IBIOBA - MPSP   22718
INSTITUTO DE INVESTIGACION EN BIOMEDICINA DE BUENOS AIRES - INSTITUTO PARTNER DE LA SOCIEDAD MAX PLANCK
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Glycinergic feedback inhibition shapes circadian oscillation in membrane potential of Drosophila clock neurons
Autor/es:
FLORENCIA FERNANDEZ-CHIAPPE; LIA FRENKEL; NARA I. MURARO; JOSE M DUHART; M FERNANDA CERIANI
Lugar:
Colonia del Sacramento
Reunión:
Congreso; XV Latin American Symposium on Chronobiology; 2019
Institución organizadora:
Latin American Symposium on Chronobiology Organizing Committee
Resumen:
The engagement of glycinergic transmission within the circadian network of Drosophila was recently unveiled. Glycine contributes to the synchronization of the circadian network alongside PDF. The impairment of glycine-mediated communication through Glycine Receptor (GlyR) downregulation in non-LNv clusters results in changes in circadian period and rhythmicity. Here we address the influence of glycine communication to the LNvs. Glycine silences action potential firing in both s- and l-LNvs clock neurons. Additionally, circadian changes in PDF-dependent sLNv architecture involves glycinergic inhibition. Several features of the temporal organization of locomotor behavior associated to the sLNvs require proper glycinergic transmission, i.e. morninganticipation under LD cycles, as well as period length and consolidation of locomotor activity under free running condition. In addition, glycinergic inhibition contributes to PDF oscillation in the dorsal projections. Hence PDF overexpression partially rescues all circadian phenotypes. Interestingly,the sLNv membrane potential gradually shifts along the day and glycine participates in its regulation. We further show that the distribution of GlyR clusters at the dorsal projections is time-of-day dependent suggesting that, in addition to a clock-control of excitability, non-cell autonomous extrinsic signals such as glycine, are recruited. Given that the LNs themselves releaseglycine it is tempting to speculate that this represents a membrane-based negative feedback loop.