Sita’s work while attending Theme J posters at the annual meeting. Giovanne Diniz and Dr. Luciane Sita at their poster during SfN’s Annual meeting. Giovanne and Dr. Sita are scientists at the University of Sao Paulo, Brazil. This past year when they started teaching the neuroanatomy course they realized that there was a blind student in their class and the instructional materials were limited to teach this population. Then they began to identify tools to use on their instruction to improve teaching for blind and visually impaired students. Most anatomy courses use illustrations, medical imaging, and cadavers; although there are didactic tools available these are for sighted individuals and most of them are in English. Thus, this team decided to develop a tool to improve the teaching of neuroanatomy concepts using low-cost materials, one that could be accessible and implemented without difficulty. Among the tools they developed for teaching neuroanatomy was a fixed brain specimen which had the gyri covered with different textured fabrics and marked with pins of various sizes. This approach was also used to teach internal structures of the brain which were presented as digitally drawn brain slides. Implementation of their tools increased the engagement of the blind student attending their class. The students’ performance was similar to the sighted peers and this motivated them to increase the repertoire of structures they have developed and to provide this as a blueprint for use of by others with blind or visually impaired students. Using tactile strategies for teaching can be difficult as there are several things to consider including the students’ needs and abilities, and the tasks that will be implemented [2]. The tools developed by Giovanne and Dr. Sita, used to teach neuroanatomy core concepts, are a great strategy for inclusiveness and effective instruction for blind and visually impaired learners. Example of a digitally drawn brain section and the textures used for teaching about specific structures. References World Health Organization. (2018). Blindness and Vision Impairment. Downing JE, Chen D. (2003). Using Tactile Strategies With Students Who Are Blind and Have Severe Disabilities. Teaching Exceptional Children. 36 (2):56-60. Alexandra Colón-Rodríguez, Ph.D. Postdoctoral scholar Genome Center University of California Davis Twitter: alexcr_1
  3. ComSciCon is an organization by and for Grad Students Full disclosure? I'm a total science communication nerd. I’m constantly distracted from research by science twitter (Sorry Ken!) and spend an inordinate amount of time thinking about how scientists can help uniform the public about all the great research going on thanks to their tax dollars. All this to say, I was immediately enamored with the ComSciCon organization. I actually first learned about the organization back in 2016, when I attended one of the satellite workshops in Chicago. I learned about data visualization from a psychologist who literally studies how our brains perceive patterns in data. I heard inspiring stories of getting involved with youtube from Emily Graslie (The Brain Scoop) at the Field Museum. Not only did I listen to panels & talks, but I also got the chance to practice my own skills with ‘pop talks.’ Basically, attendees are given one minute to describe their research for a general audience & get immediate feedback via audience cue cards that are labelled “awesome” or “jargon.” So why am I bringing up a science communication conference I attended several years ago? Well one attendee from ComSciCon’s leadership, Alie Caldwell, presented a poster about the organization and how to get involved! ComSciCon-SfN18 Poster (1).jpg1333×1436 669 KB ComSciCon’s goals are to “empower early career scientists to become leaders in their field, propagating appreciation and understanding of research results to broad and diverse audiences.” The organization accepts 50 applicants each year (out of approximately 1000 applications) to it’s Flagship conference where expert science communicators like Ed Yong from the Atlantic help train young scientists on communication skills that will benefit them both inside and outside of academia. Beyond the Flagship conference, there are also 9 satellite conferences across the US (with potentially a new one starting up in Canada!). Across all the conferences, ComSciCon has trained over 1500 graduate students and postdocs! Of course, the organization is still growing & hoping to find new areas to expand and new sponsors to help fund the work. Want to learn more about getting involved with ComSciCon? You can reach out to the leadership team at info@comscicon.org PS- Seriously though, full disclosure. I am an organizing member of ComSciCon and am leading the program organization committee for the 2019 Flagship Conference. Sadie Witkowski PhD Candidate, Northwestern University
  4. Sadie_Witkowski

    Poster Highlight: We the Scientists

    Scientists get involved in Democracy After the stress of the midterms, I definitely needed a break from political news. After being inundated with polls and stats, I just wanted to know what policies candidates supported and whether those policies were supported by scientific evidence. Too bad I only discovered We the Scientists after I cast my early vote! We the Scientists is a student-led organization from Columbia University. I spoke with Macayla Donegan about what inspired her & her collaborators to start this project. She said they were “inspired by wanting fact and evidence-based policy” but not having an easy way to organize the information that’s out there. To address this gap, Donegan and her fellow graduate students created We the Scientists as a one-stop shop to learn about national representatives from across the United States and whether their positions match up with the science. Using a map, visitors to the site can look up their state representatives and compare the Rep’s voting record to primary source scientific data (with a non-jargony shorthand version also available). The organization is continuing to grow and they also include other useful frameworks for scientists like how to write an OpEd and a Late Night Science program to engage the local public and show them the research their tax dollars support. As for We the Scientist’s next steps, they’re currently chapter-izing to help spread the reach of the program. Donegan mentioned that as grad students, it’s a lot of extra work to run this program as a side project, but they think the best way to expand is through connections with other academics. “We have a pipeline,” Donegan said. “We have some code on how to implement this.” Donegan explained to me that all they need now are some partners who care about understanding scientifically supported policies and engaging in our democracy. You can find We the Scientists at their website as well as on twitter, facebook, and instagram! Sadie Witkowski PhD Candidate
  5. Human Long-Term Memory: Encoding & Retrieval Based on my personal research interests, I was quite excited to attend this nanosymposium on encoding and retrieval in human memory. Although I tell people that I study sleep and memory, the Paller lab is really a memory lab that somehow wandered into the interesting land of memory consolidation during sleep. Most of my training has focused on the memory aspect which continues to fascinate me to this day, so I was excited to see what new insights I could glean from these talks. For better or worse though, I had a lunch that ran late and sadly missed the first two talks of the session. However, I was thrilled to hear the rest of the talks. After staying for the rest of the session, I decided that I have two favorites. The first is “Distinct cortical systems reinstate content and context information during memory search.” This presentation focused on a key element of episodic memory, contextual reinstatement. One of my major complaints with many memory tasks is that they often chose simplistic designs that are easy to test, but don’t match up to real world complexity. I thought the way James Kragel tested memory and then used intracranial recordings to understand the network dynamics of memory reinstatement was a clever way to disentangle semantic and episodic memory. My second favorite, which is perhaps no surprise considering my background, was titled “Sleep consolidates memory through diverging effects on automatic and cognitive emotional responses in children.” Common wisdom has long shown that naps are an important part of a child’s daily routine. But researcher Katharina Zinke wanted to put such traditions to the test. She & her collaborators tested whether sleep compared to wake helped kids (age 8-11 years) consolidate negative pictures over neutral ones. She tested the children after a 10-hour delay of either sleep or wake and found that sleep did indeed lead to better memory consolidation than wake. Moreover, REM sleep theta power correlated with the preference of negative emotional stimuli over neutral images. Although after sleep, the images were rated as less negative than before sleep or after a period of wake. It’s nice to see science upholding the common sense instructions of our parents. Sleep helps children process memories such that they remember the episode with out the intense emotional baggage from the event itself. Sadie Witkowski PhD Candidate
  6. Highlights on the Motor System, Exercise, and Rehabilitation Motor learning is imperative throughout development and during rehabilitation of neural injury. Several strategies to improve motor learning have gained much interest recently including non-invasive brain stimulation and exercise. The voluntary movements symposium featured several researchers examining the neural mechanisms underlying motor learning and ways to improve it. #SfN18 #motor @jasonlneva discussed how #TMS measures reveal there are separate groups of interneurons specialized for sequence motor learning and for skilled motor control. #neurostim #NIBS — Dana&TheMonsters (@DanaSwarbrick) November 4, 2018 Specifically, applying a transcranial magnetic stimulation (TMS) pulse in an anterior to posterior direction uniquely primed sequence-specific motor learning and applying a pulse in the posterior to anterior direction primed those neurons responsible for skilled motor control. #SfN18 @UBC_BrainLab @smpeters9 presented her research that complements @jasonlneva. After 20min moderate exercise: preferential activation of interneurons sensitive to anterior-posterior induced current--the same interneurons specialized for sequence specific learning. #UBC — Dana&TheMonsters (@DanaSwarbrick) November 4, 2018 Previous research has shown that an acute bout of high-intensity as opposed to moderate-intensity exercise results in the greatest enhancements to motor learning. Dr. James Coxon corroborated this using intermittent theta burst stimulation to measure neuroplasticity. Motor nanosymposium #SfN18@coxontweets discusses his research showing there may be a dose-response relationship for the effects of exercise on neuroplasticity where high-intensity is better than moderate. @MoveNeuro #neuro #HIIT #neuroexercise — Dana&TheMonsters (@DanaSwarbrick) November 4, 2018 While research has consistently shown that an acute bout of high-intensity exercise causes increased neuroplasticity and improved motor consolidation, research has also shown that genetics and fitness mediate these effects. Since non-invasive brain stimulation is more effective in women and when estradiol levels are higher, it is possible that the neuroplastic effects of exercise may be similarly moderated by menstrual cycle phase. Super cool research from El-Sayes and @cturco10 showing that contrary to #NIBS menstrual phase has no impact on exercise excitability, but: #Females who release more #BDNF in #exercise showed greater increase in excitability but not #males!!! pic.twitter.com/yfC2IZ4mrr — Dana&TheMonsters (@DanaSwarbrick) November 5, 2018 Exercise is not only useful for motor learning, but also for cognition. A poster presented by Dr. Thomas Tollner explored cognitive processing during aerobic exercise using a cognitive task and an event-related EEG approach. Conditions involving exercise (cycling and treadmill) and conditions involving standing (stationary standing and treadmill) improved visual target processing. Thomas and @GordonDodwell present research showing that standing and #exercise improve visual working #memory and there's a neurophysiological basis for these enhancements! #SfN18 #EEG pic.twitter.com/c2f5sPlXx1 — Dana&TheMonsters (@DanaSwarbrick) November 6, 2018 While much of the research on motor learning has explored the acute effects of exercise, the long-term effects of maintaining an exercise routine are very important. Adam Lundquist explored the time-course and locations of neural morphological changes associated with daily exercise. #SfN18 @lundquistaj @KeckMedUSC working with @gpetzinger presents research showing moderate #exercise causes region- and time-specific changes to #astrocyte morphology and metabolism pic.twitter.com/8gWdqE9gbA — Dana&TheMonsters (@DanaSwarbrick) November 7, 2018 Lundquist goes on to suggest that due to the morphological changes driven by daily exercise, exercise may be an important rehabilitation intervention for people with Parkinson’s disease. Other posters also highlighted the potential for neurotechnology and pharmaceutical interventions to assist in rehabilitation of spinal cord injury and stroke. #SfN18 Dr. Wagner and co. @EPFL presented #research showing #surgical implantation of #electrical array paired with #robotic assistance resulted in immediate #recovery of #walking in #paraplegic patients #SCI #rehab #neurorehab #motor @rehabINK pic.twitter.com/AJknoXOcJJ — Dana&TheMonsters (@DanaSwarbrick) November 12, 2018 Dr. JB Mignardot @EPFL presented #research showing #surgical implantation of lumbar electrical #stimulation array in combination with weight-supported #therapy allowed paraplegic #SCI injured #patients to walk with assistive #devices! #neurorehab #SfN18 pic.twitter.com/ApaddLjw5l — Dana&TheMonsters (@DanaSwarbrick) November 12, 2018 During a symposium on spinal cord injury with a special focus on inhibiting inhibitors, Dr. Martin Schwab discussed the struggles and successes he has encountered in development, financing, and execution of clinical trials. Dr. Martin Schwab discusses his inhibition of an inhibitor: Nogo-A prevents growth of neurites. Anti-Nogo-A antibodies and #rehab lead to complete #recovery in rats with #stroke @rehabINK #SfN18 #neurorehab — Dana&TheMonsters (@DanaSwarbrick) November 5, 2018 I am looking forward to hearing more about Dr. Schwab’s phase II clinical trial, and all of the other incredible progress that will be revealed at next year’s Society for Neuroscience conference! Ta ta for now! Dana Swarbrick
  7. #SfN18 Day 3 Grass Lecture: A Series of Thoughts On Monday, the annual Grass Lecture took place, highlighting the work of a high-profile researcher chosen by SfN from within its own ranks. This year, the speaker was David Tank, who has co-directed the Princeton Neuroscience Institute since 2006. Before going to Princeton, he did research at Bell Labs, helping to develop and advance fMRI techniques. While at Princeton, his work has generally focused on how the brain internally represents and encodes its own experiences. His first studies at Princeton focused primarily on how the brain represents location. In 2009, he and his student Chris Harvey invented the first virtual reality environment for mouse experiments, keeping the mouse in place on a rolling ball while IMAX-style screens surrounding the mouse display images giving the impression of motion along a linear track. Using this technique, they were able to not just observe sequences of place cells firing in the hippocampus, but they achieved enough stability to do the first intracellular identification of a place cell while spiking, which helped show that these were actually cells, and not just small regions with similar activity. A mouse in the virtual reality environment. He did more work for a while expanding this task from a 1-dimensional line in virtual reality to a 2-dimensional environment, but soon he asked an even more interesting question: are these sequences of cells firing specific to location, or is it just one aspect of a more general phenomenon? To find the answer, they allowed mice to experience sound as well as place, playing a series of tones while the mouse navigated an environment. To their surprise, they found that certain cells in the hippocampus fired in sequence to tone as well as location, but the two populations seemed to sample from each other. In other words, the brain used the same method to track multiple modes of information over time: the map was not just spatial, but possibly cognitive. Next, they took this idea one step further and fully decoupled the task from physical location, relying solely on sound. Again, a sequence of tones would play, but the mouse would remain stationary at a lever, and had to push it when the tones reached a certain frequency, all the while recording how their brain cells’ activity changed. They found the same thing here as well: their brain also represented the tone as a sequence of activity across brain cells, just like it would represent a physical sequence in space. Screen Shot 2018-11-07 at 4.14.37 PM.jpg1872×690 155 KB The sound-exclusive sequence task. Interestingly, this general purpose mapping can allow for the reverse to work as well. Sequences in space can actually get reconstructed from neural activity alone in a process known as manifold inference, based on what we know about how these sequences represent the external world. These inferred positions can then be compared to the animal’s real position throughout, and most of the time the two seem pretty similar. However, at certain points the two drift apart. The exact reason for this is unknown, but it may result from our representations coming from both an external and an internal state: when the external state dominates, the two remain similar, but when the internal state predominates, the two could drift apart. In fact, this drift may specifically represent the difference between our internal representation and external reality. The drift seems especially pronounced when mice get predictions wrong, where our external reality does not match how we represent it internally. Further, across many series of many activities, paths gradually diverge from each other as time goes on, but they generally return to the same point in the end. When an error is made, however, the paths do not return to the same point in the end, but the difference becomes even more pronounced instead. Overall, the brain seems to represent experiences as sequences of individual cells firing, regardless of what this experience actually is. This paradigm could provide a key to decoding the numerous mysteries of the brain, like how we observe the world around us or how to tell whether our internal representations are accurate. Such possibilities are immensely promising, and hopefully David Tank will have much more to show us for a long time to come. James Howe @jamesrhowe6
  8. 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
  9. The Stories We Tell I love stories. As long as I can remember, stories have played an integral part in forming my love for science, and my dreams to be a scientist. It was the story about Gregor Mendel, a gardener who became the father of modern genetics. It was Dr. Har Gobind Khorana, the first Indian-born Nobel prize winner in physiology or medicine. It was Ada Lovelace, a technological visionary and the first programmer. Which is why I could not miss the second ever SFN “Telling Stories in Science” minisymposium on Sunday chaired by the incredible Wendy Suzuki! It was an afternoon full of beautiful synchrony between the scientific values we care about and the deeply human ways in which it affects our lives, either good or bad, painful or exhilarating, easy or complex. Here I share a few of the talks and personal stories that resonated deeply with me. Who speaks for Science? Dr. Monica Feliu-Mojer started off the event with aplomb. A passionate scientist and science communicator, Dr. Feliu-Mojer is the Director of Communications and Science Outreach for Ciencia Puerto Rico, as well as the Associate Director of Diversity and Communication Training. In her talk, Dr. Feliu-Mojer reminded us that stories are a powerful way of sharing science and a compelling way to connect with people. But most importantly, she asked the question: Who speaks for science? Which community is being represented? It was a question that surprised me. Not because I didn’t immediately recognize its immense value, but because I had never thought to ask that question myself. Dr. Feliu-Mojer made her stance crystal clear and one I agree with entirely: science has consistently failed to represent minority groups, and consider race as a factor in assessing and interpreting data. Which makes one thing clear: it is integral to connect culture and context with science. In addition, as scientists, we need to ask ourselves how we can leverage our individual privilege to help other communities. Monica.jpg1000×664 346 KB I was blown away by Dr. Feliu-Mojer’s erudite and succinct summaries of the issues that impregnate the scientific field. We have the power to make all voices matter, and this is a call to action with important consequences. Our Brains on Storytelling You know when you have a conversation with someone and it feels effortless? As if there is a seamless exchange of ideas? Dr. Uri Hasson, a professor of psychology and neuroscience at Princeton University studies that very process, which is the neurological basis of human communication and storytelling. His research using fMRI shows the intriguing phenomena that people listening to the same stories show synced or aligned brain activities. The talk was fantastic, and here is his TED talk you can watch! tedtalk.jpg1540×866 79 KB Neural Entrainment. (Courtesy: TED) Personal Stories It is difficult to summarize the personal stories. The emotional effect of these narratives came so much from the speakers’ candor, personality, and courage to share difficult memories, and it almost feels like an injustice to try and surmise them in words. rachel yehuda.jpg1000×1000 100 KB Dr. Rachel Yehuda’s story was a gripping tale about the struggle to find the scientific truth about stress, trauma, and its biological underpinnings while walking the fine line of reducing people’s traumatic experiences to their science alone. To hear her story, check out this Story Collider episode. Jean_Zarate1.jpg1000×671 87.7 KB Dr. Jean Mary Zarate, a Senior Editor at Nature Neuroscience, really pulled at my heartstrings with her deeply personal narrative. She spoke about the battle between following your dreams as a musician while pursuing her career in the sciences. Zarate’s story is many of our stories, and I saw my own fears, concerns, lows, and highs in her. As an Indian Ph.D. student who loves storytelling and has a passion for writing, I too had to find a way to create a synthesis of those two worlds. Zarate spoke with understated passion, and I am ever grateful to her for recollecting this struggle. wendy.jpeg1000×667 75.3 KB Dr. Wendy Suzuki ended the event by telling us a shatteringly beautiful story about her father’s battle with Alzheimer’s disease, her struggle to help while being a memory researcher, and the unending power of love. Overall, the nanosymposium was an unmissable experience and an emotional rollercoaster that reminded me of the very humanness of the scientific practice. For those of you interested in more, here is a paper published by Journal of Neuroscience on storytelling and science with the speakers! Prabarna Ganguly PhD candidate Northeastern University @prabarna
  10. Day 3 Nanosymposium Highlight: Connect-Seq Just after lunch on Tuesday, I watched a nanosymposium talk given by Naresh Hanchate, a postdoc in Linda Buck’s lab at the Fred Hutchinson Cancer Center at the University of Washington in Seattle. There, he presented a new method he developed, which he called Connect-Seq. Connect-Seq visual summary. This method uses a combination of single cell RNA-sequencing and viral tracing to figure out which cells in one part of the brain connect to which cells in another. He was very interested in neurons in the amygdalo-piriform transition area (APir) innervating CRH neurons in the hypothalamus, which control stress hormone release after smelling an innately fearful scent, like trimethylthiazoline, an odor given off by foxes. To figure out the properties of these APir neurons, he specifically infected hypothalamic CRH neurons with a pseudorabies virus, which can actually travel backwards and infect their upstream neurons. Using microfluidic sorting, he was then able to isolate these cells into their own individual wells, and then he could perform RNA sequencing on these isolated single cells. This then allowed him to find the overall gene expression in each cell, creating a complete molecular map of each cell they isolated. This map showed a number of new and interesting things about these upstream cells that were previously unknown. The most interesting, by far, are the range of signaling molecules they use. Each cell does not simply express one neurotransmitter gene, as expected, but instead a wide range of different signaling molecules. These signaling molecules are not just GABA, glutamate, or the traditional neuromodulators like serotonin and dopamine. Instead, they include compounds like CART, vasopressin, adrenomedullin, and other obscure, poorly studied proteins. The implications of these results could be further-reaching than they may appear. Release of stress hormones may be less controlled by traditional signals from upstream neurons, but instead could result from less familiar methods that could provide fertile ground for future research, and could allow for a far richer understanding of both the intrinsic dynamics of stress and how we respond. James Howe @jamesrhowe6
  11. The Age of New Stats in Neuroscience You have heard this once. You have heard this twice. Many scientific disciplines including psychology and neuroscience are undergoing a reproducibility crisis. A critical number of social science experiments published between 2010 and 2015 in prestigious peer-reviewed journals such as Science and Nature have failed replicability [1]. A number of neuroscience-related research have also shown the same trend [2]. This is a major challenge for scientists and publishers alike because “good” science is heralded by its ability to conform to three major conditions: I. Repeatability: can the same lab using the same experimental setup obtain the same results? II. Replicability: can a different lab using the same experimental setup obtain the same results? III. Reproducibility: can a different team using a different experimental setup obtain the same results? To get a better idea of what neuroscientists are thinking as possible solutions to this challenge, I went to the Professional Development Workshop called “Improving your science: Better inference, Reproducible Analyses, and the new Publication Landscape,” and all I can say is that it has been a religious experience. The panel included Robert Calin-Jageman, Christophe Bernard, Brian Wandell, and Marina Picciotto. Here are some of the critical takeaways: The need to publish negative results “Statistical significance is the least interesting thing about the results” (Gene Glass, 2004) Confirmation bias and publication bias are common issues in scientific publications because authors are more likely to submit, and publishers are more likely to accept, papers that show positive, rather than negative or inconclusive results. This MUST change. If we do not allow negative data to be published, then a vast majority of researchers could potentially end up running experiments that have already yielded null effects. ENeuro is trying to start this trend, and it will maintain rigorous expectations of such manuscripts as well. These include multiple experimental procedures to test the hypotheses, rigorous reproduction of experimental models of other labs that you claim to refute, as well as the meticulous use of positive and negative controls. Use effect sizes and confidence intervals for better inference “Hodgkin and Huxley did not p all over their manuscripts” Robert Calin Jageman(SFN 2018) In science, there are currently two main approaches to statistics: the testing approach and the estimation approach. Most of us are quite familiar with the testing approach; this is the one associated with the nefarious p-value. In this setup we ask the qualitative question “does X have an effect on Y?” and use a p-value or a Bayes factor to generate a definitive answer. Replication is rare in the testing approach. Contrarily, the estimation approach is quantitative in nature and asks the question, “how much of an effect does X have on Y?” This is a much more reliable way of understanding and utilizing data because the estimation approach focuses on uncertainty and practical significance and encourages repeatability and replication of studies. So instead of a p-value, we would generate an effect size (the magnitude of difference between two groups) and a confidence interval (estimated range of values that is likely to include the unknown population parameter) This way scientists can also perform meta-analyses to combine results from multiple studies and identify the overall magnitude of the effect size. I came out of this workshop repeating the slogan “DON’T TEST, ESTIMATE,” iterated by Dr. Robert Calin-Jagerman, and being completely sold on the idea. As scientists, we want to do the best research and more importantly, recognize the value of our data in ways that do not jeopardize the work done, but at the same time also informs the extent of its utility in an honest manner. Thus, as journals such as Journal of Neuroscience begin to reformulate the expected statistics from our work (as intensively explained by Dr. Marina Picciotto), this workshop reveals the speedy trend scientists themselves are following towards correcting biased statistical practices and entering a space of open-access and revealing science. I for one, am extremely grateful for this road less travelled. [1] Camerer, C. F. et al. Evaluating the replicability of social science experiments in Nature and Science between 2010 and 2015. Nature Human Behaviour 2, 637–644 (2018). [2] Gilmore, R. O., Diaz, M. T., Wyble, B. A. & Yarkoni, T. Progress toward openness, transparency, and reproducibility in cognitive neuroscience. Ann. N. Y. Acad. Sci. 1396, 5–18 (2017). Prabarna Ganguly Twitter: @prabarna
  12. Animal models of neurodevelopmental disorders Using animal models of neurodevelopmental diseases is a cornerstone of the way we as neuroscientists are able to pin down mechanisms by which disease pathologies arise. Thus, I was thrilled to listen to the excellent talks given at the “Animal models of neurodevelopmental disease” nanosymposium on Sunday morning. Chaired by Melissa Bauman and co-chaired by Debra Bangasser, the talks spanned across a variety of disease models. Below I highlight two talks in particular! Zika virus: neurodegeneration in the brain and spinal cord of mouse CNS Zika virus is a human teratogen that has resulted in one of the most critical emergency responses tackled by the CDC. Pregnant women with the infection have a high risk of fetal abnormalities called Congenital Zika Syndrome. Some of the symptoms of this condition include microcephaly, calcifications, reduced spinal cord volume, epileptic seizures, and hemorrhage of the parenchyma. But what are the neuropathological consequences of Zika infection? Kevin Noguchi and his colleagues from Washington University at St. Louis investigated this question using a mouse model. In the study, neonatal mouse pups were inoculated with Zika virus and sacrificed two weeks later, revealing various neuropathologies similar to those seen in human offsprings. Using histological techniques, Noguchi found two main types of neurodegeneration: excitotoxicity and apoptosis. Excitotoxicity related neurodegeneration was observed in multiple brain regions including the cerebellum, cortex, hippocampus, and the striatum. Similarly, apoptotic degeneration was also observed in these regions, although to a lesser extent. In addition, apoptotic activity was seen in the funicular as well as focal degeneration in the axons within the corticospinal tract. fx1_lrg.jpg996×996 195 KB Fig 1. Placental pathology in Zika-infected dams is associated with severe pathology in the fetus [1] It was previously known that the Zika virus affects neural progenitor cells, which are naturally eliminated over time. These outcomes indicate persistent overstimulation after Zika infection and are valuable because they suggest that the devastating consequences of the viral infection persist far along the gestational period. Such intensive effort across the global scientific community will hopefully result in rapid development, characterization, and use of animal models for the study of Zika virus biology and effects. "Skinny" and “Branchy”: Altered dendritic morphology in the dlPFC after maternal immune activation Scientific research within the last decade has provided evidence to suggest that maternal infection during pregnancy increases the risk for formation of psychiatric disorders in the child. For example, pregnant women with gestational exposure to influenza, other infections, and elevated levels of specific pro-inflammatory cytokines are associated with an increased risk of their child forming schizophrenia later in life. Animal models have established that the maternal immune response could be the key link between maternal infection and alterations in fetal brain development. Nevertheless, much of the mechanism by which this occurs remains unknown. Dr. Cynthia Schumann (happy birthday!) from the UC Davis MIND Institute gave an excellent talk titled “Altered dendritic morphology in the dorsolateral prefrontal cortex of non-human primates prenatally exposed to maternal immune activation,” in the the nanosymposium on animal models of neurodevelopmental disease, elucidating some of the plausible ways by which maternal immune activation (MIA) could cause the deleterious effects on the growing fetus. The main aim of the study was to test the hypothesis that the development of neurodevelopmental disorders such as schizophrenia is originated by dysregulation of immune molecules, which play a pivotal role in brain development. Indeed, nonhuman primates exposed to MIA display aberrant behavioral phenotypes including self -directed behaviors and stereotypies Reduced affiliative vocalizations Inappropriate social interactions Non-attendance to salient social cues Furthermore, Schumann and her colleagues postulated that such changes can alter structural and functional connectivity, ultimately leading to disturbances in cognition, perception, and emotion. To perform this, pregnant rhesus monkeys were randomly assigned to receive saline control injections or viral mimic polyI:C for multiple days at the end of the first trimester and blood was drawn for interleukin-6 (IL-6) analysis. The dorsolateral prefrontal cortex (dlPFC) was selected as the area of interest due to preliminary evidence of neuropathology in the region. Neurons were stained with the Golgi-Cox method to measure dendritic morphology in nonhuman primate dlPFC. Fig 2. (left) Golgi-cox method labeled layer III pyramidal neurons, (right) overlaid 3-D reconstruction of dendritic arbors. Apical dendrite (yellow), basal dendrites (green, orange and red), axon (white) and spines (blue). In the pilot cohort (n=4) Schumann and others found that 4-year old rhesus monkey offsprings exposed to MIA display altered biological development. Specifically, there was an increase in the number of oblique dendrites and decreased apical dendrite diameter in the dlPFC, aka “skinny” and “branchy” phenotype. The team found no changes in dlPFC spine density. Apart from being a great talk, this is a promising research front that suggests that MIA could be a disease primer that impacts prenatal development and may induce susceptibility to formation of particular neurodevelopmental disease types. [1] Martinot, A. J. et al. Fetal Neuropathology in Zika Virus-Infected Pregnant Female Rhesus Monkeys. Cell 173, 1111-1122.e10 (2018). [2] Weir, R. K. et al. Preliminary evidence of neuropathology in nonhuman primates prenatally exposed to maternal immune activation. Brain Behav. Immun. 48, 139–146 (2015). Prabarna Ganguly PhD Candidate Northeastern University @prabarna
  13. Day 2 Keynote: The Underlying Basis of Parenting and Socialization Sunday's events finally finished with a keynote lecture from Catherine Dulac, a distinguished professor and former chair of Molecular and Cellular Biology at Harvard. Before becoming a professor, she studied pheromones at Columbia under Richard Axel (who advised my mentor as well). At Harvard, she has spent most of her career studying two topics that naturally dovetail with pheromones: social interaction and sex-specific behavior. I can hardly recount all the topics she covered in their true depth and breadth, and summarizing them while doing them justice is near-impossible. However, I can give the most important takeaways from her most impactful work over the years, which I will try (and likely fail) to do below. First, the vomeronasal organ (VNO) controls sex-specific behavior in mice. The VNO is a specialized structure in mice that allows them to smell pheromones, which animals emit as reproductive and social signals: for example, a female in heat attracts males by giving off specific pheromones, making them aware of their reproductive availability. These perceptions are dependent on one gene, TRP2, and its absence causes both males and females to lose their sex-specific behavior. Males will try to court and mate with other males, and females will attempt to mount other females. dwlogan_php6pJii4.jpg1600×1200 The vomeronasal organ. However, females will also stop lactating and lose their ability to care for their children, instead opting to kill their children, something males tend to do instead. This leads to another important insight. While males can only perform male-specific behaviors, females can do both. The vomeronasal organ ensures they act like females, but without it, they fall back on male behaviors. Second, actual control is exerted in the brain using just a few hormones. A hormone called oxytocin is required for females to prefer male mates, even if the vomeronasal organ works: if oxytocin signaling is lost, females lose their preference for males, no matter what. Further, if oxytocin signaling is manipulated in males, their mate choices change as well. Sexual and mating behavior also depends on LHRH, a hormone controlling the reproductive system. When LHRH activity changes, so does mating behavior as well. Third and finally, these functions can be localized to a few regions of the brain. Later research clarified that oxytocin is required in the medial amygdala for these effects, not the entire brain. All of the required hormones were also released from the hypothalamus: an understanding of the hypothalamus could then allow understanding of these behaviors as well. Screen Shot 2018-11-05 at 3.30.07 PM.jpg1850×1392 1.46 MB A map of the median preoptic hypothalamus using MERFISH. As a result, she has most recently been studying the molecular and spatial composition of the hypothalamus. Using single cell RNA-sequencing, her lab was able to identify all of the major cell types in the median preoptic hypothalamus, which controls the release of many different hormones. They then used MERFISH, a massively multiplexed RNA detection method, to look at these cells spatially. Through these methods, they were able to produce this complete map of this part of the hypothalamus. Over the course of Dulac’s career, she has contributed so much to neuroscience, in behavior, anatomy, and molecular biology. Her lecture serves to make this more salient than ever, while communicating these key findings in one of the most effective manners I have ever seen. James Howe @jamesrhowe6
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    Annual Meeting Tip & Tricks

    Welcome to the discussion thread for Annual Meeting Tip & Tricks. Are you attending Neuroscience 2018? How do you schedule your time to avoid burnout? What are the best networking strategies? Share your best advice below for getting the most out of SfN’s annual meeting.
  15. Join the #SfN18 Live Chat | October 17th at 12:00 p.m. EDT If you are unable to log in to post a question, please submit your questions to neuronline@sfn.org and we will post them in the thread. Whether you are an annual meeting veteran or you are attending for the first time, proper planning is key to a successful experience. From new Dual Perspectives and classic symposia to professional development workshops and on-site interviews at the NeuroJobs Career Center, this live chat will highlight the diverse learning and networking opportunities at Neuroscience 2018 On October 17th from 12-1 p.m. EDT, facilitators will discuss tips on: Navigating different types of events and meetings Making use of virtual and on-site resources Taking advantage of professional development and networking opportunities Planning your time at the meeting effectively Participants are encouraged to submit questions in advance of the live chat in the discussion thread below. You are also welcome to direct your questions to specific facilitators by tagging their usernames:@mfwells @caltimus1. Facilitators: Cara Altimus, PhD Cara Altimus is an Associate Director at The Milken Institute, Center for Strategic Philanthropy. She previously was a Staff Fellow at the Center for Devices and Radiological Health, FDA. Altimus currently uses her expertise in neuroscience to advise individuals and foundations seeking to make philanthropic investments in neurodegenerative disease and mental health. She received her undergraduate degree in genetics from the University of Georgia and her PhD in biology from the Johns Hopkins University. She completed her postdoctoral training at Johns Hopkins School of Medicine, Department of Neuroscience. image.jpg635×609 109 KB Michael F. Wells, PhD Michael F. Wells is a postdoctoral fellow at Harvard University and the Broad Institute. He previously was a graduate student at Duke University and MIT in the laboratory of Guoping Feng. Wells’ main research interests lie in stem cell models of neurodevelopmental disorders and Zika virus neuropathogenesis. He received his undergraduate degree in Biological Sciences from the University of Notre Dame and his PhD in Neurobiology from Duke University. Wells is currently a SfN Trainee Advisory Committee member and recently co-founded the Wishart Group, a mental health advocacy non-profit organization led by Passion Pit frontman Michael Angelakos. If you are unable to log in to post a question, please submit your questions to neuronline@sfn.org and we will post them in the thread. Annual Meeting Resources: Sample trainee agenda: http://neuronline.sfn.org/Articles/Professional-Development/2017/How-to-Plan-for-SfNs-Annual-Meeting-as-a-Trainee Neuronline Annual Meeting Collection: http://neuronline.sfn.org/Collections/Advice-for-SfNs-Annual-Meeting Itinerary Planner and Mobile App: https://www.sfn.org/Meetings/Neuroscience-2018/General-Information/Itinerary-Planner-and-Mobile-App Resources for trainee meeting attendees: https://community.sfn.org/t/annual-meeting-resource-for-trainees/8059 Neuroscience Meeting Planner: https://www.sfn.org/Meetings/Neuroscience-2018/General-Information/Itinerary-Planner-and-Mobile-App At the Meeting section on SfN Website: https://www.sfn.org/Meetings/Neuroscience-2018/At-the-Meeting
  16. Neuroscience 2018 Annual Meeting Forum Planning for the Annual Meeting? Post in this category to share information and ask questions about Neuroscience 2018, which will be held on November 3-7 in San Diego, CA. We encourage you to share your experiences from past annual meetings and tips for success here. You can also promote educational or social opportunities you know about or are hosting so that others attending the meeting can join. New to Neuronline? Review the illustrated guide to posting in the Neuronline Community and our community guidelines before you post. See you in San Diego! Post your thoughts in the Neuroscience 2018 Forum now.
  17. aabdullah

    Abstract Submission Live Chat

    Join the Abstract Submission Live Chat | Wednesday, April 18, 2-3 p.m. EDT Do you have any burning questions about submitting an abstract for Neuroscience 2018? Join us on April 18 for an online discussion on Neuronline with Kang Shen, Chair of the Program Committee, and Ellen Lumpkin, Theme D Chair of the Program Committee. Don’t miss your chance to chat directly with abstract reviewers! Participants are encouraged to submit questions in advance of the live chat in the discussion thread below. Related Resources: https://community.sfn.org/t/about-the-abstract-topic-matching-forum-category/279 Submit abstracts at http://www.sfn.org/cfa Facilitators image.jpg2010×2514 853 KB Kang Shen, PhD Kang Shen is a professor of neuronal cell biology in the department of biology at Stanford University. He is also an investigator in the Howard Hughes Medical Institute. Kang’s research focuses on the dendrite morphogenesis, neuronal polarization and synapse formation. He earned his Bachelor of Medicine degree from Tongji Medical University from China, his Ph. D. degree from Duke University and completed postdoctoral training from the University of California San Francisco. image.jpg960×1185 224 KB Ellen A Lumpkin, PhD Ellen A. Lumpkin is an associate professor of physiology & cellular biophysics and of somatosensory biology (in dermatology) at Columbia University. She is also Co-Director of the Thompson Family Foundation Initiative in Chemotherapy-Induced Peripheral Neuropathy & Sensory Neuroscience. She previously was a Sandler Fellow in the department of physiology at UC San Francisco and an assistant professor of neuroscience, physiology & molecular biophysics, and molecular & human genetics at Baylor College of Medicine. Lumpkin’s research focuses on genes, cells and neural signals that give rise to skin sensations such as touch, pain and itch. Dr. Lumpkin earned her BS in Animal Science from Texas Tech University and performed her PhD training at UT Southwestern Medical Center and The Rockefeller University. She completed her postdoctoral training at the University of Washington.
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