2023/24 Neuroscience Research Colloquium Schedule

FALL 2023

SEPTEMBER 8

  • Host: Anne-Sophie Sack
  • Speaker: Dr. Linda Overstreet-Wadiche, University of Alabama at Birmingham
  • Title: Adult-born neurons in the hippocampal network
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The adult dentate gyrus continually produces new neurons that integrate into the hippocampal circuit. Adult-born neurons transiently exhibit distinct cellular properties that distinguish them from the larger population of mature neurons, and these properties are thought to underlie the vital role of neurogenesis in hippocampal behaviors. I will review the developmental trajectory of adult-born neuron cellular properties and present new data focused on cellular mechanisms of “critical periods” for plasticity and information processing. The results support the idea that neurogenesis provides a substrate for experience-dependent circuit plasticity and memory precision.

SEPTEMBER 15

  • Host: Dr. Ipek Oruc
  • Speaker: Dr. Maya Koronyo, Cedars-Sinai
  • Title: Retinal manifestations of Alzheimer’s disease
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The neural retina is a key organ for vision and visual processing. As a direct extension of the brain, it emerges as a prominent site impacted by Alzheimer’s disease (AD).  The retina is the only CNS tissue not shielded by bone that can be easily accessible for noninvasive, affordable, ultra-high-resolution imaging in the clinical setting. Data from recent years strongly suggest it can serve as a window to assess AD. Early studies described retinal nerve fiber layer and ganglion cell degeneration. Our team revealed the accumulation of core AD hallmarks—amyloid β-protein (Aβ) plaques and neurofibrillary tangles—in the retina of AD and mild cognitive impairment (MCI) patients. Subsequent studies confirmed these findings, and further reported visual and electroretinography abnormalities, retinal tauopathy, Aβ oligomers, inflammation, and cell-specific degeneration in AD patients. Data from our group and others suggest that the brain and retina follow a similar trajectory during AD progression, potentially due to their shared embryonic origin and anatomical proximity. Moreover, retinal vascular irregularities—vessel density and fractal dimensions, blood flow, foveal avascular zone, curvature tortuosity, arteriole-to-venule ratio—are present in AD patients, including early-stage cases. A tight association between cerebral and retinal vasculopathy to cognitive deficits was reported in AD patients and animal models. More recently, we identified early and progressive retinal vascular platelet-derived growth factor receptor-β (PDGFRβ) deficiency and pericyte loss, as well as retinal endothelial tight junction losses in MCI and AD patients. These retinal vasculopathies strongly link to vascular amyloid accumulation as well as could predict the severity of cerebral amyloid angiopathy. Currently, we explore the complex landscape of Alzheimer’s in the retina, including AD-related molecular signatures and processes, new forms of proteinopathies, vascular and inflammatory abnormalities, synaptic loss, as well as cell-specific vulnerability and resilience. Establishing how early retinal biomarkers can be detected during AD continuum and what do they mean for brain pathology and functional decline, should guide the development of future retinal imaging technologies to improve early, noninvasive AD diagnosis and monitoring.

SEPTEMBER 22 

  • Host: Melanie Lysenko-Martin
  • Speaker: Dr. Jibran Khokhar, Western University
  • Title: Cannabis and the Vulnerable Brain: A Closer Look at Genetics, Adolescence, and Edible Overdose
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Dr. Khokhar will talk about the behavioural and neural correlates of various types of vulnerabilities to cannabis, starting from genetic risk for cannabis use, to vaping in adolescence, to the recent increases in edible overdoses in children and pets.

SEPTEMBER 29

  • Host: Dr. Doug Altshuler
  • Speaker: Dr. Richard Mooney, Duke University, North Carolina
  • Title: From song to synapse
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Vocalizations are an essential medium for social and sexual signaling in mammals and birds.  Whereas most animals only produce innate vocalizations, songbirds learn to sing in a process with many parallels to human speech learning. I will discuss recent advances from our lab highlighting the neural mechanisms that enable birdsong learning, including basal ganglia-dependent vocal exploration and reinforcement. How the learned song is integrated with innate vocalizations will also be considered, with reference to recent studies that genetically map neural circuits for innate vocalizations in mice.

OCTOBER 6

  • Host: Dr. Michael Kobor
  • Speaker: Dr. Julia Schulze-Hentrich, Saarland University, Germany
  • Title: At the nexus of genes, aging and environment: Understanding transcriptomic and epigenomic regulation in health and disease
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The DNA of every cell in our body contains the genes inherited from our parents and plays a crucial role in health and disease. While changes in the DNA itself are linked to monogenic diseases, they often fail to explain complex disorders such as neurodegenerative diseases. This can potentially be explained by additional layers of gene regulation known to be stored “above” the DNA, at the epigenetic level. Over the last years, this relatively young research field has shown that molecular structures packaging DNA in the cell nucleus influence gene activity. The DNA itself as well as its packaging structure, the so-called chromatin, can be chemically modified in many ways and is highly dynamic. With these findings, chromatin appears to be a central interface between genes and the environment, and the development and progression of diseases could be decisively influenced by epigenetic changes. Our research group investigates which epigenetic modifications are associated with complex neurological diseases – in particular Parkinson’s and Huntington’s – and how environmental factors and aging have modulating effects on them. Here, I will give an overview of current projects and highlight key findings of our work.

OCTOBER 13

  • Host: Dr. Mark Cembrowski
  • Speaker: Dr. Denise Cai, Icahn School of Medicine at Mount Sinai
  • Title: The brain in motion: stability and flexibility of memory engrams across time and experience
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Creating stable memories is critical for survival. An animal relies on past learning to navigate its environment, avoid dangerous situations, and find needed resources. Because the environment is dynamic, stable memories must be updated with new information to enable responses to changing threats (a specific danger) and rewards (such as food and water). The brain circuits involved in memory and learning require both stability and flexibility. Using in vivo calcium imaging and chemogenetics, we demonstrate how new information is updated with past memories through co-reactivation of memory ensembles during offline periods including sleep.

OCTOBER 20

  • Host: Drs. Daniela Palombo and Rebecca Todd
  • Speaker: Dr. Randy McIntosh, Simon Fraser University
  • Title: Hidden Repertoires in Cognitive Function and Dysfunction
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A hidden repertoire is a functional configuration in the brain that supports behaviour but is seldom used. As a complex system, the brain can show a broad range of configurations for the same function. This “many-to-one” property imparts our brain with resilience during normal operations but also in the face of adverse events, such as damage or disease. I will cover the evidence for these repertoires and cover strategies for investigation, and the implication for the I will also relate the existence of such repertoires to variations in the qualia of our experience.

OCTOBER 27 – THIS TALK HAS BEEN CANCELLED

  • Host: Dr. Jeremy Seamans
  • Speaker: Dr. Alla Karpova, Janelia Research Campus
  • Title: Encoding of Structured Knowledge in Anterior Cingulate Cortex
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One of the most interesting, and mysterious, aspects of biological brains is that they form representations of environments that are richer than an interlinked series of associations, and more ‘conceptual’ than partitions in a multidimensional representation of the sensory input. Our best intuition about how this happens is that brains have evolved to pick up on, and exploit, the ubiquity of structure in the natural world and in the types of tasks that animals might have to solve over their life span, efficiently forming structured relational models of the animal’s world that can be used for planning and action. But even with that intuition, we know little about how structured knowledge is acquired or updated, especially when the extraction of the relevant structure must happen incidentally, without explicit instruction or feedback. We describe an experimental framework using rat as a model system, where the relationship between the incidentally acquired structured knowledge and the neural activity is strong enough that we can begin to decode it with confidence on single trials. Going forward, this puts us in a position to probe how structured knowledge about the world is acquired by the brain, and how it is updated with experience.

NOVEMBER 3

  • Host: Dr. Doug Altshuler
  • Speaker: Dr. Douglas Wylie, University of Alberta
  • Title: Cerebellar Control of Flight in Birds: Easy as 1, 2, 3
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The cerebellum contains the majority of neurons in the brain and has been implicated with many aspects of motor control. In birds this includes the control of flight. In this talk, by synthesizing behavioral, neurophysiological, neuroanatomical and paleontological data I will emphasize three points: (i) the expansion of the cerebellum in birds is associated with the evolution of powered flight; (ii) retinal-recipient nuclei that analyze optic flow are critical for controlling flight; and (iii) three different visuomotor areas of the cerebellum are involved in controlling different aspects of flight.

NOVEMBER 17

  • Host: Dr. Lynn Raymond
  • Speaker: Dr. Rosemary Bagot, McGill University
  • Title: At the intersection of threat and reward in nucleus accumbens glutamatergic afferents.
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The nucleus accumbens integrates diverse inputs, balancing threat and reward to orchestrate motivated behaviour. Glutamatergic projections from the ventral hippocampus and medial prefrontal cortex converge in the accumbens medial shell and are implicated in reward processing as well as adaptation to chronic stress. How these pathways integrate aversive or appetitive events to modulate behaviour is not fully understood and largely unstudied in females, despite known sex-differences in stress-related psychopathologies. I will present new data using pathway-specific in vivo fibre-photometry and chemogenetic silencing to uncover how these projections encode aversive experiences to shape behavioural responding to threat and integrate information about the outcome of actions to shape learning about reward.

NOVEMBER 24

  • Host: Dr. Jason Snyder
  • Speaker: Dr. Irene Vavasour, UBC
  • Title: Diving into neuroimaging research with FINS
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The Fipke Integrated Neuroimaging Suite (FINS) hosts state-of-the-art neuroimaging equipment including a 3T Philips MRI scanner and a 3T GE PET/MR scanner. Our translational research includes developing better imaging tools for disorders such as multiple sclerosis, Parkinson’s, Alzheimer’s, stroke, traumatic brain injury and mental health, as well as healthy aging. This presentation will discuss many of our novel imaging techniques, including myelin water imaging, how and why they are used and what up and coming developments are available.

DECEMBER 1

  • Host: Dr. Lynn Raymond
  • Speaker: Dr. Mark Bevan, Northwestern University
  • Title: Dysregulation and rescue of subthalamic nucleus locomotor function in Huntington’s disease mice
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In this seminar I will focus on our recent studies on the role of the subthalamic nucleus in motor control and its dysregulation in movement disorders.  We found that 1) subthalamic locomotor encoding and gait are highly dysregulated in Q175 Huntington’s disease (HD) mice 2) analogous gait deficits could be generated in wild type mice through optogenetic manipulation of subthalamic activity 3) subthalamic locomotor encoding and gait could be rescued in HD mice through suppression of subthalamic mutant huntingtin expression. Together, these findings argue that subthalamic activity normally optimizes movement, whereas dysregulated subthalamic activity contributes to gait deficits in HD and is a potential target for therapeutic intervention.

DECEMBER 8

  • Host: Dr. Tim Murphy
  • Speaker: Dr. Adrienne Fairhall, University of Washington
  • Title: Cognitive rule-switching in macaques.
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What is the neural basis of abstraction? Working in collaboration with experimental groups who have trained monkeys and humans on a decision task, we analyze how subjects make use of visual information and feedback to infer a hidden rule, where the rule switches in an uncued fashion. We fit a suite of behavioral models and learn that while humans are close to optimal Bayesian agents, monkey behavior is better fit as reinforcement learning, with a novel additional factor included. We use this behavioral model to elucidate structure in neural activity recorded from 200 sites across the brain, finding low-dimensional and dynamic representations of stimulus, feedback and  reward prediction error that support the notion of internal states captured by the behavioral model.

TERM 2

(WINTER 2024)

JANUARY 12

  • Host: Dr. Stan Floresco
  • Speaker: Dr. Joshua Berke, University of California, San Francisco
  • Title: Time, Space and Dopamine
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Dopamine is famously involved in reward, but exactly how continues to be the subject of debate. Two key functions include signaling reward expectations to promote motivated, effortful work, and signaling errors in reward expectation to promote learning. I will present new studies from my laboratory examining each of these processes. We combine recent technological advances for measuring dopamine with novel behavioral tasks, to probe how animals compute reward expectations over multiple temporal and spatial scales.

JANUARY 19 – THIS TALK HAS BEEN CANCELLED AND HAS BEEN RESCHEDULED TO MAY 31

  • Host: Dr. Jason Snyder
  • Speaker: Dr. Khaled Abdelrahman, UBC
  • Title: Decoding the Intricacies of GPCR Signaling in neurodegenerative diseases
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Our research focuses on the intricate role of specific G protein-coupled receptors (GPCRs) in the pathophysiology of neurodegenerative diseases. A key aspect of our focus is unraveling the sex-specific regulation of GPCR signaling in these conditions. Through exploring these intricacies, we aim to illuminate novel therapeutic avenues and enhance our understanding of the complex interplay between GPCRs and neurodegeneration.

JANUARY 26

  • Host: Dr. Jason Snyder
  • Speaker: UBC Kickstart Updates
  • Speakers:
  • Dr. Anthony Phillips : Assessment of novel drugs for attenuation of opiod withdrawal-induced hyperalgesia
  • Dr. Kamyar Keramatian: Evaluation of a novel psychoeducational intervention for individuals at high risk for bipolar disorder: a feasibility study.
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FEBRUARY 2

  • Host: Dr. Jason Snyder
  • Speaker: UBC Kickstart Updates
  • Speakers:
  • Dr. Daniela Palombo: Neural Correlates of Emotional Memory: Basic Findings and Implications for PTSD.
  • Dr. Catharine Winstanley: Applying metabolomics to explore origins of sex differences in risk-taking caused by D2/3 agonists.
  • Dr. Ipek Oruc: Automated detection of Alzheimer’s Disease from retinal fundus images using deep learning.
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FEBRUARY 9

  • Host: Dr. Christian Schütz
  • Speaker: Dr. Harriet de Wit, University of Chicago
  • Title: Microdosing:  Fact or Fiction?
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Dr. Harriet de Wit will review evidence for the purported beneficial effects of ‘microdosing’ psychedelic drugs, specifically LSD.  She will describe recent studies from her laboratory investigating behavioral and neural effects of low doses of LSD in healthy adults.  She will illustrate some of the methodological challenges researchers face in investigating the effects of very low doses of drugs.

FEBRUARY 16

  • Host: Dr. Eric Accili
  • Guest: Dr. Emily Liman, University of Southern California
  • Title: The secret of sour: Discovery structure and function of the sour receptor OTOP1.
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Identifying and discriminating among compounds prior to ingestion is essential for animals to survive and thrive. Taste receptor cells encode five basic taste qualities, for which receptors and signaling pathways had been described for all but sour taste.  Here I will describe the identification from a screen of genes enriched in sour taste cells of the sour receptor, OTOP1. OTOP1 forms a proton channel, structurally unrelated to previously described ion channels. OTOP1 assembles as a dimer, with three putative pathways, gated by protons and Zn2+. Our recent findings expand the role of OTOP1 in taste cells to the detection of ammonium chloride, a potent taste stimulus used in salty licorice. OTOP1 is a member of a small family of ion channels found throughout the body and conserved across evolution. Ongoing work is aimed at discovering the roles of OTOP channels to various physiological and pathophysiological processes.

FEBRUARY 23
  • Host: Dr. Cheryl Wellington
  • Guest: Dr. Ramon Diaz-Arrastia, University of Pennsylvania
  • Title: Traumatic brain injury-related neurodegeneration:  What is the pathology.”
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Evidence accumulated over the past decades has shown that for many patients, traumatic brain injury (TBI) triggers cellular and molecular processes that continue to evolve long after the acute period and initial recovery. While these mechanisms result in short-term tissue repair and regeneration, the reparative process is often incomplete, and can also be maladaptive. Long-term outcomes after TBI are not fixed, but rather there can be improvement or deterioration years, even decades, after injury. TBI can result in long-term impairment and disability and increases risk of remote neurodegeneration and dementia.  It is estimated that 5-10% of the population-wide burden of dementia is associated with TBI.

Despite the substantial societal burden imposed by long-term neurodegeneration and dementia after TBI, little is known about the underlying pathophysiological mechanisms of trauma-related neurodegeneration (TReND). For decades it was believed that TBI was associated with an increased risk for Alzheimer’s disease, but recent work indicates that other pathologies, including microvasculopathy, axonal degeneration, and neuroinflammation play prominent roles.

This presentation will review the epidemiologic data regarding TReND and will then discuss insights from neuropathologic studies on long-term survivors after TBI.  Recent work using neuroimaging and molecular biomarkers measured years after TBI will be reviewed.  Finally, we will discuss recent work pointing to potential therapeutic interventions.

MARCH 1

  • Host: Dr. Annie Ciernia
  • Speaker: Dr. Janine Kwapis, Pennsylvania State University
  • Title: Time to learn: Diurnal regulation of memory by the clock gene Per1.
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Many biological processes, including memory formation, are strongly influenced by the circadian system, which synchronizes animals’ internal states with the external time of day. Long-term memory performance changes across the day/night cycle in both humans and rodents, yet the mechanisms that support this process are largely unknown. In this talk, I will present my lab’s research suggesting that a circadian clock gene, Period1 (Per1) may serve as a molecular interface between the circadian clock and memory formation. Per1 oscillates in tandem with memory in memory-relevant brain regions, like the hippocampus, with both memory and Per1 levels peaking during the day and showing a trough at night. Interestingly, old animals have repressed hippocampal Per1 levels even during the day, suggesting that they may show impairments in memory due to this persistent “nighttime state” that limits memory across the diurnal cycle. Together, our data suggest that Per1 may function locally in memory-relevant brain regions to exert diurnal control over memory.

MARCH 8

  • Host: Dr. Tim Murphy
  • Speaker: Dr. Nick Steinmetz, University of Washington
  • Title: Brain-wide coordinated dynamics and Neuropixels Ultra
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In this talk, I will describe two recent projects in my lab. In the first, we discovered that brain-wide spatiotemporal dynamics (i.e. traveling waves) are coordinated on a moment-to-moment basis between neocortex and striatum, thalamus, and midbrain. We used widefield calcium imaging and Neuropixels 2.0 recordings in combination to reveal the structure of these waves in the mouse brain, including a link to the underlying axonal architecture that supports them. Second, I will talk about our work developing a new version of the Neuropixels probe, called ‘Neuropixels Ultra’, which has much smaller and denser recording sites than previous versions. This configuration yields improved characteristics for some applications and reveals new observations about the biophysical phenomena observable with extracellular electrophysiology.

MARCH 15

  • Host: Dr. Cheryl Wellington
  • Speaker: Dr. David Holtzman,  Washington University in St. Louis
  • Title: The role of APOE and the immune response in amyloid-induced tauopathy and tau-mediated neurodegeneration
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MARCH 22

  • Host: Dr. Stan Floresco
  • Speaker: Dr. Alicia Izquierdo, University of California, Irvine
  • Title: Translational models of frontocortical circuits in learning and decision making
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Orbitofrontal cortex (OFC) and Anterior cingulate cortex (ACC) have been assigned various overlapping roles ranging from learning and responding to reward, signaling value and uncertainty, and supporting economic decisions, to name a few. Both of these regions share reciprocal anatomical connections with basolateral amygdala, contributing to functional similarities among these circuits. Using a combination of novel behavioral paradigms, DREADDs, and 1P calcium imaging in freely-moving rats, our lab has sought better resolution of diverse frontocortical processes. In this talk I will present data comparing subregional frontal cortex contributions, together with basolateral amygdala, in reward learning and value-based decisions. With few exceptions, our results suggest mostly overlapping, less specialized, roles for ACC and OFC that point to complementary roles in keeping track of expected uncertainty, or the range of typically-experienced outcomes. Collectively these findings may have implications for how we view frontocortical contributions across rodent and primate species.

APRIL 5

  • Host: Dr. Helen Tremlett
  • Speaker: Dr. Kaarina Kowalec, University of Manitoba
  • Title:  Depression polygenicity and its association with multiple sclerosis disease activity and progression.
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Depression is a common comorbidity in those with multiple sclerosis (MS) and is associated with faster MS disability progression. Identifying who may be at higher risk for depression or faster disease activity or progression may facilitate earlier identification. We will examine the polygenicity of comorbid depression in MS and whether it is associated with MS disease activity & disability progression in multiple cohorts from Canada, the USA, Sweden, and UK Biobank.

APRIL 12

  • Host: Dr. Catharine Winstanley
  • Speaker: Dr. Carrie Ferrario, University of Michigan
  • Title: Alterations in brain & behavior that contribute to obesity
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While urges to eat are regulated by hunger, satiety, and energy demand, they are also strongly influenced by sights, sounds, and smells that are associated with food (food cues). These food cues can influence feeding behavior, triggering cravings that can promote overeating. Dr. Ferrario’s lab examines the neurobiological mechanisms of cue-triggered food craving, and how these processes are influenced by susceptibility to diet-induced obesity and by consumption of sugary, fatty, “junk-food” diets. In her talk, she will discuss how enhanced responsivity to food cues contributes to obesity, and how eating “junk-foods” enhances excitatory transmission within the NAc to influence food “craving”. She will also highlight sex differences in these effects, and the role that susceptibility to obesity plays in diet-induced plasticity.

APRIL 19

  • Host: Dr. Kota Mizumoto
  • Speaker: Dr. Aki Taruno,  Kyoto Prefectural University of Medicine
  • Title: A chemical synapse that lacks vesicles
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Chemical neurotransmission is essential for a variety of neural processes and is traditionally understood to be mediated by Ca2+-dependent exocytosis of synaptic vesicles. Nevertheless, it has been recognized for decades that taste receptor cells in taste buds do not possess synaptic vesicles, yet they can transmit gustatory information to the nervous system. Here I will describe the identification of a unique synapse of taste receptor cells where the ion-conducting pore of a voltage-gated channel, CALHM1/3, serves as the conduit for action potential-dependent neurotransmitter (ATP) release. This mechanism has been termed a ‘channel synapse.’ Anatomically, a channel synapse is characterized by its tripartite structure, which includes a presynaptic mitochondrion adjacent to a CALHM1/3-enriched plasma membrane that faces a post-synaptic afferent nerve. Our recent discoveries extend the roles of channel synapses to various extraoral physiological and pathophysiological processes.

MAY 3

  • Host: Mathias Delhaye
  • Speaker: Dr. Edward Boyden, Massachusetts Institute of Technology
  • Title: Tools for Analyzing and Repairing the Brain
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Understanding and repairing complex biological systems, such as the brain, requires technologies for systematically observing and controlling these systems.  We are discovering new molecular principles that enable such technologies.  For example, we discovered that one can physically magnify biological specimens by synthesizing dense networks of swellable polymer throughout them, and then chemically processing the specimens to isotropically swell them.  This method, which we call expansion microscopy, enables ordinary microscopes to do nanoimaging – important for mapping molecules throughout cells, and cells throughout brain circuits.  Expansion of biomolecules away from each other also decrowds them, enabling previously invisible nanostructures to be labeled, and seen.  As a second example, we discovered that microbial opsins, genetically expressed in neurons, could enable their electrical activities to be precisely controlled in response to light.  These molecules, called optogenetic tools, enable causal assessment of how neurons contribute to behaviors and pathological states, and are yielding insights into new treatment strategies for brain diseases.  They are also beginning to be used in human patients, in experimental clinical contexts like treating blindness. Finally, we are developing, using new strategies such as robotic directed evolution, fluorescent reporters that enable the precision measurement of signals such as voltage.  In order to reveal relationships between different molecular signals within a cell, we are developing spatial and temporal multiplexing strategies that enable many such signals to be imaged at once in the same living cell, using ordinary microscopes, and requiring only fully genetically encoded constructs.  We share all these tools freely, and aim to integrate the use of these tools so as to enable comprehensive understandings of neural circuits.

MAY 10 

  • Host: Dr. Annie Ciernia
  • Speaker: Dr. Anne West, Duke University
  • Title: From chromatin regulation to synapse development in neurodevelopmental disorders
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Chromatin regulatory proteins are a major class of gene products for which sequence variants are associated with autism spectrum disorders and intellectual disability; however, the functional consequences of these mutations for brain development remain poorly understood. We are identifying molecular mechanisms through which chromatin regulatory enzymes promote the expression of synaptic gene products and functional neuronal maturation. I will discuss how our studies are working to build a foundation for understanding how dysregulation of chromatin regulation in the developing brain leads to neurodevelopmental disorders.

MAY 24

  • Host: Dr. Doug Altshuler
  • Speaker: Dr. Brian Corneil, University of Western Ontario
  • Title: TBD
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MAY 31

  • Host:  Dr. Jason Snyder
  • Speaker: Dr. Khaled Abdelrahman
  • Title: Decoding the Intricacies of GPCR Signaling in neurodegenerative diseases
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Our research focuses on the intricate role of specific G protein-coupled receptors (GPCRs) in the pathophysiology of neurodegenerative diseases. A key aspect of our focus is unraveling the sex-specific regulation of GPCR signaling in these conditions. Through exploring these intricacies, we aim to illuminate novel therapeutic avenues and enhance our understanding of the complex interplay between GPCRs and neurodegeneration.