Temperature is an essential environmental stimulus with affecting animal’s biochemistry. Animals can respond to temperature changes through altered physiology. Yet, how animals habituate to ambient temperature is poorly known. Nematode C. elegans stores temperature experience that induces temperature habituation-linked cold tolerance. We show here that a light and pheromone-sensing neuron (ASJ) regulates cold habituation through insulin signaling. Cold habituation is abnormal in a mutant impairing trimetic G protein signaling in ASJ. Ca²⁺ imaging and genetic analysis indicate that ASJ neuron acts as temperature sensing neuron. Insulin molecules released from synapses of ASJ is received by the intestine and neurons, which regulates gene expression for cold habituation. Essential molecular physiological systems are conserved throughout human to C. elegans, and the systems found in this study can therefore provide a useful model for studying temperature habituation.

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Food likes and dislikes can change with experience; conditioned taste aversion (CTA) is one of the examples. When animals consume a novel taste (conditioned stimulus, CS) followed by an experience of a poisoning symptom (unconditioned stimulus, US), they develop aversion to the CS (CTA learning), resulting in the acquisition of the CTA memory. If the animals experience the repeated presentations of the CS without the US after CTA learning, they can exhibit preference to the CS (extinction learning), resulting in the acquisition of the extinction memory. Recently, a number of studies have suggested that sex hormones play a crucial role in neural and hormonal control of behavior. In this review, we focus on some roles of androgens on brain mechanisms relevant for the extinction memory after CTA learning from the viewpoint of the sexual maturation in mice. Our behavioral experiments show that the retention process of the extinction memory after CTA learning is affected by one of androgens, testosterone, which promotes sexual maturation. The maturation of the retention mechanism of the extinction memory requires exposure of the amygdala and the ventral medial prefrontal cortex (vmPFC), which are related to the CTA and extinction memories, to testosterone in two steps (sexual pre- and post- maturation period). In male mice, the exposure during the sexual pre-maturation period is essential for testosterone-dependent maturation of the retention mechanism of the extinction memory during the sexual post-maturation period.

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Pheromone is defined as chemical released by one organism that modulates the behavior or physiology of a second organism of the same species. Releaser pheromones induce specific behavior by exerting acute effects on the neuronal response, whereas primer pheromones induce physiological changes with long-lasting effects by changing the neuroendocrine status of the recipients. In mammals, although several types of releaser pheromones have been identified, the identities of primer pheromones remain largely unknown. In sheep and goats, the seasonally anestrous endocrine state of females is changed to the estrous state upon exposure to male scents. This so-called “male effect” is one of the most conspicuous primer pheromone effects in mammals. We have identified an olfactory signal molecule that activates the central regulator of reproduction, the gonadotropin-releasing hormone (GnRH) pulse generator, in goats. Using gas chromatography-mass spectrometry to analyze male goat headspace volatiles, we identified several ethyl-branched aldehydes and ketones. We electrophysiologically demonstrated that one of these compounds, 4-ethyloctanal, activates the GnRH pulse generator in female goats. This discovery opens a new avenue toward a deeper understanding of the pheromone-dependent regulation of reproduction in mammals, as well as the development of novel and more natural technology for increasing the reproductive efficiency of livestock animals.

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