RESUMO
Monoamines provide chemical codes of behavioral states. However, the neural mechanisms of monoaminergic orchestration of behavior are poorly understood. Touch elicits an escape response in Caenorhabditis elegans where the animal moves backward and turns to change its direction of locomotion. We show that the tyramine receptor SER-2 acts through a Gαo pathway to inhibit neurotransmitter release from GABAergic motor neurons that synapse onto ventral body wall muscles. Extrasynaptic activation of SER-2 facilitates ventral body wall muscle contraction, contributing to the tight ventral turn that allows the animal to navigate away from a threatening stimulus. Tyramine temporally coordinates the different phases of the escape response through the synaptic activation of the fast-acting ionotropic receptor, LGC-55, and extrasynaptic activation of the slow-acting metabotropic receptor, SER-2. Our studies show, at the level of single cells, how a sensory input recruits the action of a monoamine to change neural circuit properties and orchestrate a compound motor sequence.
Assuntos
Caenorhabditis elegans/fisiologia , Reação de Fuga/fisiologia , Neurotransmissores/fisiologia , Tiramina/fisiologia , Aldicarb/farmacologia , Animais , Caenorhabditis elegans/citologia , Proteínas de Caenorhabditis elegans/metabolismo , Inibidores da Colinesterase/farmacologia , Neurônios GABAérgicos/metabolismo , Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/genética , Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo , Neurônios Motores/metabolismo , Contração Muscular , Junção Neuromuscular/efeitos dos fármacos , Junção Neuromuscular/fisiologia , Neurotransmissores/farmacologia , Receptores de Amina Biogênica/genética , Receptores de Amina Biogênica/metabolismo , Deleção de Sequência , Transmissão Sináptica , Tiramina/farmacologiaRESUMO
A key feature of escape responses is the fast translation of sensory information into a coordinated motor output. In C. elegans, anterior touch initiates a backward escape response in which lateral head movements are suppressed. Here, we show that tyramine inhibits head movements and forward locomotion through the activation of a tyramine-gated chloride channel, LGC-55. lgc-55 mutant animals have defects in reversal behavior and fail to suppress head oscillations in response to anterior touch. lgc-55 is expressed in neurons and muscle cells that receive direct synaptic inputs from tyraminergic motor neurons. Therefore, tyramine can act as a classical inhibitory neurotransmitter. Activation of LGC-55 by tyramine coordinates the output of two distinct motor programs, locomotion and head movements that are critical for a C. elegans escape response.
