RESUMO
The N-methyl-D-aspartate (NMDA) subtype of glutamate receptor is important for synaptic plasticity and nervous system development and function. We have used genetic and electrophysiological methods to demonstrate that NMR-1, a Caenorhabditis elegans NMDA-type ionotropic glutamate receptor subunit, plays a role in the control of movement and foraging behavior. nmr-1 mutants show a lower probability of switching from forward to backward movement and a reduced ability to navigate a complex environment. Electrical recordings from the interneuron AVA show that NMDA-dependent currents are selectively disrupted in nmr-1 mutants. We also show that a slowly desensitizing variant of a non-NMDA receptor can rescue the nmr-1 mutant phenotype. We propose that NMDA receptors in C. elegans provide long-lived currents that modulate the frequency of movement reversals during foraging behavior.
Assuntos
Proteínas de Caenorhabditis elegans , Caenorhabditis elegans/genética , Locomoção/fisiologia , Receptores de N-Metil-D-Aspartato/genética , Transmissão Sináptica/fisiologia , Animais , Animais Geneticamente Modificados , Eletrofisiologia , Deleção de Genes , Expressão Gênica/fisiologia , Interneurônios/química , Interneurônios/fisiologia , Aprendizagem em Labirinto/fisiologia , Potenciais da Membrana/fisiologia , Dados de Sequência Molecular , Mutagênese/fisiologia , Fenótipo , Receptores de AMPA , Receptores de Glutamato/análise , Receptores de Glutamato/genética , Receptores de Glutamato/metabolismo , Receptores de N-Metil-D-Aspartato/análise , Receptores de N-Metil-D-Aspartato/metabolismo , Homologia de Sequência de AminoácidosRESUMO
How simple neuronal circuits control behavior is not well understood at the molecular or genetic level. In Caenorhabditis elegans, foraging behavior consists of long, forward movements interrupted by brief reversals. To determine how this pattern is generated and regulated, we have developed novel perturbation techniques that allow us to depolarize selected neurons in vivo using the dominant glutamate receptor mutation identified in the Lurcher mouse. Transgenic worms that expressed a mutated C. elegans glutamate receptor in interneurons that control locomotion displayed a remarkable and unexpected change in their behavior-they rapidly alternated between forward and backward coordinated movement. Our findings suggest that the gating of movement reversals is controlled in a partially distributed fashion by a small subset of interneurons and that this gating is modified by sensory input.
