Negative regulation of gamma-aminobutyric acid type A receptor on free calcium ion levels following facial nerve injury

Previous studies have demonstrated that muscarinic, and nicotinic receptors increase free Ca2＋ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca2＋ overload can trigger either necrotic or apoptotic cell death. Gamma-aminobutyric acid （GABA）, an important inhibitory neurotransmitter in the central nervous system, exists in the facial nerve nucleus. It is assumed that GABA negatively regulates free Ca2＋ levels in the facial nerve nucleus. The present study investigated GABA type A （GABAA） receptor expression in the facial nerve nucleus in a rat model of facial nerve injury using immunohistochemistry and laser confocal microscopy, as well as the regulatory effects of GABAA receptor on nicotinic receptor response following facial nerve injury. Subunits α1, α3, α5, β1, β2, δ, and γ3 of GABAA receptors were expressed in the facial nerve nucleus following facial nerve injury. In addition, GABAA receptor expression significantly inhibited the increase in nicotinic receptor-mediated free Ca2＋ levels in the facial nerve nucleus following facial nerve injury in a concentration-dependent fashion. These results suggest that GABAA receptors exhibit negative effects on nicotinic receptor responses following facial nerve injury.

Muscarinic receptor-mediated calcium changes in a rat model of facial nerve nucleus injury

The muscarinic receptor modulates intracellular free calcium ion levels in the facial nerve nucleus via different channels. In the present study, muscarinic receptor-mediated free calcium ions levels were detected by confocal laser microscopy in the facial nerve nucleus following facial nerve injury in rats. There was no significant difference in muscarinic receptor expression at the affected facial nerve nucleus compared with expression prior to injury, but muscarinic receptor-mediated free calcium ion levels increased in the affected side following facial nerve injury （P 〈 0.01）. At day 30 after facial nerve injury, 50 pmol/L muscarinic-mediated free calcium ion levels were significantly inhibited at the affected facial nerve nucleus in calcium-free artificial cerebrospinal fluid, and the change range was 82% of artificial cerebrospinal fluid （P 〈 0.05）. These results suggest that increased free calcium ion concentrations are achieved by intracellular calcium ion release, and that the transmembrane flow of calcium ions is also involved in this process.

Metal-organic frameworks-derived nitrogen-doped carbon supported nanostructured PtNi catalyst for enhanced hydrosilylation of 1-octene

Here,we successfully developed nano structured PtNi particles supported on n itroge rrdoped carbon(NC),which were obtai ned by carbon izati on of metal-organic frameworks under different temperatures,forming the nano-PtNi/NC-600,nano-PtNi/NC-800,nano-PtNi/NC-900 and nano-PtNi/NC-1000 catalysts.For hydrosilylation of 1-octene,we found that the nano-PtNi/NC-1000 catalyst exhibits higher activity for anti-Markovnikov hydrosilylation of 1-octene than those of nano-PtNi/NC-600,nano-PtNi/NC-800,nano-PtNi/NC-900 catalysts.Experiments have verified that benefiting from obvious charge transfer from nano-PtNi particles to NC support carbonized at 1,000℃,the nano-PtNi/NC-1000 catalyst achieved almost complete conversion and produce exclusive adduct for anti-Markovnikov hydrosilylation of 1-octene.Importantly,the nano-PtNi/NC-1000 catalyst exhibited good reusability for the hydrosilylation reaction.This work provides a new path to optimize electronic structure of catalysts by support modification to enhance electron transfer between metal active species and supports for highly catalytic performance.