bioRxiv Science⌕ Search

Biology subjects

Dimtsi, A.

Publications and source records attributed to Dimtsi, A..

2 recordsLinked to original sources

Mating proximity blinds threat perception.

Romantic engagement can bias sensory perception. This love blindness reflects a common behavioral principle across organisms: favoring pursuit of a coveted reward over potential risks. In the case of animal courtship, such sensory biases may support reproductive success but can also expose individuals to danger, such as predation. How do neural networks balance the trade-off between risk and reward? Here, we discover a dopamine-governed filter mechanism in male Drosophila that reduces threat perception as courtship progresses. We show that during early courtship stages, threat-activated visual neurons inhibit central courtship nodes via specific serotonergic neurons. This serotonergic inhibition prompts flies to abort courtship when they see imminent danger. However, as flies advance in the courtship process, the dopaminergic filter system reduces visual threat responses, shifting the balance from survival to mating. By recording neural activity from males as they approach mating, we demonstrate that progress in courtship is registered as dopaminergic activity levels ramping up. This dopamine signaling inhibits the visual threat detection pathway via Dop2R receptors, allowing male flies to focus on courtship when they are close to copulation. Thus, dopamine signaling biases sensory perception based on perceived goal proximity, in order to prioritize between competing behaviors.

neuroscience↗

Altered synaptic connectivity in an in vitro human model of STXBP1 encephalopathy

Early infantile developmental and epileptic encephalopathies are devastating conditions, generally of genetic origin, but the pathological mechanisms often remain obscure. A major obstacle in this field of research is the difficulty of studying cortical brain development in humans, in utero. To address this, we established an in vitro assay to study the impact of gene variants on the developing human brain, using living organotypic cultures of the human subplate and neighbouring cortical regions, prepared from ethically sourced, 14-17 post conception week brain tissue (www.hdbr.org). We were able to maintain cultures for several months, during which time, the gross anatomical structures of the cortical plate, subplate and marginal zone persisted, while neurons continued to develop morphologically, and form new synaptic networks. This preparation thus permits the study of genetic manipulations, and their downstream effects upon an intact developing human cortical network. We focused upon STXBP1 haploinsufficiency, which is among the most common genetic causes of developmental and epileptic encephalopathy. This was induced using shRNA interference, leading to impaired synaptic function and a drop in the number of glutamatergic synapses. We thereby provide a critical proof-of-principle for how to study the impact of any gene of interest on the development of the human cortex.

neuroscience↗