The abstract is read at the publisher; the summary is JClub's.
Overexpressing nlp-58 in Caenorhabditis elegans causes abnormal thermotaxis behavior without disrupting thermosensory neuron temperature responses, implicating conserved tachykinin signaling.
- Why it matters: Mammalian NKB signaling is linked to thermoregulatory dysfunction in menopause, but the neural circuit mechanisms are not fully defined.
- What they did: The authors used a genetically tractable thermotaxis assay, mapped nlp-58 expression to multiple neurons including AIY, and tested neuron-specific overexpression and receptor genetics, focusing on TKR-1.
- The result: Thermotaxis defects are mediated mainly by TKR-1 acting in ASG and/or ASJ sensory neurons, interact with dhs-4, decline with age via endogenous NLP-58/TKR-1 signaling, and are partially improved by fezolinetant.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.