The development of color centers in diamond as the basis for emerging quantum technologies has been limited by the need for ion implantation to create the appropriate defects. We present a versatile method to dope diamond without ion implantation by synthesis of a doped amorphous carbon precursor and transformation at high temperatures and high pressures. To explore this bottom-up method for color center generation, we rationally create silicon vacancy defects in nanodiamond and investigate them for optical pressure metrology. In addition, we show that this process can generate noble gas defects within diamond from the typically inactive argon pressure medium, which may explain the hysteresis effects observed in other high-pressure experiments and the presence of noble gases in some meteoritic nanodiamonds. Our results illustrate a general method to produce color centers in diamond and may enable the controlled generation of designer defects.

An orphan member of the solute carrier family SLC10, SLC10A4 has been found to be enriched in midbrain and brainstem neurons and has been found to co-localize with and to affect dopamine homeostasis. We generated an SLC10A4 knockout mouse (Slc10a4Δ/Δ) using Cre targeted recombination, and characterized behavioral measures of motor and cognitive function as well as dopamine and acetylcholine levels in midbrain and brainstem. In agreement with previous studies, Slc10a4 mRNA was preferentially expressed in neurons in the brains of wild-type (Slc10a4+/+) mice and was enriched in dopaminergic and cholinergic regions. Slc10a4Δ/Δ mice had no impairment in motor function or novelty-induced exploratory behaviors but performed significantly worse in measures of spatial memory and cognitive flexibility. Slc10a4Δ/Δ mice also did not differ from Slc10a4+/+ in measures of anxiety. HPLC measures on tissue punches taken from the dorsal and ventral striatum reveal a decrease in dopamine content and a corresponding increase in the metabolite DOPAC, indicating an increase in dopamine turnover. Punches taken from the brainstem revealed a decrease in acetylcholine as compared with Slc10a4+/+ littermates. Together, these data indicate that loss of SLC10A4 protein results in neurotransmitter imbalance and cognitive impairment.

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