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Coexpressed D1- And D2-Like Dopamine Receptors Antagonistically Modulate Acetylcholine Release In Caenorhabditis Elegans., Andrew T. Allen, Kathryn N. Maher, Khursheed A. Wani, Katherine E. Betts, Daniel Chase
Coexpressed D1- And D2-Like Dopamine Receptors Antagonistically Modulate Acetylcholine Release In Caenorhabditis Elegans., Andrew T. Allen, Kathryn N. Maher, Khursheed A. Wani, Katherine E. Betts, Daniel Chase
Daniel Chase
Dopamine acts through two classes of G protein-coupled receptor (D1-like and D2-like) to modulate neuron activity in the brain. While subtypes of D1- and D2-like receptors are coexpressed in many neurons of the mammalian brain, it is unclear how signaling by these coexpressed receptors interacts to modulate the activity of the neuron in which they are expressed. D1- and D2-like dopamine receptors are also coexpressed in the cholinergic ventral-cord motor neurons of Caenorhabditis elegans. To begin to understand how coexpressed dopamine receptors interact to modulate neuron activity, we performed a genetic screen in C. elegans and isolated mutants defective in …
A Specific Subset Of Transient Receptor Potential Vanilloid-Type Channel Subunits In Caenorhabditis Elegans Endocrine Cells Function As Mixed Heteromers To Promote Neurotransmitter Release, Antony M. Jose, Amy Bany, Daniel Chase, Michael R. Koelle
A Specific Subset Of Transient Receptor Potential Vanilloid-Type Channel Subunits In Caenorhabditis Elegans Endocrine Cells Function As Mixed Heteromers To Promote Neurotransmitter Release, Antony M. Jose, Amy Bany, Daniel Chase, Michael R. Koelle
Daniel Chase
Transient receptor potential (TRP) channel subunits form homotetramers that function in sensory transduction. Heteromeric channels also form, but their physiological subunit compositions and functions are largely unknown. We found a dominant-negative mutant of the C. elegans TRPV (vanilloid-type) subunit OCR-2 that apparently incorporates into and inactivates OCR-2 homomers as well as heteromers with the TRPV subunits OCR-1 and -4, resulting in a premature egg-laying defect. This defect is reproduced by knocking out all three OCR genes, but not by any single knockout. Thus a mixture of redundant heteromeric channels prevents premature egg laying. These channels, as well as the G-protein …