Abstract
Aversive learning and memories are crucial for animals to avoid previously encountered stressful stimuli and thereby increase their chance of survival. Neuropeptides are essential signaling molecules in the brain and are emerging as important modulators of learned behaviors, but their precise role is not well understood. Here, we show that neuropeptides of the evolutionarily conserved MyoInhibitory Peptide (MIP)-family modify salt chemotaxis behavior in Caenorhabditis elegans according to previous experience. MIP signaling, through activation of the G protein-coupled receptor SPRR-2, is required for short-term gustatory plasticity. In addition, MIP/SPRR-2 neuropeptide-receptor signaling mediates another type of aversive gustatory learning called salt avoidance learning that depends on de novo transcription, translation and the CREB transcription factor, all hallmarks of long-term memory. MIP/SPRR-2 signaling mediates salt avoidance learning in parallel with insulin signaling. These findings lay a foundation to investigate the suggested orphan MIP receptor orthologs in deuterostomians, including human GPR139 and GPR142.
Highlights
In a dynamic environment animals have to adapt their choices and behavioral responses according to previous experiences to increase their chances of survival
We found that the C. elegans receptor SPRR-2 and its ligands, the MyoInhibitory Peptide (MIP)-1 neuropeptides— which are members of the evolutionarily conserved myoinhibitory peptide system—are required for aversive gustatory learning
To test our hypothesis that MIP signaling mediates learning in C. elegans, we examined lossof-function mutants of the three MIP receptor orthologs for their performance in an established associative learning test for gustatory plasticity [11,12,13]
Summary
In a dynamic environment animals have to adapt their choices and behavioral responses according to previous experiences to increase their chances of survival. Animals evolved the ability to learn and generate memories through associative and non-associative neural mechanisms [1,2]. Knowledge on the molecular pathways underlying learning and memory is essential to uncover the complex regulation of experience-dependent plasticity in neural circuits and its decline with age or in associated diseases. Studies in invertebrate model systems, such as Aplysia, have been vital to our current knowledge on the molecular basis of learning and memory [1,3]. Caenorhabditis elegans has become a popular model for uncovering genes and mechanisms of circuit plasticity that regulate learning and memory [2,5]. C. elegans shows associative and non-associative learning in response to a variety of sensory cues and can form both short-term and long-term memories [2,7]
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