Hypothalamic warm-sensitive neurons require TRPC4 channel for detecting internal warmth and regulating body temperature in mice.

Precise monitoring of internal temperature is vital for thermal homeostasis in mammals. For decades, warm-sensitive neurons (WSNs) within the preoptic area (POA) were thought to sense internal warmth, using this information as feedback to regulate body temperature (Tcore). However, the cellular and molecular mechanisms by which WSNs measure temperature remain largely undefined. Via a pilot genetic screen, we found that silencing the TRPC4 channel in mice substantially attenuated hypothermia induced by light-mediated heating of the POA. Loss-of-function studies of TRPC4 confirmed its role in warm sensing in GABAergic WSNs, causing additional defects in basal temperature setting, warm defense, and fever responses. Furthermore, TRPC4 antagonists and agonists bidirectionally regulated Tcore. Thus, our data indicate that TRPC4 is essential for sensing internal warmth and that TRPC4-expressing GABAergic WSNs function as a novel cellular sensor for preventing Tcore from exceeding set-point temperatures. TRPC4 may represent a potential therapeutic target for managing Tcore.

Cooling-activated dorsomedial hypothalamic BDNF neurons control cold defense in mice.

BDNF and its expressing neurons in the brain critically control feeding and energy expenditure (EE) in both rodents and humans. However, whether BDNF neurons would function in thermoregulation during temperature challenges is unclear. Here, we show that BDNF neurons in the dorsomedial hypothalamus (DMHBDNF ) of mice are activated by afferent cooling signals. These cooling-activated BDNF neurons are mainly GABAergic. Activation of DMHBDNF neurons or the GABAergic subpopulations is sufficient to increase body temperature, EE, and physical activity. Conversely, blocking DMHBDNF neurons substantially impairs cold defense and reduces energy expenditure, physical activity, and UCP1 expression in BAT, which eventually results in bodyweight gain and glucose/insulin intolerance. Therefore, we identify a subset of DMHBDNF neurons as a novel type of cooling-activated neurons to promote cold defense. Thus, we reveal a critical role of BDNF circuitry in thermoregulation, which deepens our understanding of BDNF in controlling energy homeostasis and obesity.

Sufficient nitrogen promoted high phosphorus tolerance and phosphorus-accumulating capability of Polygonum hydropiper in relation to changes of phytohormones and phenols.

Nitrogen (N) application is efficient to enhance phosphorus (P)-phytoextraction efficiency of P-accumulating plants. However, there is little available information on growth, P uptake and physiological changes of P-accumulating plants in high P media with different N application, and that whether the improved growth or P uptake is related with changes of phytohormones and phenols. This study investigated growth, P-accumulating capability, phytohormones and phenols of a mining ecotype (ME) and a non-mining ecotype (NME) of Polygonum hydropiper in high P media (400 mg L-1) with sufficient N (SN, 50 mg L-1) and low N (LN, 12.5 mg L-1) supply. SN supply greatly increased tissue biomass, P-accumulating capability of P. hydropiper in high P media, and the ME showed higher P bioaccumulation coefficient, and tissue P accumulation than the NME. The greatest tissue biomass and P accumulation was found at 5 weeks. At 5 weeks, SN supply greatly decreased concentrations of indole-3-acetic acid (IAA), zeatin, abscisic acid (ABA), total phenolic and flavonoid in tissues of P. hydropiper, compared with LN supply. The ME produced lower concentrations of IAA, zeatin, ABA, total phenolic and flavonoid than the NME in leaf and stem in high P media with N supply. Significantly negative correlations were found between IAA, zeatin, ABA, flavonoid concentrations and biomass as well as P accumulation in leaf. Thus, SN supply promoted high P tolerance and P-accumulating capability of the ME in relation to modulating phytohormones and phenols to suitable concentrations, ultimately improving P-phytoextraction ability.