Devon A. Thompson

Eli Lilly and Company; San Diego CA, United States of America

Dawn A Thompson

Broad Institute of MIT and Harvard; Cambridge MA, United States of America

Picture from Krause MW et al. (1997) Development "A C. elegans E/Daughterless bHLH protein marks neuronal but not striated muscle ...."

Figure 3. CeE/DA antibody-positive pharyngeal nuclei. (A) Exploded view of the pharynx showing the location of muscle cell groups (pm1-8) (from Albertson and Thompson, 1975). (B) Abbreviated cell lineage diagram showing the origin of posterior pharyngeal nuclei relative to the founder blastomeres (AB, MS, E, C, D and P4). CeE/DA-positive nuclei are indicated by bold type; smaller, normal type indicates similar nuclei that are undetectable with the antibody. For pm5, CeE/DA-positive nuclei are AB descendants and negative nuclei are MS descendants. For g1 and g2 nuclei, no clear lineage distinction exists for CeE/DA-positive versus -negative nuclei.

Da nucleus

nucleus of pedigree Da

dopaminergic neuron

Neuron that uses dopamine (DA) as a neurotransmitter.

McDonald PW et al. (2006) Cell Mol Neurobiol "Dopamine signaling architecture in Caenorhabditis elegans."

Jessen T, McDonald PW, Blakely RD, Field JR

[Cell Mol Neurobiol, 2006]

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.

AVDL

Ventral cord interneuron, synapses onto VA, DA, AS motorneurons; formerly called delta.

AVDR

Ventral cord interneuron, synapses onto VA, DA, AS motorneurons; formerly called delta.

Y38A8.4 : hmr-1 : ulp-2

mild hmr-1 RNAi (feeding with diluted bacteria) caused severe epidermal phenotypes and embryonic arrest of ulp-2(gk916250) hypomorph (Thompson et al., 2013), which otherwise developed normally.

Bernhard N et al. (2000) Learn Mem "A behavioral and genetic dissection of two forms of olfactory plasticity in Caenorhabditis elegans: adaptation and habituation."

Bernhard N, van der Kooy D

[Learn Mem, 2000]

Continuous presentation of an olfactory stimulus causes a decrement of the chemotaxis response in the nematode Caenorhabditis elegans. However, the differences between the learning process of habituation (a readily reversible decrease in behavioral response) and other types of olfactory plasticity such as adaptation (a decrement in response due to sensory fatigue, which cannot be dishabituated) have not been addressed. The volatile odorant diacetyl (DA) was used within a single paradigm to assess the distinct processes of olfactory adaptation and habituation. Preexposing and testing worms to 100% DA vapors caused a chemotaxis decrement that was not reversible despite the presentation of potentially dishabituating stimuli. This DA adaptation was abolished in worms with an odr-10 mutation (encoding a high-affinity DA receptor on the AWA neuron), even though naive chemotaxis remained unaffected. Conversely, DA adaptation remained intact in odr-1 mutants (defective in AWC neuron-mediated olfactory behavior), even though naive chemotaxis to DA decreased. Surprisingly, exposure to vapors of intermediate concentrations of DA (0.01% and 25%) did not cause worms to exhibit any response decrement. In contrast to preexposure to high DA concentrations, preexposure to low DA concentrations (0.001%) produced habituation of the chemotaxis response (a dishabituating stimulus could reverse the response decrement back to baseline levels). The distinct behavioral effects produced by DA preexposure highlight a concentration-dependent dissociation between two decremental olfactory processes: adaptation at high DA concentrations versus habituation at low DA concentrations.