Abstract
Co-localization and co-transmission of neurotransmitters and neuropeptides is a core property of neural signaling across species. While co-transmission can increase the flexibility of cellular communication, understanding the functional impact on neural dynamics and behavior remains a major challenge. Here we examine the role of neuropeptide/monoamine co-transmission in the orchestration of the C. elegans escape response. The tyraminergic RIM neurons, which coordinate distinct motor programs of the escape response, also co-express the neuropeptide encoding gene flp-18. We find that in response to a mechanical stimulus, flp-18 mutants have defects in locomotory arousal and head bending that facilitate the omega turn. We show that the induction of the escape response leads to the release of FLP-18 neuropeptides. FLP-18 modulates the escape response through the activation of the G-protein coupled receptor NPR-5. FLP-18 increases intracellular calcium levels in neck and body wall muscles to promote body bending. Our results show that FLP-18 and tyramine act in different tissues in both a complementary and antagonistic manner to control distinct motor programs during different phases of the C. elegans flight response. Our study reveals basic principles by which co-transmission of monoamines and neuropeptides orchestrate in arousal and behavior in response to stress.
Highlights
Co-localization of classical neurotransmitters and neuropeptides is a common feature of the animal nervous system [1]
It is commonly found in nervous systems across species that monoamines and neuropeptides are co-released and affect the properties of target cells
Adrenaline and neuropeptide Y are co-released from sympathetic neurons where they increase blood pressure and heart rate during the fight-or-flight response
Summary
Co-localization of classical neurotransmitters and neuropeptides is a common feature of the animal nervous system [1]. Studies in mammals have shown that the stress related modulatory functions of NPY and NA co-transmission are complex, with complementary actions in some tissues and antagonistic actions in others. Both NA and NPY increase blood pressure through peripheral vasoconstriction, NPY inhibits presynaptic NA release from sympathetic neurons and opposes the action of NA on cardiac contraction [9–19]. Unraveling the precise effects of co-transmission of neural stress hormones is very challenging in vertebrates given the complexity of the nervous system, the multiple central and peripheral release sites and the diversity of target tissues expressing NA and NPY receptor (NPYR) subtypes
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