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      Conserved role of dopamine in the modulation of behavior

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          Abstract

          Dopamine is an ancient signaling molecule. It is responsible for maintaining the adaptability of behavioral outputs and is found across taxa. The following is a summary of the role of dopamine and the mechanisms of its function and dysfunction. We discuss our recent findings on dopaminergic control of behaviors in C. elegans and discuss its potential implications for work in the fields of C. elegans and Parkinson research.

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          Most cited references89

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          Modulation of intracellular cyclic AMP levels by different human dopamine D4 receptor variants.

          To investigate whether polymorphic forms of the human dopamine D4 receptor have different functional characteristics, we have stably expressed cDNAs of the D4.2, D4.4, and D4.7 isoforms in several cell lines. Chinese hamster ovary CHO-K1 cell lines expressing D4 receptor variants displayed pharmacological profiles that were in close agreement with previous data from transiently expressed D4 receptors in COS-7 cells. Dopamine stimulation of the D4 receptors resulted in a concentration-dependent inhibition of the forskolin-stimulated cyclic AMP (cAMP) levels. The potency of dopamine to inhibit cAMP formation was about twofold reduced for D4.7 (EC50 of approximately 37 nM) compared with the D4.2 and D4.4 variants (EC50 of approximately 16 nM). Antagonists block the dopamine-mediated inhibition of cAMP formation with a rank order of potency of emonapride > haloperidol = clozapine > raclopride. There was no obvious correlation between the efficacy of inhibition of forskolin-stimulated cAMP levels and the D4 subtypes. Dopamine could completely reverse prostaglandin E2-stimulated cAMP levels for all three D4 receptor variants. Deletion of the repeat sequence does not affect functional activity of the receptor. The data presented indicate that the polymorphic repeat sequence causes only small changes in the ability of the D4 receptor to block cAMP production in CHO cells.
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            Neurotoxin-induced degeneration of dopamine neurons in Caenorhabditis elegans.

            Parkinson's disease is a complex neurodegenerative disorder characterized by the death of brain dopamine neurons. In mammals, dopamine neuronal degeneration can be triggered through exposure to neurotoxins accumulated by the presynaptic dopamine transporter (DAT), including 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium. We have established a system for the pharmacological and genetic evaluation of neurotoxin-induced dopamine neuronal death in Caenorhabditis elegans. Brief (1 h) exposure of green fluorescent protein-tagged, living worms to 6-OHDA causes selective degeneration of dopamine neurons. We demonstrate that agents that interfere with DAT function protect against 6-OHDA toxicity. 6-OHDA-triggered neural degeneration does not require the CED-3/CED-4 cell death pathway, but is abolished by the genetic disruption of the C. elegans DAT.
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              A C. elegans stretch receptor neuron revealed by a mechanosensitive TRP channel homologue.

              The nematode Caenorhabditis elegans is commonly used as a genetic model organism for dissecting integration of the sensory and motor systems. Despite extensive genetic and behavioural analyses that have led to the identification of many genes and neural circuits involved in regulating C. elegans locomotion behaviour, it remains unclear whether and how somatosensory feedback modulates motor output during locomotion. In particular, no stretch receptors have been identified in C. elegans, raising the issue of whether stretch-receptor-mediated proprioception is used by C. elegans to regulate its locomotion behaviour. Here we have characterized TRP-4, the C. elegans homologue of the mechanosensitive TRPN channel. We show that trp-4 mutant worms bend their body abnormally, exhibiting a body posture distinct from that of wild-type worms during locomotion, suggesting that TRP-4 is involved in stretch-receptor-mediated proprioception. We show that TRP-4 acts in a single neuron, DVA, to mediate its function in proprioception, and that the activity of DVA can be stimulated by body stretch. DVA both positively and negatively modulates locomotion, providing a unique mechanism whereby a single neuron can fine-tune motor activity. Thus, DVA represents a stretch receptor neuron that regulates sensory-motor integration during C. elegans locomotion.
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                Author and article information

                Journal
                Commun Integr Biol
                Commun Integr Biol
                CIB
                Communicative & Integrative Biology
                Landes Bioscience
                1942-0889
                01 September 2012
                01 September 2012
                : 5
                : 5
                : 440-447
                Affiliations
                Section of Neurobiology; The University of Texas at Austin; Austin, TX USA
                Author notes
                [* ]Correspondence to: Jonathan T. Pierce-Shimomura, Email: jonps@ 123456mail.utexas.edu
                Article
                2012CIB0047R 20978
                10.4161/cib.20978
                3502204
                23181157
                8e906751-3008-45fa-90f2-9c6859dc5333
                Copyright © 2012 Landes Bioscience

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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                Molecular biology
                parkinson’s disease,gait transitions,caenorhabditis elegans
                Molecular biology
                parkinson’s disease, gait transitions, caenorhabditis elegans

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