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  1. 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
  2. 18555968_10154641381361527_2346768722613592822_n.jpg960×960 170 KB Hello everyone! My name is Prabarna Ganguly and I am a Behavioral Neuroscience PhD candidate at Northeastern University in Boston. I study the effects of early life stress on neuroinflammation and its associated effects on adolescent drug-addiction behavior. If you want to learn more about how stress can induce vulnerability to addiction, come see me and my poster (499.19) on Tuesday, Nov 6 between 10-12pm! This year I am excited to cover all the exciting work being done in the field of development and cognition. Specifically, I will be highlighting research on stem cells and reprogramming, autism, as well as human cognition and behavior. Cheers and looking forward to making great SFN connections in sunny San Diego! Prabarna Ganguly PhD Candidate Brenhouse Lab Northeastern University Neuronline: @ganguly_p Twitter: @prabarna Website: prabarnaganguly.com Email: prabarna@gmail.com
  3. The Wide Applicability of Stem Cells What a stem cell novice can pick up in only a few lectures I have a confession to make. I’m not what most people would consider to be a typical neuroscientist. My BS is in Chemistry and I’m actually in the Toxicology department at the University of Maryland, Baltimore. My research is based in neurotoxicology and I have taken neuroscience courses to better understand the brain but before graduate school I was completely uninitiated with anything neuro. Therefore, I have taken it upon myself to attend symposiums here at SfN 2017 on topics about which I know very little, to try and expand my neuroscience base. I started with stem cells. Photo courtesy of med.stanford.edu First, advantages of stem cells quickly became obvious. You can transplant human organoids into other animal models. Often these cells can last a really long time (in some instances over a year!) The implantations will send axonal projections throughout the host brain (successful graft/host connectivity) Incredibly malleable, you can grow almost any neuronal subtype you want Can grow cells from human subjects with diseases to study and understand how those diseases arise during differentiation/development Can provide a model for disease that do not have representative animal models (such as Leigh Syndrome, a pediatric neurological mitochondria disorder) Can use CRISPR/Cas9 to induce different disease states (if the genetic causes/underpinnings are known) All of these points show an exciting future for stem cell research, but what surprised me the most was the ability to co-culture induced pluripotent stem cell (iPSC) derived motor neurons and skeletal muscle cells to create a functioning neuromuscular junction. Advances of this nature are building blocks for the future of all medical research. If we are truly working to limit animal-use (a topic for a completely different discussion), then these studies may give us a glimpse into that very-distant future. Talking with others around the conference there have been some skeptics around stem cells, mostly because we are in the infancy of that research. I would argue, however, that with anything related to the field of medicine you absolutely have to start somewhere. Even if issues may arise moving forward, particularly with the specificity in differentiation, we cannot understand and improve on those issues without pushing forward. More information on stem cells is still ahead of us at this conference! The prestigious “14th Annual Christopher Reeve Hot Topics in Stem Cell Biology Evening of Data Blitzes” is TOMORROW NIGHT from 6.30p to 9.20p in Room 146 of the Washington Convention Center! Eleven speakers from around the field will discuss their latest work regarding stem cell biology. You do not have to register as it is an open event, so do not panic if you felt you missed out on these earlier symposiums! You can see a bigger description, as well as the full list of satellite events for the year, here. Eric Lumsden
  4. 20150923-ADV-torrey_truszkowski-0E3A0083.jpg1919×2879 2.62 MB My name is Torrey Truszkowski and I’ll be blogging about themes A (development) and D (sensory systems) as well as anything else that strikes my fancy. I’ll likely post about navigating the meeting for newbies, professional development workshops and more. I’m a graduate student at Brown University working to understand multisensory integration in the lab of Carlos Aizenman. I am planning to transition to full time science communication after graduating. Find me online: torreysci.com - my website and personal blog @TorreyTruszko on Twitter @salmont3 on Neuronline Find me at the meeting: Leading the workshop “A Practical Guide to Science Communication” on Sunday, Nov 12, noon-2pm. Presenting a Dynamic Poster on Wednesday afternoon (located at DP06). “Network properties of multisensory integration in the developing optic tectum” Check out this brief TED-style introduction to my research:
  5. eric.lumsden

    Eric Lumsden, SfN 2017 Blogger

    Hello, my name is Eric Lumsden and I am one of the 2017 Society for Neuroscience Bloggers. I am a graduate student at the University of Maryland School of Medicine studying under Dr. Edson Albuquerque. My research focuses on how prenatal exposure to organophosphorus pesticides affects synaptic activity in the hippocampus and how that relates to learning and memory deficits in those exposed. Due to these interests I will primarily be posting on two subjects: Neural Excitability, Synapses and Glia (B) Development (A). I also plan to keep a running journal detailing my experiences as a first time attendee of SfN. Outside of the lab I am very interested in science policy and communications. You can read some of my previous work at the UMB student blog as well as my personal Medium account. I will also be live tweeting SfN so you can follow my twitter account (@lumsden_eric) for live updates! You can also find me on LinkedIn. If you see me walking around feel free to say hello! I’m excited to meet many new and exciting scientists at the event this year! Eric Lumsden eric.lumsden@umaryland.edu University of Maryland, Baltimore
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