A5000638413- Photoreceptor and optogenetics research
- Cellular transport and secretion
- Congenital heart defects research
- Phosphodiesterase function and regulation
- Functional Brain Connectivity Studies
- Congenital Heart Disease Studies
- Neural dynamics and brain function
- Genetics and Neurodevelopmental Disorders
- Receptor Mechanisms and Signaling
- Neuroscience and Neuropharmacology Research
Center for Neuroscience and Cognitive Systems
2022-2025
Italian Institute of Technology
2022-2025
University of Trento
2022-2025
Amsterdam Neuroscience
2019
Abstract While shaped and constrained by axonal connections, fMRI-based functional connectivity reorganizes in response to varying interareal input or pathological perturbations. However, the causal contribution of regional brain activity whole-brain fMRI network organization remains unclear. Here we combine neural manipulations, resting-state vivo electrophysiology probe how inactivation a cortical node causally affects brain-wide coupling mouse. We find that chronic inhibition medial...
Chromosome 22q11.2 deletion increases the risk of neuropsychiatric disorders like autism and schizophrenia. Disruption large-scale functional connectivity in 22q11 syndrome (22q11DS) has been widely reported, but biological factors driving these changes remain unclear. We used a cross-species design to uncover developmental trajectory neural underpinnings brain dysconnectivity 22q11DS. In LgDel mice, model for 22q11DS, we found age-specific patterns dysconnectivity, with widespread fMRI...
Abstract Chromosome 22q11.2 deletion is among the strongest known genetic risk factors for neuropsychiatric disorders, including autism and schizophrenia. Brain imaging studies have reported disrupted large-scale functional connectivity in people with 22q11 syndrome (22q11DS). However, significance biological determinants of these alterations remain unclear. Here, we use a cross-species design to investigate developmental trajectory neural underpinnings brain dysconnectivity 22q11DS. We find...
Abstract To support frequency-coded information transfer, mammalian synapses tightly synchronize neurotransmitter release to action potentials (APs). However, desynchronizes during AP trains, especially at room temperature. Here we show that suppression of asynchronous by Synaptotagmin-1 (Syt1), but not triggering, is highly temperature sensitive, and enhances synchronous high-frequency stimulation. In Syt1-deficient synapses, increased with temperature, opposite wildtype synapses. Mutations...