Arnaud Monteil

This paper develops an AI-driven drug discovery framework for NALCN channelopathy, identifying aprepitant as a lead therapeutic candidate through HTS, structural modeling, and experimental validation.

The paper shows that YEATS2 regulates calcium homeostasis in dopaminergic neurons, and its disruption leads to neuronal loss and behavioral deficits, which can be rescued by inhibiting Orai channels.

This study shows that NALCN deficiency preferentially affects GABAergic interneurons, reducing their intrinsic excitability and impairing contextual adaptation and spatial memory in mice.

The paper compares TMUV cluster 1 and 2 strains, finding cluster 2 has higher replication efficiency in human cells and induces stronger innate immune responses.

This study uses automated and manual patch-clamp techniques to analyze Cav3.1 channel variants, identifying gain- and loss-of-function properties linked to neurological disorders.

This study identifies the ancient eukaryotic origins and conservation of NALCN/Cch1 channelosome subunits across animals, fungi, and apusomonads.

This study investigates the role of dopamine D2 autoreceptors in regulating VTA dopamine neuron responses to aversive stimuli and finds they act as a regulatory brake with sex-biased effects on threat processing.

This study investigates the sex-specific effects of NALCN deletion in Drd2-expressing striatal spiny projection neurons, revealing sex differences in excitability and behavior.

This study identifies de novo NALCN mutations causing a new syndrome with congenital contractures, hypotonia, and developmental delay, distinct from known DA2A.