Or Yudco's research while affiliated with Hebrew University of Jerusalem and other places

Publications (2)

Article
The brain undergoes rapid, dramatic, and reversible transitioning between states of wakefulness and unconsciousness during natural sleep and in pathological conditions such as hypoxia, hypotension, and concussion. Transitioning can also be induced pharmacologically using general anesthetic agents. The effect is selective. Mobility, sensory percepti...
Article
In light of the general shift from rats to mice as the leading rodent model in neuroscience research we used c-Fos expression as a tool to survey brain regions in the mouse in which neural activity differs between the states of wakefulness and pentobarbital-induced general anesthesia. The aim was to complement prior surveys carried out in rats. In...

Citations

... These include the preoptic area, which is considered as a sleep-promoting area, and the basal forebrain, lateral hypothalamic area, ventral tegmental area, and locus coeruleus that are brain regions involved in mediating sleep-arousal and anaesthesia-arousal transitions [1]. Remarkably, recent studies have identified an ensemble of neuroendocrine cells in the supraoptic nucleus (SON) of the hypothalamus persistently activated by GA [6,7]. In elegant studies Jiang-Xie et al., [6] demonstrated that GA diminishes the expression of the immediate early gene Fos, commonly used as a marker for activated neurons, throughout the entire brain except for a subset of neurones in the SON that were persistently and commonly activated by several types of general anaesthetics. ...
... nucleus (SON) and the zona inserta (ZI). Looking at higher resolution large numbers of brain structures, maybe all, include at least some such "anesthesia-on" neurons, neurons that are excited by GABAergic anesthetics (Lu et al., 2008;Abulafia et al., 2009;Yatziv et al., 2020Yatziv et al., , 2021. It is premature, however, to rule out the possibility that some of this excitation reflects a direct drug action mediated by GABA A -R expressing neurons in the presence of a reversed Cl −1 gradient, rather than by network effects such as disinhibition (Wagner et al., 1997;Ben-Ari, 2002;Price et al., 2005). ...