Adult-specific electrical silencing of pacemaker neurons uncouples

CERIANI, MF

Destin, Florida

Congreso; XII Meeting of the Society for Biological Rhythms; 2010

Society for Biological Rhythms

Circadian rhythms regulate different aspects of physiology and behavior by means of self-sustained 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 clearly crucial. The preservation of molecular oscillations within the sLNvs is sufficient to command rhythmic behavior under free running conditions. The s-LNvs transmit this time information releasing a neuropeptide known as pigment dispersing factor (PDF), and likely changing synaptic partners by remodeling their axonal terminals in a circadian fashion. 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 gain insight into this process avoiding developmental defects 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 inability of these neurons to transmit information rather than an effect on the clock. Accordingly, both the complexity of the axonal terminals as well as PDF accumulation were severely affected during the silenced phase, suggesting that changes in the s-LNvs membrane potential impact additional processes as opposed to directly influence molecular oscillations.