A Postdoc position is now available in the Dura-Bernal Lab at the State University of New York (SUNY) Downstate Health Sciences University (Brooklyn, New York), working on a new exciting multidisciplinary project entitled "Restoring motor function after spinal cord injury using multiscale modeling to decode neural latent dynamics from motor cortex EEG." The position is funded by New York State (NYS) Department of Health (DOH) Spinal Cord Injury Research program. The project aims to improve brain-machine interface decoders by combining multiscale modeling of motor cortex circuits, analysis of low-dimensional neural manifolds associated with behavior, and realistic simulation of EEG signals.

The lab of Dr. Kendrick Kay at the Center for Magnetic Resonance Research at the University of Minnesota is recruiting one or more postdocs. The lab seeks to integrate broad interdisciplinary insights to understand function in the visual system. One postdoc position is on a newly funded NIH R01 to develop, design, and collect a large-scale 7T fMRI dataset that samples a wide range of cognitive tasks on a common set of visual stimuli. The project is being conducted in close collaboration with co-PI Dr. Clayton Curtis (New York University). Activities in this grant include either (i) designing, collecting, and analyzing the large-scale neuroimaging dataset, (ii) technical work focused on extending and expanding the GLMsingle analysis method, and/or (iii) other related experimental or modeling work in visual/cognitive neuroscience. Another postdoc position is aimed towards integrating fMRI and intracranial EEG measurements during visual tasks (NSD-iEEG) and electrical stimulation. The general goal of this effort is to better understand signaling across the visual hierarchy (from early visual to higher order areas ventral temporal cortex and frontal/parietal areas). This project is in collaboration with PI Dr. Dora Hermes (Mayo Clinic).

The postdoc position is under the joint co-mentoring of Dr. Demian Battaglia and Dr. Romain Goutagny at the University of Strasbourg, France, in the Functional System's Dynamics team – FunSy. The position starts as soon as possible and can last up to two years. The job offer is funded by the French ANR 'HippoComp' project, which focuses on the complexity of hippocampal oscillations and the hypothesis that such complexity can serve as a computational resource. The team performs electrophysiological recordings in the hippocampus and cortex during spatial navigation and memory tasks in mice (wild type and mutant developing various neuropathologies) and have access to vast data through local and international cooperation. They use a large spectrum of computational tools ranging from time-series and network analyses, information theory, and machine-learning to multi-scale computational modeling.

A postdoc position is available under the shared supervision of Prof. Maxime Baud and Dr. Timothée Proix, who both specialize in quantitative neuroscience research. Together, they are running a three-year clinical trial involving patients with epilepsy who received a minimally invasive EEG device beneath the scalp for the chronic recording (months) of brain signals during wake and sleep. The postdoc will help with the analysis of massive amounts of EEG data, with a desire to build forecasting algorithms aiming at estimating the risk of seizures 24 hours in advance. The project lies at the interface between machine learning and EEG data analysis. The goal of the project is to develop machine learning algorithms to forecast seizures.

An NIH-funded collaboration between David Prober (Caltech), Thai Truong (USC) and Geoff Goodhill (Washington University in St Louis) aims to gain new insight into the neural circuits underlying sleep, through a combination of whole-brain neural recordings in zebrafish and theoretical/computational modeling. A postdoc position is available in the Goodhill lab to contribute to the modeling and computational analysis components. Using novel 2-photon imaging technologies Prober and Truong are recording from the entire larval zebrafish brain at single-neuron resolution continuously for long periods of time, examining neural circuit activity during normal day-night cycles and in response to genetic and pharmacological perturbations. The Goodhill lab is analyzing the resulting huge datasets using a variety of sophisticated computational approaches, and using these results to build new theoretical models that reveal how neural circuits interact to govern sleep.

The postdoc position is focused on the development of BrainSTEM, a web application designed as an electronic lab notebook for describing neurophysiological experiments as well as a data-sharing platform for the community. The role involves the design of a standard language for describing experimental neuroscience, semantic search functionality, stronger adoption of the FAIR principles, and stimulating and supporting community uptake. The project is primarily funded by the NIH, through the Brain Initiative U19 Oxytocin grant. The project will include occasional travels, e.g., to New York (NYU), Brain Initiate meetings, SfN, FENS, and to pilot user labs.

We have an opening for a postdoc position investigating the neural bases of deep multimodal learning in the brain. The project involves EEG and laminar 7T imaging (in collaboration with Dr. Peter Bandettini’s lab at NIMH) to test computational hypotheses for how the brain learns multimodal concept representations. Responsibilities of the postdoc include running EEG and fMRI experiments, data analysis and manuscript preparation. Georgetown University has a vibrant neuroscience community with over fifty labs participating in the Interdisciplinary Program in Neuroscience and a number of relevant research centers, including the new Center for Neuroengineering (cne.georgetown.edu). Interested candidates should submit a CV, a brief (1 page) statement of research interests, representative reprints, and the names and contact information of three references to Interfolio via https://apply.interfolio.com/148520. Faxed, emailed, or mailed applications will not be accepted. Questions about the position can be directed to Maximilian Riesenhuber (mr287@georgetown.edu).

Claude Desplan is a Silver Professor of Biology and Neuroscience at NYU. He was born in Algeria and was trained at Ecole Normale Supérieure St. Cloud, France. He received his DSc at INSERM in Paris in 1983 and joined Pat O’Farrell at UCSF as a postdoc. There he demonstrated that the homeodomain, a conserved signature of many developmental genes, is a DNA binding motif. Currently, Dr. Desplan works at NYU where he investigates the generation of neural diversity using the Drosophila visual system.

Corticospinal neurons (CSN) are the cortical projection neurons that innervate the spinal cord and some brainstem targets with segmental precision to control voluntary movement of specific functional motor groups, limb sections, or individual digits, yet molecular regulation over CSN segmental target specificity is essentially unknown. CSN subpopulations exhibit striking axon targeting specificity from development into maturity: Evolutionarily newer rostrolateral CSN exclusively innervate bulbar-cervical targets (CSNBC-lat), while evolutionarily older caudomedial CSN (CSNmed) are more heterogeneous, with distinct subpopulations extending axons to either bulbar-cervical or thoraco-lumbar segments. The cervical cord, with its evolutionarily enhanced precision of forelimb movement, is innervated by multiple CSN subpopulations, suggesting inter-neuronal interactions in establishing corticospinal connectivity. I identify that Lumican, previously unrecognized in axon development, controls the specificity of cervical spinal cord innervation by CSN. Remarkably, Lumican, an extracellular matrix protein expressed by CSNBC-lat, non-cell-autonomously suppresses axon collateralization in the cervical cord by CSNmed. Intersectional viral labeling and mouse genetics further identify that Lumican controls axon collateralization by multiple subpopulations in caudomedial sensorimotor cortex. These results identify inter-axonal molecular crosstalk between CSN subpopulations as a novel mechanism controlling corticospinal connectivity and competitive specificity. Further, this mechanism has potential implications for evolutionary diversification of corticospinal circuitry with finer scale precision. "" Complementing this work, to comprehensively elucidate related axon projection mechanisms functioning at tips of growing CSN axons in vivo, I am currently applying experimental and analytic approaches recently developed in my postdoc lab (Poulopoulos*, Murphy*, Nature, 2019) to quantitatively and subcellularly “map” RNA and protein molecular machinery of subtype-specific growth cones, in parallel to their parent somata, isolated directly in vivo from developing subcerebral projection neurons (SCPN; the broader cortical output neuron population targeting both brainstem and spinal cord; includes CSN). I am investigating both normal development and GC-soma dysregulation with mutation of central CSN-SCPN transcriptional regulator Ctip2/Bcl11b.

This seminar is part of our “Emergent Scientists” series, an initiative that provides a platform for scientists at the critical PhD/postdoc transition period to share their work with a broad audience and network. Summary: These talks cover Alzheimer’s disease (AD) research in both mice and humans. Christiana will discuss in particular the translational aspects of applying mouse work to humans and the importance of timing in disease pathology and intervention (e.g. timing between AD biomarkers vs. symptom onset, timing of therapy, etc.). Siddharth will discuss a rare variant of Alzheimer’s disease called “Logopenic Progressive Aphasia”, which presents with temporo-parietal atrophy yet relative sparing of hippocampal circuitry. Siddharth will discuss how, despite the unusual anatomical basis underlying this AD variant, degeneration of the angular gyrus in the left inferior parietal lobule contributes to memory deficits similar to those of typical amnesic Alzheimer’s disease. Christiana’s abstract: Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder that causes severe deterioration of memory, cognition, behavior, and the ability to perform daily activities. The disease is characterized by the accumulation of two proteins in fibrillar form; Amyloid-β forms fibrils that accumulate as extracellular plaques while tau fibrils form intracellular tangles. Here we aim to translate findings from a commonly used AD mouse model to AD patients. Here we initiate and chronically inhibit neuropathology in lateral entorhinal cortex (LEC) layer two neurons in an AD mouse model. This is achieved by over-expressing P301L tau virally and chronically activating hM4Di DREADDs intracranially using the ligand dechloroclozapine. Biomarkers in cerebrospinal fluid (CSF) is measured longitudinally in the model using microdialysis, and we use this same system to intracranially administer drugs aimed at halting AD-related neuropathology. The models are additionally tested in a novel contextual memory task. Preliminary findings indicate that viral injections of P301L tau into LEC layer two reveal direct projections between this region and the outer molecular layer of dentate gyrus and the rest of hippocampus. Additionally, phosphorylated tau co-localize with ‘starter cells’ and appear to spread from the injection site. Preliminary microdialysis results suggest that the concentrations of CSF amyloid-β and tau proteins mirror changes observed along the disease cascade in patients. The disease-modifying drugs appear to halt neuropathological development in this preclincial model. These findings will lead to a novel platform for translational AD research, linking the extensive research done in rodents to clinical applications. Siddharth’s abstract: A distributed brain network supports our ability to remember past events. The parietal cortex is a critical member of this network, yet, its exact contributions to episodic remembering remain unclear. Neurodegenerative syndromes affecting the posterior neocortex offer a unique opportunity to understand the importance and role of parietal regions to episodic memory. In this talk, I introduce and explore the rare neurodegenerative syndrome of Logopenic Progressive Aphasia (LPA), an aphasic variant of Alzheimer’s disease presenting with early, left-lateralized temporo-parietal atrophy, amidst relatively spared hippocampal integrity. I then discuss two key studies from my recent Ph.D. work showcasing pervasive episodic and autobiographical memory dysfunction in LPA, to a level comparable to typical, amnesic Alzheimer’s disease. Using multimodal neuroimaging, I demonstrate how degeneration of the angular gyrus in the left inferior parietal lobule, and its structural connections to the hippocampus, contribute to amnesic profiles in this syndrome. I finally evaluate these findings in the context of memory profiles in other posterior cortical neurodegenerative syndromes as well as recent theoretical models underscoring the importance of the parietal cortex in the integration and representation of episodic contextual information.