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Heim, M.-M.

Publications and source records attributed to Heim, M.-M..

3 recordsLinked to original sources

Avoidance engages dopaminergic punishment in Drosophila

It was classically suggested that behaviour can cause emotions (Darwin 1872). For example, smiling can make us feel happier, and in rodents the induced patterns of cardiac activity and breathing that are indicative of fear can in turn evoke it (Coles et al. 2022, Hsueh et al. 2023, Jhang et al. 2024). However, the adaptive significance of such feedback is unclear. We show that inducing backward movement, an element of avoidance behaviour in Drosophila, engages negative valence signals in these animals, and reveal the neuronal mechanisms and adaptive significance of this effect. We develop a paradigm with odours as conditioned stimuli paired with optogenetically induced backward movement instead of a punishing unconditioned stimulus, and combined these experiments with pharmacology, high-resolution video tracking, functional imaging, connectome analyses, and modelling. Our results show that backward movement engages dopaminergic punishment neurons and supports aversive memories. Such avoidance-to-punishment feedback counterbalances extinction learning and maintains learned avoidance, reducing the risk of further punishment. This can explain the long-standing "avoidance paradox", the observation that avoidance adaptively persists even when it is successful and no punishment is received (Bolles 1972). Our results provide a neurobiologically grounded argument for an integrated view of behaviour organization and valence processing.

neuroscience↗

Postsynaptic plasticity of cholinergic synapses underlies the induction and expression of appetitive memories in Drosophila

In vertebrates, several forms of memory-relevant synaptic plasticity involve postsynaptic rearrangements of glutamate receptors. In contrast, previous work indicates that Drosophila and other invertebrates store memories using presynaptic plasticity of cholinergic synapses. Here, we provide evidence for postsynaptic plasticity at cholinergic output synapses from the Drosophila mushroom bodies (MBs). We find that the nicotinic acetylcholine receptor (nAChR) subunit 5 is required within specific MB output neurons (MBONs) for appetitive memory induction, but is dispensable for aversive memories. In addition, nAChR 2 subunits mediate memory expression and likely functions downstream of 5 and the postsynaptic scaffold protein Dlg. We show that postsynaptic plasticity traces can be induced independently of the presynapse, and that in vivo dynamics of 2 nAChR subunits are changed both in the context of associative and non-associative memory formation, underlying different plasticity rules. Therefore, regardless of neurotransmitter identity, key principles of postsynaptic plasticity support memory storage across phyla.

neuroscience↗

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↗