An intestinal gap-junction protein is needed for normal acetylcholine response in Caenorhabditis elegans
The Caenorhabditis elegans (C. elegans) nervous system is understood in detail, yet predicting the behavior it controls is challenging. Dynamic regulation of the nervous system may be caused by neuromodulators released in response to calcium. In the C. elegans intestine, a calcium wave regulates peptide release that triggers muscle contractions associated with defecation. Intestinal calcium waves require gap junctions that include the innexin-16 (inx-16) subunit for normal propagation and patterning. Upon observing that inx-16 mutants exhibit abnormal movement, we hypothesize that calcium-triggered peptide release from the intestine regulates locomotory circuits. We determined the relationship between an intestinal calcium wave and locomotion signaling by assessing neurotransmission rates in the intestinal calcium wave mutant, inx-16. Two assays of acetylcholine responsiveness, one using an acetylcholine agonist and the other an acetylcholinesterase inhibitor, were performed in the inx-16 mutant. The results suggest a pre-synaptic deficit in acetylcholine release. We propose that peptides released in response to intestinal calcium waves acts as neuromodulators of acetylcholine-based neurotransmission. Our study suggests a connection between defecation-related signaling and nervous system function.
Moore, Gabriel, Phoebe Hammer, and Maureen Peters. 2014. "An intestinal gap-junction protein is needed for normal acetylcholine response in Caenorhabditis elegans." FASEB Journal 28(1): 1129.8.
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