I would like to cordially invite you to the habilitation lecture which will take place on the 11th of June at 3pm in the Konorski lecture hall. We will host dr Monika Bijata (Laboratory of Cell Biophysics, Nencki Institute of Experimental Biology, PAS). Her habilitation is processed by the Scientific Council of the Nencki Institute of Experimental Biology, Polish Academy of Sciences. She will give a lecture entitled: “The role of selected serotonin receptors in synaptic plasticity underlying stress-related diseases”

Abstract:

In my talk, I will present research on the roles of three serotonin receptors—5-HT1AR, 5-HT4R, and 5-HT7R—in neuronal signaling and the development of depressive-like behaviors. These receptors, coupled with different G proteins, affect various effector proteins and signaling pathways. Activation of 5-HT7R, coupled with Gαs and Gα12 proteins, has a pro-depressive effect by increasing MMP-9 activity in the hippocampus, leading to spine remodeling and depressive-like behaviors. Silencing 5-HT7R expression in the CA1 hippocampal subregion prevents anhedonia under chronic stress. Additionally, modulation of NMDAR activity, an effector of the 5-HT7R/MMP-9 pathway, using Nitrosynapsin reverses chronic stress-induced pathological changes. Conversely, activation of 5-HT1AR, coupled with Gαi protein, alleviates depressive symptoms. Palmitoylation of 5-HT1AR is essential for proper signal transmission. Reduced palmitoylation in the prefrontal cortex (PFC) is observed in anhedonic animals and depressed humans who committed suicide. Activation of 5-HT4R, coupled with Gαs and Gα13 proteins, also exhibits an antidepressant effect. Stimulation of 5-HT4R leads to dendritic spine maturation through Gα13 protein and RHOA activation, increasing active synapses and neuronal excitability. This process is dependent on ROCK kinase, activated by RHOA GTPase. My research highlights the complex roles of these serotonin receptors in depressive-like behaviors and synaptic plasticity, providing insights for understaiding in pathopsysiology of depression.