Objective To investigate the modulatory effect of different dosage of sufentanil on I GABA in rat dorsal root ganglion neurons. Methods The rat root ganglion neurons were enzymatically dissociated. The whole-cell patch clamp techniquewas applied to record the effect of 0.02 , 0.1, 0.5, 2.5 μmol/L sufentanil and 0.5 mol/L sufentanil + 1 nmol/L Naloxone, a non-specific ityopioid receptor antagonist on IGABA. Results 0.02, 0.1, 0.5, 2.5 μmol/L sufentanil potentiated IGABA to (108.7 ± 6.7)%,(122.0 ± 2.3)%, (146.7 ± 7.9)% and (130.1 ± 5.6)%, respectively (n = 10; *P < 0.05, **P < 0.01). The potentiation role of 0.1,0.5, 2.5 μmol/L sufentanil on IGABA lasted 10 to 20 min The potentiation could be blocked by Naloxone (n = 7; *P < 0.05, **P < 0.01). Conclusion Sufentanil activates μ opioid receptor and potentiates the action of GABAA receptor, and the potentiation could be blocked by Naloxone. The enhancement of currents by sufentanil may increase GABA A receptor-mediated presynaptic inhibition at the spinal cord level.

Objective To investigate the effects of ketamine on the voltage-gated sodium channels in hippocampal pyramidal neurons, trying to elucidate the possible mechanism of general anesthesia with ketamine.Methods Hippocampal pyramidal neurons were isolated from Wistar rats of 2 weeks old. Whole-cell patch-clamp recordings were made from cultured hippocampal pyramidal neurons before and after the application of ketamine The effect of ketamine on the sodium current amplitude and the kinetics of the channel were studied. Results The sodium channels were reversibly inhibited by ketamine in a dose-dependent manner. IC50 of ketamine was (794?21) ?mol/L.The hyperpolarizing shift of both steady-activation and steady-inactivation was observed.Conclusion Ketamine inhibits the voltage-gated sodium channels to some degree. Sodium channel inhibition may be involved in the mechanism of general anesthesia induced with ketamine.

Objective:To evaluate the role of synapsin-Ⅰ phosphorylation in herkinorin-induced reduction of oxygen-glucose deprivation/restoration (OGD/R)-caused damage to cortical neurons and the relationship with conventional protein kinase C (cPKC)γ in newborn mice.Methods:Primary cortical neurons of cPKCγ + /+ and cPKCγ -/- mice (within 24 h after birth) were cultured for 7 days.Each type of neurons were then divided into 3 groups ( n=5 each) using a random number table method: control group (group C), OGD/R group and herkinorin group (group H). The neurons were subjected to oxygen-glucose deprivation (OGD) for 1 h followed by restoration of oxygen-glucose supply for 24 h. Herkinorin 10 μmol/L was added immediately after onset of OGD, the neurons were then incubated for 1 h, and herkinorin was washed out at the end of OGD in group H. At 24 h of oxygen-glucose restoration, cells were collected for measurement of the cell survival rate by methyl thiazolyl tetrazolium assay, and immunofluorescence was used to measure the number of neurites and the length of dendrites.Western blot was applied to detect the expression of phosphorylated synapsin-Ⅰ (p-synapsin-Ⅰ). Results:Compared with group C, the cell survival rate and the number of neurites were significantly decreased, the length of dendrites was shortened, and the expression of p-synapsin-Ⅰ was down-regulated in cPKCγ + /+ and cPKCγ -/- mice in group OGD/R and group H ( P<0.05). Compared with group OGD/R, the cell survival rate and the number of neurites were significantly increased, the length of dendrites was prolonged, the expression of p-synapsin-Ⅰ was up-regulated in cPKCγ + /+ mice in group H ( P<0.05), and no significant change was found in the parameters mentioned above in cPKCγ -/- mice in group H ( P>0.05). There was no significant differences in the expression of synapsin-Ⅰ in neurons among the three groups of cPKCγ + /+ mice and among the three groups of cPKCγ -/- mice ( P>0.05). Conclusion:Herkinorin can reduce OGD/R-caused damage to cortical neurons through decreasing cPKCγ membrane translocation and inhibiting synapsin-Ⅰ phosphorylation in newborn mice.