We report the formation of a series of metal-containing hydrogenated silicon clusters using an ion trap. Mass analyses reveal that many types of transition metal ions M(+) ( M = Hf, Ta, W, Re, Ir, etc.) react with silane (SiH4) to form dehydrogenated MSi( +)(n) cluster ions ( n = 14, 13, 12, 11, 9, respectively) as an end product, indicating that the metal atom is endohedral and stabilizes the Si polyhedral cage. This finding is confirmed by our ab initio calculation that WSi12 is a W-encapsulating Si12 cage cluster, and is very stable owing to both the electronic and the geometrical shell closures.

Atomic-sized fluorescent defects in diamond are widely recognized as a promising solid state platform for quantum cryptography and quantum information processing. For these applications, single photon sources with a high intensity and reproducible fabrication methods are required. In this study, we report a novel color center in diamond, composed of a germanium (Ge) and a vacancy (V) and named the GeV center, which has a sharp and strong photoluminescence band with a zero-phonon line at 602 nm at room temperature. We demonstrate this new color center works as a single photon source. Both ion implantation and chemical vapor deposition techniques enabled fabrication of GeV centers in diamond. A first-principles calculation revealed the atomic crystal structure and energy levels of the GeV center.

The neural mechanisms underlying memory regulation during sleep are not yet fully understood. We found that melanin concentrating hormone–producing neurons (MCH neurons) in the hypothalamus actively contribute to forgetting in rapid eye movement (REM) sleep. Hypothalamic MCH neurons densely innervated the dorsal hippocampus. Activation or inhibition of MCH neurons impaired or improved hippocampus-dependent memory, respectively. Activation of MCH nerve terminals in vitro reduced firing of hippocampal pyramidal neurons by increasing inhibitory inputs. Wake- and REM sleep–active MCH neurons were distinct populations that were randomly distributed in the hypothalamus. REM sleep state–dependent inhibition of MCH neurons impaired hippocampus-dependent memory without affecting sleep architecture or quality. REM sleep–active MCH neurons in the hypothalamus are thus involved in active forgetting in the hippocampus.