@article {69669,
	title = {ONIX: a unified open-source platform for multimodal neural recording and perturbation during naturalistic behavior.},
	journal = {Nat Methods},
	year = {2024},
	month = {2024 Nov 11},
	abstract = {<p>Behavioral neuroscience faces two conflicting demands: long-duration recordings from large neural populations and unimpeded animal behavior. To meet this challenge we developed ONIX, an open-source data acquisition system with high data throughput (2 GB s) and low closed-loop latencies (\&lt;1 ms) that uses a 0.3-mm thin tether to minimize behavioral impact. Head position and rotation are tracked in three dimensions and used to drive active commutation without torque measurements. ONIX can acquire data from combinations of passive electrodes, Neuropixels probes, head-mounted microscopes, cameras, three-dimensional trackers and other data sources. We performed uninterrupted, long (~7 h) neural recordings in mice as they traversed complex three-dimensional terrain, and multiday sleep-tracking recordings (~55 h). ONIX enabled exploration with similar mobility as nonimplanted animals, in contrast to conventional tethered systems, which have restricted movement. By combining long recordings with full mobility, our technology will enable progress on questions that require high-quality neural recordings during ethologically grounded behaviors.</p>
},
	issn = {1548-7105},
	doi = {10.1038/s41592-024-02521-1},
	url = {https://doi.org/10.1038/s41592-024-02521-1},
	author = {Newman, Jonathan P and Zhang, Jie and Cuevas-L{\'o}pez, Aar{\'o}n and Miller, Nicholas J and Honda, Takato and van der Goes, Marie-Sophie H and Leighton, Alexandra H and Carvalho, Filipe and Lopes, Gon{\c c}alo and Lakunina, Anna and Siegle, Joshua H and Harnett, Mark T and Wilson, Matthew A and Voigts, Jakob}
}
@article {68448,
	title = {NAD$^{+}$/NADH metabolism and NAD$^{+}$-dependent enzymes in cell death and ischemic brain injury: current advances and therapeutic implications.},
	journal = {Curr Med Chem},
	volume = {22},
	year = {2015},
	month = {2015},
	pages = {1239-47},
	abstract = {<p>NAD(+) and NADH play crucial roles in a variety of biological processes including energy metabolism, mitochondrial functions, and gene expression. Multiple studies have indicated that NAD(+) administration can profoundly decrease oxidative cell death as well as ischemic and traumatic brain injury, suggesting NAD(+) metabolism as a promising therapeutic target for cerebral ischemia and head injury. Cumulating evidence has suggested that NAD(+) can produce its protective effects by multiple mechanisms, including preventing mitochondrial alterations, enhancing energy metabolism, preventing virtually all forms of cell death including apoptosis, necrosis and autophagy, inhibiting inflammation, directly increasing antioxidation capacity of cells and tissues, and activating SIRT1. Increasing evidence has also suggested that NADH metabolism is a potential therapeutic target for treating several neurological disorders. A number of studies have further indicated that multiple NAD(+)-dependent enzymes such as sirtuins, polymerase(ADP-ribose) polymerases (PARPs) and CD38 mediate cell death and multiple biological processes. In this article, an overview of the recent findings regarding the roles of NAD(+)/NADH and NAD(+)-dependent enzymes in cell death and ischemic brain injury is provided. These findings have collectively indicated that NAD(+)/NADH and NAD(+)-dependent enzymes play fundamental roles in oxidative stress-induced cell death and ischemic brain injury, which may become promising therapeutic targets for brain ischemia and multiple other neurological disorders.</p>
},
	keywords = {ADP-ribosyl Cyclase 1, Animals, Brain Injuries, Brain Ischemia, Cell Death, Humans, NAD, Poly(ADP-ribose) Polymerases, Sirtuins},
	issn = {1875-533X},
	doi = {10.2174/0929867322666150209154420},
	author = {Ma, Yingxin and Nie, Hui and Chen, Heyu and Li, Jiefu and Hong, Yunyi and Wang, Ban and Wang, Caixia and Zhang, Jie and Cao, Wei and Zhang, Mingchao and Xu, Yongning and Ding, Xianting and Yin, Shan Kai and Qu, Xinkai and Ying, Weihai}
}
