Role of the ATP receptor P2X7 in experimental schizophrenia: a focus onprefrontal microglia
Visitor at the Laboratory of Neuronal Excitability, ACHUCARRO
Contemporary psychiatry identifies at the core of schizophrenia the progressive decline of social skills and cognitive abilities, symptoms displaying quintessential resistance to the available treatments. The deterioration of the dorso-lateral prefrontal cortex plays a central role in the paradigmatic downfall of working memory in schizophrenic individuals.
Research on extracellular ATP-signaling in rodent's models of psychiatric conditions is suggesting new pathways with potential to counteract cognitive-like symptoms. The purinergic receptor P2X7 (P2X7R) ontologically refers to immunological functions in the body and brain, where it is coherently expressed by hematopoietically derived microglia. Microglial cells, in turn, are driven and controlled by extracellular purines.
I will discuss selected results from our recent publication entitled "P2X7 Receptor-Dependent Layer-Specific Changes in Neuron-Microglia Reactivity in the Prefrontal Cortex of a Phencyclidine Induced Mouse Model of Schizophrenia", product of a fruitful collaboration between my PhD host lab of Beata Sperlàgh in Budapest and at Achucarro. Once introduced the murine pharmacological models adopted in the study and the impact of the P2X7R functional expression, the focus will narrow on the microglia-neuron interactions in the medial prefrontal cortex, questioning the role of P2X7R in the maintenance of homeostatic conditions.