Global S&T Development Trend Analysis Platform of Resources and Environment
Coupling the spins of many nitrogen-vacancy centres in a trapped diamond to its orientation produces a spin-dependent torque and spin-cooling of the motion of the diamond.
Observing and controlling macroscopic quantum systems has long been a driving force in quantum physics research. In particular, strong coupling between individual quantum systems and mechanical oscillators is being actively studied(1-3). Whereas both read-out of mechanical motion using coherent control of spin systems(4-9) and single-spin read-out using pristine oscillators have been demonstrated(10,11), temperature control of the motion of a macroscopic object using long-lived electronic spins has not been reported. Here we observe a spin-dependent torque and spin-cooling of the motion of a trapped microdiamond. Using a combination of microwave and laser excitation enables the spins of nitrogen-vacancy centres to act on the diamond orientation and to cool the diamond libration via a dynamical back-action. Furthermore, by driving the system in the nonlinear regime, we demonstrate bistability and self-sustained coherent oscillations stimulated by spin-mechanical coupling, which offers the prospect of spin-driven generation of non-classical states of motion. Such a levitating diamond-held in position by electric field gradients under vacuum-can operate as a '
Neural control of the function of visceral organs is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence, and is often dysregulated in gastrointestinal disorders(1). Luminal factors, such as diet and microbiota, regulate neurogenic programs of gut motility(2-5), but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor aryl hydrocarbon receptor (AHR) functions as a biosensor in intestinal neural circuits, linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons that represent distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles that are controlled by the combined effects of host genetic programs and microbial colonization. Microbiota-induced expression of AHR in neurons of the distal gastrointestinal tract enables these neurons to respond to the luminal environment and to induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr, or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in the enteric neurons of mice treated with antibiotics partially restores intestinal motility. Together, our experiments identify AHR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits to maintain gut homeostasis and health.
In a mouse model, aryl hydrocarbon receptor signalling in enteric neurons is revealed as a mechanism that helps to maintain gut homeostasis by integrating the luminal environment with the physiology of intestinal neural circuits.
