István Katona

This study investigates how prenatal cannabinoid exposure affects endocannabinoid-mediated synaptic plasticity in dopamine neurons, revealing a switch to nitric oxide signaling that alters excitatory and inhibitory plasticity.

The paper introduces fluorescent activity-based probes to map MAGL activity in brain tissues, revealing its spatial distribution in mouse and human brains.

The paper identifies nanoscale synaptic remodeling at corticostriatal circuits that predicts flexible action control and shows its absence in aging and rigidity.

This study shows that CB1 agonists like CP55,940 and THC cause respiratory depression in awake mice, contradicting previous beliefs about their minimal respiratory impact.

The paper proposes an on-demand release model for endocannabinoid 2-AG via microvesicles, showing stimulus-dependent release regulated by PKC, DAGL, and Arf6.

This study shows that prenatal THC exposure in male rats increases vulnerability to addiction-like behaviors by enhancing cue-driven dopamine responses and striatal encoding during reward seeking.

This study shows that genetic deletion of NAPE-PLD in mice leads to anxiety-like behaviors and context-dependent dysregulation of the HPA axis, with sex-specific effects on corticosterone levels.

This study identifies somatic purinergic junctions between microglia and developing neurons across developmental stages, suggesting they facilitate communication and regulation of neurogenesis.

The paper identifies ABHD4 as a mediator of developmental anoikis that protects the prenatal brain from pathological insults by eliminating abnormally detached progenitor cells.

The paper identifies specialized somatic microglia-neuron junctions that enable microglia to monitor and protect neuronal function through purinergic signaling.