Dopamine Signaling Architecture in Caenorhabditis elegans
PW McDonald, T Jessen, JR Field… - Cellular and molecular …, 2006 - Springer
PW McDonald, T Jessen, JR Field, RD Blakely
Cellular and molecular neurobiology, 2006•Springer1. Aims: In this review, we highlight the identification and analysis of molecules orchestrating
dopamine (DA) signaling in the nematode Caenorhabditis elegans, focusing on recent
characterizations of DA transporters and receptors. 2. Methods: We illustrate the isolation
and characterization of molecules important for C. elegans DA synthesis, packaging,
reuptake and signaling and examine how mutations in these proteins are being exploited
through in vitro and in vivo paradigms to yield novel insights of protein structure, DA …
dopamine (DA) signaling in the nematode Caenorhabditis elegans, focusing on recent
characterizations of DA transporters and receptors. 2. Methods: We illustrate the isolation
and characterization of molecules important for C. elegans DA synthesis, packaging,
reuptake and signaling and examine how mutations in these proteins are being exploited
through in vitro and in vivo paradigms to yield novel insights of protein structure, DA …
1. Aims: In this review, we highlight the identification and analysis of molecules orchestrating dopamine (DA) signaling in the nematode Caenorhabditis elegans, focusing on recent characterizations of DA transporters and receptors.
2. Methods: We illustrate the isolation and characterization of molecules important for C. elegans DA synthesis, packaging, reuptake and signaling and examine how mutations in these proteins are being exploited through in vitro and in vivo paradigms to yield novel insights of protein structure, DA signaling pathways and DA-supported behaviors.
3. Results: DA signaling in the worm, as in man, arises by synaptic and nonsynaptic release from a small number of cells that exert modulatory control over a larger network underlying C. elegans behavior.
4. Conclusions: The C. elegans model system offers unique opportunities to elucidate ill-defined pathways that support DA release, inactivation, and signaling in addition to clarifying mechanisms of DA-mediated behavioral plasticity. Further use of the model offers prospects for the identification of novel genes and proteins whose study may yield benefits for DA-supported neural disorders in man.
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