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GU, J.

Publications and source records attributed to GU, J..

2 recordsLinked to original sources

The Serotonergic Neural Circuit Between The Dorsal Raphe Nucleus And The Basolateral Amygdala Is Implicated In Modulating The Arousal from Sevoflurane Anesthesia

Although some advancements concerning the arousal involved in mediating the delayed emergency from general anesthesia, which will lead to the serious complications, had been made, the role by arousal in modulating in delayed emergency still remains to be unclear. In our models, based on our previous working that activation of the 5-Hydroxytryptamine (5-HT) neurons in the dorsal raphe nucleus (DRN) by optogenetics can significantly reduce the emergency time by activating arousal pathway, we further test whether the serotonergic neural circuit between the DRN and the basolateral amygdala (BLA) is implicated in modulating the arousal from the sevoflurane anesthesia and the emergency time of sevoflurane anesthesia by the pharmacological, optogenetics and fiber photometry. Our findings showed that whether the serotonergic neural circuit between the DRN and the basolateral amygdala (BLA) plays a key role in modulating the arousal from the sevoflurane anesthesia and the emergency time of sevoflurane anesthesia. Based on the serotonergic neural circuit, the 5-HT 1 A receptor is of great significance to mediate the arousal and the emergency time of the sevoflurane anesthesia. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=143 SRC="FIGDIR/small/511924v2_ufig1.gif" ALT="Figure 1"> View larger version (58K): org.highwire.dtl.DTLVardef@34621eorg.highwire.dtl.DTLVardef@115ae09org.highwire.dtl.DTLVardef@54eb12org.highwire.dtl.DTLVardef@11515ff_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure1C_FLOATNO C_FIG

neuroscience↗

Sirt3 mediated by lentiviral vectors in the periaqueductal gray suppresses morphine withdrawal in rats: A preliminary study

Opioid use disorder (OUD) is a significant clinical and social problem, inducing dependence/addiction and over-dose death. Opioid dependence/withdrawal contributes to the addiction vulnerability. Limited understanding of the exact mechanisms of morphine withdrawal leads to failure to adequately manage opioid withdrawal symptoms. Determining new molecular mechanisms of morphine withdrawal (MW) may allow development of novel therapeutic strategies for treating this disorder. Chronic morphine with naloxone precipitation induces MW behavioral response. Sirt3 (one member of sirtuins family) as a mitochondrial fidelity, plays an important role in mitochondrial homeostasis through the direct regulation of mitochondrial energy metabolism, ATP synthesis, detoxification of mitochondrial ROS, etc. In the pilot study, we found that (1) cultured neurons infected with lentiviral vector expressing Sirt3 induced over-expression of Sirt3, (2) microinjection of LV-Sirt3 into the vlPAG increased Sirt3 protein expression in rats, (3) MW lowered the expression of Sirt3 in the vlPAG, and (4) microinjection of LV-Sirt3 into the vlPAG decreased the MW behavioral response. Current preliminary study demonstrates that complement of Sirt3 in the PAG suppressed MW, providing a novel therapeutic approach to morphine physical withdrawal symptoms. The exact up-and/or down-stream factors of Sirt3 in the model are under the investigation.

neuroscience↗