The electrical silencing of pacemaker neurons cause reversible disruption of circadian locomotor activity in Drosophila melanogaster.

A DEPETRIS CHAUVIN; J BERNI; EJ ARANOVICH; MF CERIANI

Casa Serrana, Huerta Grande, Córdoba

Congreso; I Reunión Conjunta de Neurociencias; 2009

TAN, SAN

Circadian rhythms regulate differents aspect of physiology and behavior, based on self-sustaining transcriptional feedback loops of clock genes. Over 150 neurons are implicated in circadian regulation of locomotor behavior in the fly brain but the small ventral lateral neurons (sLNvs) are at the top of the hierarchy. The preservation of molecular oscilation specifically in the sLNvs is necessary to command rhythmic behavior. The sLNvs express the neuropeptide PIGMENT DISPERSING FACTOR (PDF). Rhythmic release of PDF is thought to be important for the transmission of time information; daily structural changes of axonal terminals of this circuit might be relevant too. Electrical activity of PDF neurons is also required for rhythmicity. Silencing PDF neurons by expressing a K+ channel (KIR) during the lifetime leads to behavioral arrythmicity and blocks molecular oscillations in the sLNvs. To study this process avoiding developmental defects that might interfere with the analysis, we developed a new tool for temporal control of gene expression in PDF neurons. Silencing the PDF circuit only during the adult stage led to behavioral arrythmicity as previously described. Surprisingly, once kir expression was shut down, flies recovered rhythmicity in a phase reminiscent to that of the initial training. PERIOD oscillations in the sLNvs showed that the molecular clock remained intact through the silenced phase, supporting that arrhythmicity is a consequence of the incapability of these neurons to transmit information rather than an effect on the clock. Thus, electrical silencing could be directly affecting structural plasticity of PDF terminals, consequently changing the synaptic partners, and finally impacting circadian behavior.