Molecular Neuroscience seminars

Matthew J. Girgenti discusses how research on individual brain cells and the three-dimensional organization of DNA is changing the biological understanding of post-traumatic stress disorder. The seminar examines how these approaches reveal trauma-associated brain changes and identify possible targets for more effective, personalized treatments. Girgenti is a neuroscientist in Yale School of Medicine’s Department of Psychiatry. Jeffrey Borenstein moderates this Meet the Scientist session. Online via the BBRF Zoom webinar. Tuesday 13 October 2026, 14:00 EDT (America/New_York; UTC−4). Follow Register Today on the organizer’s event page to the event-specific Zoom form. Advance registration is available to researchers, students, healthcare providers, mental-health organizations, patients and family members.

Brain metabolism supplies the energy underlying brain injury, recovery and aging. This webinar brings together three complementary approaches to understanding how repetitive mild traumatic brain injury affects these processes. Sakthivel Ravi examines repetitive mild TBI and aging through multimodal imaging and molecular profiling. Adam Khalifa presents wireless brain glucose sensing for TBI research, and Joe Abisambra discusses disruption of bioenergetic pathways following repetitive mild TBI. The talks are followed by a moderated question-and-answer discussion.

Astrocytes help sustain neural signaling and tissue stability, but injury and implanted devices cause them to change their functions. Tim O'Shea examines how the extent and timing of this response determine tissue protection, regeneration and implant durability. Limited renewal of adult astrocytes contrasts with the greater proliferation and migration of immature cells in newborn mammals. Around implants, continuing movement, infection and other stimuli can prolong the response and affect device performance. The talk uses astrocyte-specific transcriptomic assays to investigate this reprogramming and considers how to improve repair without sacrificing normal astrocyte functions. It also presents biomaterial and cell-transplant approaches being studied in preclinical stroke, spinal cord injury and implant-response models.

Junjie Guo investigates how an intronic nucleotide-repeat expansion in C9orf72 causes familial and some sporadic cases of amyotrophic lateral sclerosis and frontotemporal dementia. The talk presents progress in understanding how the expansion changes gene expression, alongside functional-genomics approaches that identify potential therapeutic targets controlling expression of the pathogenic mutation. It also considers which mechanisms and modifiers extend to other disease-causing repeat expansions. Guo is Associate Professor of Neuroscience at Yale School of Medicine; the seminar is hosted by J. Wren Kim. Online via CUNY ASRC Zoom. Thursday 8 October 2026, 12:00–13:00 EDT (America/New_York; UTC−4). Follow the Zoom link on the official seminar page; meeting details are also supplied in its abstract PDF. Organized by the Advanced Science Research Center at the CUNY Graduate Center, Neuroscience Initiative. This listing advertises remote attendance.

UCL Department of Neuroinflammation Seminar by Professor Emad Moeendarbary (Professor of Cell Mechanics and Mechanobiology, UCL Mechanical Engineering) on how biophysical factors such as substrate stiffness and axon geometry regulate oligodendrocyte behavior and myelin formation, presenting the AxoMetic in vitro myelination platform for discovery of remyelinating therapies.

Thalamic networks, at the core of thalamocortical and thalamosubcortical communications, underlie processes of perception, attention, memory, emotions, and the sleep-wake cycle, and are disrupted in mental disorders, including schizophrenia and autism. However, the underlying mechanisms of pathology are unknown. I will present novel evidence on key organizational principles, structural, and molecular features of thalamocortical networks, as well as critical thalamic pathway interactions that are likely affected in disorders. This data can facilitate modeling typical and abnormal brain function and can provide the foundation to understand heterogeneous disruption of these networks in sleep disorders, attention deficits, and cognitive and affective impairments in schizophrenia and autism, with important implications for the design of targeted therapeutic interventions

The cortex comprises many neuronal types, which can be distinguished by their transcriptomes: the sets of genes they express. Little is known about the in vivo activity of these cell types, particularly as regards the structure of their spike trains, which might provide clues to cortical circuit function. To address this question, we used Neuropixels electrodes to record layer 5 excitatory populations in mouse V1, then transcriptomically identified the recorded cell types. To do so, we performed a subsequent recording of the same cells using 2-photon (2p) calcium imaging, identifying neurons between the two recording modalities by fingerprinting their responses to a “zebra noise” stimulus and estimating the path of the electrode through the 2p stack with a probabilistic method. We then cut brain slices and performed in situ transcriptomics to localize ~300 genes using coppaFISH3d, a new open source method, and aligned the transcriptomic data to the 2p stack. Analysis of the data is ongoing, and suggests substantial differences in spike time coordination between ET and IT neurons, as well as between transcriptomic subtypes of both these excitatory types.

Cellular crosstalk is an essential process during brain development and is influenced by numerous factors, including cell morphology, adhesion, the local extracellular matrix and secreted vesicles. Inspired by mutations associated with neurodevelopmental disorders, we focus on understanding the role of extracellular mechanisms essential for the proper development of the human brain. Therefore, we combine 2D and 3D in vitro human models to better understand the molecular and cellular mechanisms involved in progenitor proliferation and fate, migration and maturation of excitatory and inhibitory neurons during human brain development and tackle the causes of neurodevelopmental disorders.

Nervous system function relies on the polarized architecture of neurons, established by directional transport of pre- and postsynaptic cargoes. While delivery of postsynaptic components depends on the secretory pathway, the identity of the membrane compartment(s) that supply presynaptic active zone (AZ) and synaptic vesicle (SV) proteins is largely unknown. I will discuss our recent advances in our understanding of how key components of the presynaptic machinery for neurotransmitter release are transported and assembled focussing on our studies in genome-engineered human induced pluripotent stem cell-derived neurons. Specifically, I will focus on the composition and cell biological identity of the axonal transport vesicles that shuttle key components of neurotransmission to nascent synapses and on machinery for axonal transport and its control by signaling lipids. Our studies identify a crucial mechanism mediating the delivery of SV and active zone proteins to developing synapses and reveal connections to neurological disorders. In the second part of my talk, I will discuss how exocytosis and endocytosis are coupled to maintain presynaptic membrane homeostasis. I will present unpublished data regarding the role of membrane tension in the coupling of exocytosis and endocytosis at synapses. We have identified an endocytic BAR domain protein that is capable of sensing alterations in membrane tension caused by the exocytotic fusion of SVs to initiate compensatory endocytosis to restore plasma membrane area. Interference with this mechanism results in defects in the coupling of presynaptic exocytosis and SV recycling at human synapses.

Binary and analog variation of synapses between cortical pyramidal neurons

Neocortical synaptic engrams for remote contextual memories

Astrocytes release glutamate by regulated exocytosis in health and disease Vladimir Parpura, International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, P.R. China Parpura will present you with the evidence that astrocytes, a subtype of glial cells in the brain, can exocytotically release the neurotransmitter glutamate and how this release is regulated. Spatiotemporal characteristic of vesicular fusion that underlie glutamate release in astrocytes will be discussed. He will also present data on a translational project in which this release pathway can be targeted for the treatment of glioblastoma, the deadliest brain cancer.

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord. A major function of TDP-43 is as a repressor of cryptic exon inclusion during RNA splicing. By re-analyzing RNA-sequencing datasets from human FTD/ALS brains, we discovered dozens of novel cryptic splicing events in important neuronal genes. Single nucleotide polymorphisms in UNC13A are among the strongest hits associated with FTD and ALS in human genome-wide association studies, but how those variants increase risk for disease is unknown. We discovered that TDP-43 represses a cryptic exon-splicing event in UNC13A. Loss of TDP-43 from the nucleus in human brain, neuronal cell lines and motor neurons derived from induced pluripotent stem cells resulted in the inclusion of a cryptic exon in UNC13A mRNA and reduced UNC13A protein expression. The top variants associated with FTD or ALS risk in humans are located in the intron harboring the cryptic exon, and we show that they increase UNC13A cryptic exon splicing in the face of TDP-43 dysfunction. Together, our data provide a direct functional link between one of the strongest genetic risk factors for FTD and ALS (UNC13A genetic variants), and loss of TDP-43 function. Recent analyses have revealed even further changes in TDP-43 target genes, including widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B) and providing evidence that alternative polyadenylation is a new facet of TDP-43 pathology.

Synaptic architecture of a memory engram in the mouse hippocampus

Join Us for the Memory Decoding Journal Club! A collaboration of the Carboncopies Foundation and BPF Aspirational Neuroscience. This time, we’re diving into a groundbreaking paper: "Motor learning selectively strengthens cortical and striatal synapses of motor engram neurons