Join us for the Bruker Online Neuroscience Summit 2025, a two-day virtual event on April 22 and 23, 2025, from 8 AM to 10:30 AM (PDT) each day. This summit will showcase groundbreaking research from leading scientists utilizing advanced imaging technologies, including Bruker two-photon microscopes, miniscopes from Inscopix, and Bruker Spatial Biology equipment, to explore neuronal activity in the brain.
Over the course of the summit, attendees will have the opportunity to hear from leading scientists presenting their latest findings across five key areas of neuroscience:
Each topic will feature a series of three experts, providing in-depth insights and fostering discussions on the latest advancements and applications in neuroscience research. Don’t miss this chance to connect with the scientific community and stay at the forefront of neuroscience innovation.
Register now to secure your spot and be part of this exciting event!
TABLE OF CONTENTS:
Track A: OPTOGENETICS | Track B: PSYCHIATRIC DISORDERS | ||
---|---|---|---|
8:00 am PDT | Welcome Remarks | 8:00 am PDT | Welcome Remarks |
8:10 am | Austin Coley, Assistant Professor of Neurobiology, UCLA | 8:10 am | Christina Kim, Assistant Professor of Neuroscience, Princeton |
8:40 am | Q&A | 9:00 am | Q&A |
8:50 am | Benjamin Scholl, Assistant Professor of Physiology, University of Colorado | 9:10 am | Jonathan Nassi, Senior Director Translational Science, Inscopix, a Bruker Company |
9:20 am | Q&A | 9:40 am | Q&A |
9:30 am | David Anderson, Seymour Benzer Professor of Biology, Caltech/HHMI Investigator | 9:50 am | Jamie Maguire, Kenneth and JoAnn G. Wellner Professor of Neuroscience, Tufts University |
10:20 am | Q&A | 10:20 am | Q&A |
10:30 am | Thank You Remarks | 10:30 am | Thank You Remarks |
Track A: LEADING-EDGE TECHNOLOGY | Track B: NEUROVASCULAR RESEARCH | Track C: BEHAVIORAL STUDIES | |
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8:00 am PDT | Welcome Remarks | Welcome Remarks | Welcome Remarks |
8:10 am | Kevin Mann, Applications Scientist, Bruker | Philip O'Herron, Assistant Professor of Physiology, Augusta University | Hyung Jin Choi, Associate Professor, Seoul National University |
9:00 am | Q&A | Q&A | Q&A |
9:10 am | Flavio Donato, Assistant Professor of Neuroscience, University of Basel | Kimberly Young, Research Associate, Bruker Spatial Biology | Thomas Clandinin, The Shooter Family Professor of Neurobiology, Stanford University |
9:40 am | Q&A | Q&A | Q&A |
9:50 am | Waylin Yu, Lead Application Scientist, Inscopix, a Bruker Company | Hajime Hirase, Professor of Translational Neuromedicine, University of Copenhagen | Yvette Fisher, Assistant Professor, University of California, Berkeley |
10:20 am | Q&A | Q&A | Q&A |
10:30 am | Thank You Remarks | Thank You Remarks | Thank You Remarks |
Assistant Professor, Dept. of Neurobiology, Brain Research Institute, Integrative Center for Learning and Memory, University of California - Los Angeles {Lab Link}
Assistant Professor, Dept. of Physiology and Biophysics, University of Colorado School of Medicine {Bio Link}
Seymour Benzer Professor of Biology, California Institute of Technology/HHMI Investigator {Lab Link}
Lead Application Scientist, Inscopix, a Bruker Company
Presentation: Two-Photon Imaging in Freely Behaving Animals
Assistant Professor, Dept. of Physiology, August University
Presentation: Manipulating Blood Flow with Optogenetics
Research Associate, Bruker Spatial Biology
Professor, Center for Translational Neuromedicine, University of Copenhagen {Lab Link}
Associate Professor, Dept. of Biomedical Sciences/Anatomy and Cell Biology, Seoul National University {Lab Link}
The Shooter Family Professor of Neurobiology, Stanford University
Presentation: How Does Connectomics Constrain Computation?
Assistant Professor, Dept. of Molecular and Cell Biology and Helen Wills Neuroscience Institute, University of California, Berkeley {Lab Link}
The mental health field lacks granularity in diagnostic practices, which may contribute to the variability in efficacy of existing treatments. Anhedonia, a condition identified in multiple neuropsychiatric disorders, is described as the inability to experience pleasure and is linked to anomalous medial prefrontal cortex (mPFC) activity. The mPFC is responsible for higher order functions, such as valence processing; however, it remains unknown how mPFC valence-specific neuronal population activity is affected during anhedonic conditions. To test this, we implemented the unpredictable chronic mild stress (CMS) protocol in mice and examined hedonic behaviors following stress and ketamine treatment. We performed in vivo 2-photon calcium imaging to longitudinally track mPFC valence-specific neuronal population activity and dynamics during Pavlovian conditioning tasks. Also, we utilized behavioral pose-estimation tracking systems to predict anhedonia based on facial features during Pavlovian conditioning tasks. Lastly, we applied a linear classifier to test whether we can decode susceptibility to chronic mild stress based on mPFC valence-encoding properties prior to stress-exposure and behavioral expression of susceptibility. These results indicate that mPFC valence encoding properties are predictive of anhedonic states. Altogether, these experiments point to the need for increased granularity in the measurement of both behavior and neural activity, as these factors can predict the induction conditions of stress-induced anhedonia.
Cortical computations arise from dynamic interactions between neurons, which shift with sensory context to either amplify or suppress activity. While suppressive interactions between similarly tuned neurons have been reported in mouse V1, it is unclear whether such feature competition generalizes to columnar cortices like ferret V1, where nearby neurons and long-range excitatory projections are functionally aligned. We combined two-photon calcium imaging and optogenetics to examine how excitatory interactions in layer 2/3 of ferret V1 depend on stimulus contrast. Responses to drifting gratings at low and high contrast were recorded while single excitatory neurons were photostimulated. A Poisson generalized linear model quantified the influence of each stimulated neuron on surrounding activity and tuning. We observed widespread net suppression, strongest across large cortical distances and enhanced at high contrast. Nearby neurons (<100 μm) were least suppressed. Among similarly tuned neurons, pairwise noise correlations predicted interaction strength and sign: low contrast led to local facilitation between correlated pairs, while high contrast induced widespread suppression. These results are consistent with stabilized supralinear network models, in which weak inputs are amplified and strong inputs are sublinearly integrated. Contrast-dependent shifts in interaction patterns were associated with improved stimulus decoding, suggesting dynamic recruitment of inhibition optimizes sensory encoding in columnar cortex.
Innate survival behaviors such as fighting, mating and predator defense are associated with affective internal states, such as fear. The identification of neural representations of such states using supervised analyses has been challenged by a lack of direct measures and inter-trial variability. To overcome these limitations, we have performed unsupervised modeling of single-trial neural data acquired during naturalistic social behaviors, using recurrent Switching Linear Dynamical Systems (rSLDS). rSLDS learns a dynamics matrix based on latent factor activity in a state-space approximated by a set of linear substates, yielding a probabilistic model of neural dynamics. When used to model single-trial calcium imaging data recorded from hypothalamic "attack" neurons during aggressive encounters, rSLDS discovered an approximate line attractor that represents the intensity and duration of an internal state of aggressiveness. In this talk, I will discuss features of this representation, evidence for its local instantiation in the hypothalamus, mechanistic implementation and generalization to other social behaviors. Together, these recent results extend the potential role of continuous attractor dynamics beyond the representation of cognitive variables, to the representation of scalable and persistent affective internal states. They also identify a tractable experimental platform to investigate how circuit-level mechanisms give rise to emergent network dynamics at the manifold level in the mammalian brain.
Probing the molecular and functional properties of neuronal ensembles is essential for understanding how these networks give rise to circuit function and animal behavior. Our group specializes in developing molecular and optical approaches to study different types of neuronal signaling in the brains of awake, behaving mice. We utilize real-time, cellular-resolution imaging techniques for recording activity during behavior, in addition to next-generation molecular activity integrators for tagging and manipulating activated neuronal circuits. To allow investigations into the molecular cell-types of these neurons, we engineer technologies that encode the cellular activity history into the transcriptome of individual neurons. This activity tag is read-out during single-cell RNA sequencing, and can then be linked to specific set of relevant cell-types. Alternatively, the activity tag can encode an actuator, such as an opsin, to enable subsequent manipulation of the tagged neurons. Here I will discuss our work using two-photon guided light- and calcium-dependent tagging and manipulation of neurons that respond to psychedelic drugs in mice.
Major depressive disorder and related psychiatric conditions present a major societal challenge, with a large proportion of patients not responding to available treatments. The Inscopix Discovery Lab was established to address this challenge, leveraging miniscope-based calcium imaging in partnership with pharma and biotech to develop preclinical assays in support of psychiatric drug development. Here, we describe some of our latest work profiling candidate antidepressants based on pharmacodynamic measurements in prefrontal cortex of freely behaving mice. Through these efforts we have built up a library of neurobehavioral drug profiles that includes the recently approved antidepressant Ketamine as well as some of the most promising psychedelics and related analogs including DMT, MDMA, DOI, Psilocin, Tabernanthalog and Lisuride. We have identified key differences and similarities among these drugs on locomotor activity, neuronal activity levels and inter-neuronal correlations. Through unsupervised modeling and hierarchical clustering, we find that, in some respects, Ketamine's impact on prefrontal cortical circuits is more similar to certain serotonergic psychedelics than to other NMDA modulators. Such similarities may point toward shared therapeutic mechanism of action among distinct pharmacology, underscoring the importance of measuring drug responses in vivo in the intact brain rather than relying solely on receptor affinity characterizations and other in vitro assays. These powerful new capabilities to comparatively profile how candidate treatments impact disease relevant circuits in the brain promises to critically inform preclinical drug discovery and accelerate development of more effective treatments for depression and related psychiatric conditions.
The basolateral amygdala (BLA) is an emotional processing hub which governs both positive and negative valence processing. Work from our laboratory has demonstrated a critical role for oscillations in the BLA in the neural computations of valence. Parvalbumin interneurons orchestrate network states in the BLA that drive divergent behavioral outcomes. Our research program focuses on how these neural computations become disrupted in association with pathological states. For example, chronic stress, a major risk factor for psychiatric illnesses, alters the neural computations of valence processing, favoring negative valence states, a process which involves altered cellular and circuit dynamics. The use of the Inscopix nVue system has been instrumental in our ability to understand how the cellular dynamics of BLA neurons becomes altered following chronic stress and may contribute to pathological behavioral outcomes.
Two-photon microscopy has been instrumental in neuroscience, revealing insights into perception, computation, and connectivity across diverse models. Ca2+ imaging, in particular, has enabled precise visualization of brain activity at the level of small networks, single cells, dendrites, and individual spines. Light-based manipulations, such as optogenetics, have allowed real-time perturbation of neural circuits from single synapses to entire ensembles. More recently, fast fluorescent indicators for voltage and neurotransmitters have extended two-photon capabilities beyond Ca2+ imaging, enabling more temporally precise measurements of neural activity using the same optical platforms. I will discuss how Bruker’s advanced two-photon microscopy systems support these modern imaging and stimulation approaches, offering high-speed acquisition, deep tissue access, and precise control for probing neural function.
Memories are dynamic constructs whose properties change with time and experience. The biological mechanisms underpinning these dynamics remain elusive, particularly concerning how shifts in the composition of memory-encoding neuronal ensembles influence the evolution of a memory over time. By targeting developmentally distinct subpopulations of principal neurons, we discovered that memory encoding resulted in the concurrent establishment of multiple memory traces in the mouse hippocampus. Two of these traces were instantiated in subpopulations of early- and late-born neurons and followed distinct reactivation trajectories after encoding. The divergent recruitment of these subpopulations underpinned the gradual reorganization of memory ensembles and modulated memory persistence and plasticity across multiple learning episodes. Thus, our findings reveal profound and intricate relationships between ensemble dynamics and the progression of memories over time.
Inscopix aims to offer rapid and robust end-to-end data acquisition and processing capabilities through an easy-to-use product portfolio supporting surgical procedures, data acquisition, management, and analysis. Its latest development, the nVista 2P, is a plug-and-play system for free-behaving two-photon miniature microscope imaging. The nVista 2P has been validated for compatibility with GRIN lenses and cranial windows to enable deep and shallow brain imaging, as well as precise cell identification and registration over time. In this presentation, our lead application scientist, Dr. Waylin Yu, will highlight the user-friendly features of the Inscopix 2P workflow and the range of applications enabled by the nVista 2P and the Inscopix Data Exploration, Analysis & Sharing (IDEAS) platform.
We have developed a mouse model to alter blood flow using optogenetic stimulation. These mice express the red-shifted depolarizing opsin ReaChR in vascular mural cells, leading to vasoconstriction when stimulated with light. Using the Bruker Ultima 2P-Plus system, we are able to stimulate the vessels to change their diameter while simultaneously monitoring neural and vascular signals with two-photon fluorescence imaging. An LED module provides full-field stimulation for widespread vasoconstriction. Using a second laser line combined with a spatial light modulator (SLM), we can target individual vessel segments across multiple depth planes for more precise vessel control. This presentation will discuss the methodology and demonstrate the properties of vasoconstriction under different conditions. We will additionally explain how we are using this tool to study the interaction between neural activity and blood flow changes in the cerebral cortex.
Microglia, the brain's primary immune cells, are highly responsive to changes in their environment, adapting their behavior through intricate molecular signaling. These functional shifts, from surveillance to injury response, are associated with morphological changes, which can serve as markers of their functional state. Our study uniquely combines cutting edge, high-plex spatial proteomics and traditional immunohistochemistry (IHC) to quantify and correlate microglial morphology with functional changes after ischemic stroke at different timepoints.
Adult male mice were subjected to transient middle cerebral artery occlusion and reperfusion using the filament method. Following this procedure, stroke severity was confirmed using a Bruker Biospec 70/20 7.0T MRI scanner. Brains were extracted at 24 hours, 2 weeks, or 4 weeks post-stroke (3 animals/timepoint), fixed, and sectioned at 10μm (spatial proteomics) or 50μm (IHC). We stained microglia with an IBA1 antibody or, utilizing the high plex Mouse CosMx® Neuroscience Protein Panel and the CosMx Spatial Molecular Imager (SMI), we detected 68 proteins with single cell resolution, focusing on regions proximal and distal to the infarct.
Leveraging the many microglial and immune markers in the Mouse CosMx Neuroscience Protein Panel, we captured precise cell morphology and quantified it by skeleton analysis focused on microglial process length and endpoints. Our results showed strong correlation between CosMx SMI and IHC morphometric data over time and distance from stroke injury, supporting CosMx SMI as a viable alternative to traditional IHC. Additionally, principal component analysis of select proteins in the CosMx SMI data revealed correlations between microglial form and function across various brain regions. Utilizing the InSituCor analysis toolkit, we further identified a module of spatially correlated proteins in the infarct region two weeks post-stroke, including Cathepsin B—a promising therapeutic target—and phagocytic markers CD11b, CD11c, and DAP12, with their colocalization shifting gradually with distance from the infarct core. By pairing spatial proteomic data with microglial morphology analysis, we gained deeper insights into the complex interactions between microglia and the recovering brain following ischemic stroke, highlighting how these interactions evolve over time and with proximity to the infarct core.
Studying blood microcirculation is crucial for understanding vascular diseases. Blood flow is currently imaged following invasive administration of fluorescent dyes that attenuate within one hour. We developed three new molecular genetic approaches for longitudinal vasculature study.
Liver-secreted albumin is the most abundant protein in plasma and cerebrospinal fluid. We created liver-targeting AAVs expressing fluorescent protein-tagged albumin to visualize blood plasma in mice after a single systemic injection (DOI: 10.1016/j.crmeth.2022.100302). While effective in adults, AAV genome dilution in the growing liver limits use in neonates.
To overcome this, we established a virally induced CRISPR/Cas9 knock-in of fluorescent albumin (DOI: 10.1007/978-1-0716-4011-1_6). An AAV carrying ~1 kb homologous arms around Alb exon 14 enabled expression of Alb-mNeonGreen after postnatal day 3 injection, with stable expression for at least three months.
As an alternative, we generated a mouse with mScarlet knocked into Alb exon 14, including a SpyTag, which is utilized for biosensor attachment or blood–brain barrier assessment. These approaches enable powerful imaging of murine vasculature (DOI: 10.1101/2025.03.18.643859).
Understanding how individual neurons contribute to specific behaviors requires precise neural activity imaging aligned with well-designed behavioral paradigms. This talk presents a framework for investigating behavior-time-locked neuronal roles using single-cell-level neural activity imaging in freely moving mice. We emphasize the importance of designing behavioral tasks that directly test neuroscience hypotheses, ensuring precise temporal alignment between neural activity and behavioral events. Understanding how individual neurons contribute to specific behavioral processes, such as food discovery, approach, consumption, reward learning, and extinction memory, requires precise neural activity imaging aligned with well-structured behavioral paradigms. We emphasize the importance of designing behavioral tasks that capture key moments in reward-related behaviors, ensuring precise temporal alignment between neural activity and behavioral transitions. By integrating advanced single-cell-level neural activity imaging techniques with hypothesis-driven behavioral paradigms, we aim to elucidate the neuronal mechanisms underlying reward processing and learning, providing new insights into neural circuit function.
Recent work has leveraged connectomics to predict the function of cells and circuits in the brains of many species. However, many of these hypotheses have not been compared with physiological measurements. We characterized the visual responses of many cell types in the fruit fly and quantitatively compared them to connectomic predictions. Our results establish a powerful set of constraints for improving the accuracy of connectomic predictions.
In the Drosophila brain, head direction neurons form a network whose activity tracks the angular position of the fly using both external visual signals and internal self-motion information. Previous work discovered that plasticity allows these external signals to be combined with internal cues to form a coherent sense of direction. Yet the synaptic mechanisms that implement plasticity in this network are still unknown. In this talk I will discuss a role for multiple monoaminergic neuromodulators in shaping synaptic plasticity. We recently published evidence that dopamine provides a "when-to-learn" signal that allows the head direction network to update synaptic weights when new spatial information is available—that is, when a fly is rotating. We show that dopamine neurons that innervate the head direction network are active when the fly turns, and that manipulating dopamine alters the influence of visual cues. Thus, dopamine seems to accelerate learning as the fly’s turning maneuvers provide a new visual scene, this allows learning rates to be low at other times to protect stored information. Interestingly, because dopamine release is global, it is not well positioned to instruct coincidence detection that would be required for the network to store a "snapshot" of the flies' current surroundings. Moreover, I will discuss unpublished evidence that a second neuromodulator, octopamine, is critical for coincidence detection during plasticity induction.
Attending the Bruker Online Neuroscience Summit 2025 offers several key benefits:
This summit is a unique opportunity to stay at the forefront of neuroscience innovation and connect with the scientific community. Don’t miss out!