The proper functioning of neocortical circuits is central for sensory information processing, motor command, language, memory storage, cognition, and behavior. Neocortical circuits are composed of a great variety of neurons that receive information from hundreds-to-thousands other neurons belonging to many different brain regions, integrate (and perhaps store) this information, and then pass it on to numerous other connected neurons. Thus, the specific connections and the integrative properties of neurons are central to the operation of neocortical circuits. Both are malleable features that have been demonstrated to be altered by activity, during plasticity, or in physiopathological conditions. Consequently, their plastic modification or pathological alteration may change the operation of neocortical circuits and contribute to memory formation and neurological/psychiatric disorders.
Our research program aims at gaining a better understanding of the operation of neocortical circuits. To tackle this issue, we examine the connectivity of specific neocortical neuron types and their intrinsic excitability, and study the role of plastic modifications of these features for memory formation, as well as of their pathological alterations in autism spectrum disorders. Our ultimate goal is to find core mechanisms for the functioning or dysfunction of neocortical circuits and to provide a causal link between these mechanisms and cognitive abilities/behavior.
To address these questions we focus on the sensory and prefrontal cortex circuits of mice. To define neurons engaged in specific memory tasks, and to study the cellular and circuit mechanisms of autism spectrum disorders, we employ transgenic mice. In addition, we employ in vitro/in vivo single-cell and multi-electrode electrophysiological as well as calcium imaging approaches, opto-/chemogenetic approaches, viral tracing, whole-brain imaging and quantification of connectivity, and behavioral tasks.
Autism spectrum disorders (ASD) are a set of complex neurodevelopmental disorders for which there is currently no targeted therapeutic approach. It is thought that alterations of genes regulating migr
Metabotropic glutamate receptor subtype 5 (mGluR5) is crucially implicated in the pathophysiology of Fragile X Syndrome (FXS); however, its dysfunction at the sub-cellular level, and related synaptic
In fragile X syndrome (FXS), sensory hypersensitivity and impaired habituation is thought to result in attention overload and various behavioral abnormalities in reaction to the excessive and remanent
Fragile X syndrome (FXS) is a developmental disorder caused by a mutation in the X-linked FMR1 gene, coding for the FMRP protein which is largely involved in synaptic function. FXS patients present se
The function of cortical GABAergic interneurons is largely determined by their integration into specific neural circuits, but the mechanisms controlling the wiring of these cells remain largely unknow
