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Ender, A.

Publications and source records attributed to Ender, A..

2 recordsLinked to original sources

A novel enteric pacemaker activity in Drosophila

Enteric organs such as the gut and stomach display the intrinsic ability to generate slow-wave potentials, rhythmic electrochemical events acting as key regulators of gastrointestinal motility. In mammals, slow waves occur as a result of the pacemaker activity of Interstitial Cells of Cajal (ICCs) which, by recruiting visceral muscles, ultimately lead to peristalsis. Here, we uncover and characterize a novel mechanism in Drosophila by which the midgut is able to generate strong muscular whip-like contractions. This pacemaker activity, here named superstalsis, is only active at certain physiological conditions and is selectively linked to longitudinal visceral muscle activation. Furthermore, we identify in Subdued, an ortholog gene of the ANO1/TMEM16A family, a marker for peristalsis in Drosophila, specifically associated with circular muscle activity. As fasting and bacterial infections cause specific changes in the intestinal motility profiles in vivo, we propose that the gut can autonomously alter the peristalsis/superstalsis balance to efficiently respond to diverse pathological and homeostatic events.

physiology↗

Network-specific synchronization of electrical slow-wave oscillations regulates sleep in Drosophila

Slow-wave rhythms characteristic of deep sleep oscillate in the delta band (0.5-4 Hz) and can be found across various brain regions in vertebrates. Across systems it is however unclear how oscillations arise and whether they are the causal functional unit steering behavior. Here, for the first time in any invertebrate, we discover sleep-relevant delta oscillations in Drosophila. We find that slow-wave oscillations in the sleep-regulating R2 network increase with sleep need. Optical multi-unit voltage recordings reveal that single R2 neurons get synchronized by sensory and circadian input pathways. We show that this synchronization depends on NMDA receptor (NMDARs) coincidence detector function and on an interplay of cholinergic and glutamatergic inputs setting a resonance frequency. Genetically targeting the coincidence detector function of NMDARs in R2, and thus the uncovered mechanism underlying synchronization, abolished network-specific slow-wave oscillations. It also disrupted sleep and facilitated light-induced wakening, directly establishing a causal role for slow-wave oscillations in regulating sleep and sensory gating. We therefore propose that the synchronization-based increase in oscillatory power likely represents an evolutionarily conserved, potentially optimal, strategy for constructing sleep-regulating sensory gates.

neuroscience↗