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The Journal of Neuroscience, July 9, 2008, 28(28):7104-7112; doi:10.1523/JNEUROSCI.0378-08.2008

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Cellular/Molecular
Behavioral Impact of Neurotransmitter-Activated G-Protein-Coupled Receptors: Muscarinic and GABA_B Receptors Regulate Caenorhabditis elegans Locomotion

Jeremy S. Dittman and Joshua M. Kaplan

Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114

Correspondence should be addressed to Joshua M. Kaplan, Department of Molecular Biology, Massachusetts General Hospital, Simches Research Building, 7th Floor, 185 Cambridge Street, Boston, MA 02114. Email: kaplan{at}molbio.mgh.harvard.edu

Neurotransmitter released from presynaptic terminals activates both ligand-gated ion channels (ionotropic receptors) and a variety of G-protein-coupled receptors (GPCRs). These neurotransmitter receptors are expressed on both presynaptic and postsynaptic cells. Thus, each neurotransmitter acts on multiple receptor classes, generating a large repertoire of physiological responses. The impact of many ionotropic receptors on neuronal activity and behavior has been clearly elucidated; however, much less is known about how neurotransmitter-gated GPCRs regulate neurons and circuits. In Caenorhabditis elegans, both acetylcholine (ACh) and GABA are released in the nerve cord and mediate fast neuromuscular excitation and inhibition during locomotion. Here we identify a muscarinic receptor (GAR-2) and the GABA_B receptor dimer (GBB-1/2) that detect synaptically released ACh and GABA, respectively. Both GAR-2 and GBB-1/2 inhibited cholinergic motor neurons when ACh and GABA levels were enhanced. Loss of either GPCR resulted in movement defects, suggesting that these receptors are activated during locomotion. When the negative feedback provided by GAR-2 was replaced with positive feedback, animals became highly sensitive to ACh levels and locomotion was severely impaired. Thus, conserved GPCRs act in the nematode motor circuit to provide negative feedback and to regulate locomotory behaviors that underlie navigation.

Key words: C. elegans; feedback; GABA_B receptor; GPCR; locomotion; muscarinic

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Received Jan. 28, 2008; revised May 14, 2008; accepted June 5, 2008.

Correspondence should be addressed to Joshua M. Kaplan, Department of Molecular Biology, Massachusetts General Hospital, Simches Research Building, 7th Floor, 185 Cambridge Street, Boston, MA 02114. Email: kaplan{at}molbio.mgh.harvard.edu

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