A neuronal amine-gated chloride channel governs satiety in C.elegans

BLANCO, MARÍA GABRIELA; RAYES D; VEUTHEY, TANIA; DE ROSA MJ; AGUIRRE, NICOLÁS

Buenos Aires

Congreso; 2nd Falan Congress; 2016

Food intake is a conserved behavior that depends on molecules that communicate the animal nutritional status to the brain. A key process in apettite control is satiety which implies a specific sequence of behaviors: completion of food, reduced locomotion and sleep. This has also been also described in C elegans, as these animals become quiescent by stopping feeding and moving after achieving satiation. Nevertheless, the neural circuit and the molecular basis of satiety in this animal are poorly understood. Amphetamine is a well known anorexigenic drug that has been used for obesity treatments in humans. In C.elegans, it activates LGC-55, an amine-gated chloride channel. We found that lgc-55 null mutants deplete their food about 40% faster than wild-type controls. This is due to an increased food intake per worm in the mutants, as the number of offsprings and the growth rates do not exhibit significant differences compared to that of wild-type worms. Strikingly, quiescence experiments, an assay that evaluate satiety in worms, revealed that the fraction of satiated worms in the mutant strain is 2.5-fold lower. Our results suggest that the amphetamine-sensitive receptor LGC-55 is essential for satiety in C.elegans. Amine-gated inhibitory signaling have been also evidenced in mammals and LGC-55 exhibits 35-45 % identity with human orphans receptors. This study could contribute to the elucidation of a conserved mechanism of food intake regulation throughout the animal kingdom.