Through the activity patterns of calcium image, we identify that an oxygen-sensation neuron regulates the behavior of ethanol stimulation. In this study, we focused on feeding behavior for functional mapping of a neural pathway in response to ethanol stimuli. However, it is still unclear whether a neuron senses the ethanol, or a neural circuit regulates the behavioral response to ethanol stimuli. In cellular level, a voltage- and calcium-activated potassium (BK) channel slo-1 and a neuropeptide receptor npr-1, both are activated by high concentration ethanol, and loss of function mutants exhibit strong ethanol resistance and acute tolerance respectively. High concentration ethanol, more than 100 mM, results in a decrease of locomotion, lifespans, feeding and egg laying, , ], and low concentration ethanol (1 mM) results in surprisingly double lifespan in ethanol-treated L1 larvae.
In C.elegans, previous studies have demonstrated that different ethanol concentration produces distinctive effects on animals.
So C. elegans has served as an ideal model for neural function and its resulting behavior.Ĭ. elegans exhibits many reversible, dose-dependent behaviors in response to exogenous alcohol, as Drosophila and mammals. Although mammals and nematodes show great diversity in neural composition and genomic structure, the nematode C. elegans develops similar neural modules as mammals for highly efficient integration of information. And worms show extraordinary sensitive sense to various environmental cues as bacteria, metal ions, odor and ethanol. So it is still a challenge to identify whether a neural pathway, though widely accepted, mediates or modulates the ethanol response.ĭue to merely 302 neurons with about 7000 synapses and clear anatomical connections between the neurons, C. elegans becomes an attractive subject for fundamental neurological mechanism. Nevertheless, an increased food intake is not associated with pleasure of delicious food and sensor satiety. Neurologically, Ethanol stimulates opioid, GABA and dopamine neurotransmission with the rewarding properties, , ]. But the neural mechanism underlying ethanol-induced food intake remains largely uncertain. After ethanol consumed, the subjective feelings of hunger arise and then increase the short-term food intake, particularly high-fat savoury foods. These findings revealed a neural circuit to understand how the nervous system responds to ethanol and generates corresponding behavior.Įthanol (alcohol) is widely used for drug and beverage in ordinary people's lives. So BAG neurons respond to alcohol through the promotion of intracellular calcium signaling, and then the downstream motor neurons NSM release serotonin to regulate the feeding behavior in C. elegans.
And the rescue experiment of double mutant indicated the guanylate cyclases and serotonin in the same signaling pathway.
In addition, serotonin, released from NSM motor neurons, promoted feeding behavior under ethanol stimulation. And both guanylate cyclases GCY-31 and GCY-33 were crucial signaling protein of calcium response in BAG neurons. We recorded the intracellular calcium signaling of seven sensory neurons in response to ethanol, and only found a significant increase of calcium signaling in BAG among the seven sensor neurons. To understand the neural mechanisms of these ethanol-induced behaviors, we investigated a neural pathway of ethanol-induced feeding behavior by guanylate cyclases and serotonin signals in C. elegans. Ethanol affects the nervous system of animals to cause a boost of feeding, sexual, verbal, and locomotor behaviors.
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