Developmental Neuroscience

The 2026 symposium presents research by the foundation’s achievement-prize recipients. Steven A. Kushner discusses precision psychiatry and its remaining challenges; Andrew H. Miller examines an inflammatory subtype of depression; Cynthia Rogers explores how early experience affects brain development and children’s mental health; Sheena Josselyn addresses memory and engrams; and Christine Yu Moutier considers translating suicide-prevention science into action. Jeffrey Borenstein gives the welcome and Carol A. Tamminga moderates. The programme runs on 30 October from 09:30 to 12:30 EDT. Participants may attend at Kaufman Music Center, 129 West 67th Street, New York City, or virtually. Registration through the linked event portal requires an account and selection of attendance mode.

A Keystone Symposium connecting genetics, functional genomics, developmental neurobiology, and industry to identify convergent mechanisms and therapeutic opportunities in neurodevelopmental disorders.

This EMBO Workshop integrates developmental biology, sensory neuroscience, central circuits, motor control, behavior, population genetics, genomics, and ecology to advance comparative insect neuroscience. Early-career researchers are prioritized for selected talks, and all accepted participants present their work.

2024 BACN Early-Career Prize Lecture Many of our decisions affect other people. Our choices can decelerate climate change, stop the spread of infectious diseases, and directly help or harm others. Prosocial behaviours – decisions that help others – could contribute to reducing the impact of these challenges, yet their computational and neural mechanisms remain poorly understood. I will present recent work that examines prosocial motivation, how willing we are to incur costs to help others, prosocial learning, how we learn from the outcomes of our choices when they affect other people, and prosocial preferences, our self-reports of helping others. Throughout the talk, I will outline the possible computational and neural bases of these behaviours, and how they may differ from young adulthood to old age.

Cognitive processing requires directed interactions between several brain areas of the limbic system, such as the hippocampus (HP) and lateral entorhinal cortex (LEC). They are modulated by multiple sensory systems. During development, the olfactory system might have a particular impact on these areas in mice that at birth are blind, deaf, do not whisker and have poor motor abilities. We previously showed that neonatal olfactory activation boosts the oscillatory entrainment of LEC via mono-and polysynaptic projections from the olfactory bulb (OB). However, the long-lasting impact of olfactory inputs on the limbic function and cognitive abilities of later life is fully unknown. Thus, we chemogenetically decreased the synaptic outputs of mitral/tufted cells (M/TCs), the main projecting neurons in the OB, during postnatal days 8-10 and monitored the long-lasting consequences on the downstream areas LEC and HP, and on cognitive performance. In vivo extracellular recordings revealed that after the transient decrease of the olfactory output, the oscillatory activities of downstream areas were diminished along development, in line with the long-lasting decrease in the dendritic complexity of HP-projecting pyramidal neurons in LEC. Correspondingly, pre-juvenile mice experiencing early life manipulation had declined performance in cognitive tasks. These results indicate that the early olfactory processing before eye-opening might be critical for the functional development of cognitive abilities.

One of the most prominent features of the human brain is the fabulous size of the cerebral cortex and its intricate folding, both of which emerge during development. Over the last few years, work from my lab has shown that specific cellular and genetic mechanisms play central roles in cortex folding, particularly linked to neural stem and progenitor cells. Key mechanisms include high rates of neurogenesis, high abundance of basal Radial Glia Cells (bRGCs), and neuron migration, all of which are intertwined during development. We have also shown that primary cortical folds follow highly stereotyped patterns, defined by a spatial-temporal protomap of gene expression within germinal layers of the developing cortex. I will present recent findings from my laboratory revealing novel cellular and genetic mechanisms that regulate cortex expansion and folding. We have uncovered the contribution of epigenetic regulation to the establishment of the cortex folding protomap, modulating the expression levels of key transcription factors that control progenitor cell proliferation and cortex folding. At the single cell level, we have identified an unprecedented diversity of cortical progenitor cell classes in the ferret and human embryonic cortex. These are differentially enriched in gyrus versus sulcus regions and establish parallel cell lineages, not observed in mouse. Our findings show that genetic and epigenetic mechanisms in gyrencephalic species diversify cortical progenitor cell types and implement parallel cell linages, driving the expansion of neurogenesis and patterning cerebral cortex folds.

Focal Cortical Dysplasia (FCD) is the most common focal cortical malformation leading to intractable childhood focal epilepsy. In recent years, we and others have shown that FCD type II is caused by mosaic mutations in genes within the PI3K-AKT-mTOR-signaling pathway. Hyperactivation of the mTOR pathway accounts for neuropathological abnormalities and seizure occurrence in FCD. We further showed from human surgical FCDII tissue that epileptiform activity correlates with the density of mutated dysmorphic neurons, supporting their pro-epileptogenic role. The level of mosaicism, as defined by variant allele frequency (VAF) is thought to correlate with the size and regional brain distribution of the lesion such that when a somatic mutation occurs early during the cortical development, the dysplastic area is smaller than if it occurs later. Novel approaches based on the detection of cell-free DNA from the CSF and from trace tissue adherent to SEEG electrodes promise future opportunities for genetic testing during the presurgical evaluation of refractory epilepsy patients or in those that are not eligible for surgery. In utero-based electroporation mouse models allow to express somatic mutation during neurodevelopment and recapitulate most neuropathological and clinical features of FCDII, establishing relevant preclinical mouse models for developing precision medicine strategies.

Develop an independent neuroscience research programme as part of the Iowa Neuroscience Institute. The search spans neurodevelopment, neurodegeneration, neuroimmunology and cancer neuroscience, and is open at assistant, associate and full professor levels. Faculty contribute to research, teaching and collaborative scientific activity. The university states that applications will remain open until the positions are filled.