ABSTRACT
@#【Objective】To unmask the effect of Orexin B on the synaptic transmission between feed-forward projection from the lateral geniculate nucleus（LGN）to orexin-sensitive neurons in layer 6b（L6b）of visual cortex（VC）.【Methods】C57 mice at P25-P30 were used for micro-injection of CTB555 and ChR2-EGFP into LGN to label the neurons feedback projection to LGN from L6b and the feed-forward projection from LGN to the neurons in L6b of VC respectively. The EPSC in L6b cells was intracellularly recorded from the neurons labeled by CTB555.【Results】The neurons feedback projection to LGN in L6b are mainly pyramidal neurons, and the most of these cells are activated by orexin B，called orexin- sensitive neurons. Orexin B enhanced the NMDAR-mediated postsynaptic current in orexin-sensitive neurons in L6b by electrical or optical stimulation on the LGN projection to VC［electrical stimulation：（125.1 ± 3.7）%，optical stimulation：（123.8 ±3.8）%. In the case of OX2R′s blocker，the effect of Orexin B on EPSC amplitude disappeared with significant statistical significance，P < 0.05］，thus，strengthening the synaptic transmission between LGN and orexin-sensitive neurons in L6b.【Conclusions】Orexin B enhances the synaptic transmission between LGN to pyramidal neurons in L6b of VC.
ABSTRACT
Objective To study the neuroprotective effect of orexin-B on rat model of cerebral ischemia-reperfusion injury and its molecular mechanism. Methods The artery occlusion model of male Wister rats(middle cerebral ar-tery occlusion,MCAO) was established which has been ischemic 2 h and reperfusion 24 h. Rats were randomly di-vided into sham group (control), ischemia-reperfusion group (I/R), ischemia-reperfusion +PBS group (I/R+PBS),and ischemia-reperfusion +orexin-B group (I/R+OXB). The neurological deficit scores were processed to inclusion and exclusion. Infarct size was determined by TTC staining;Using Western blot,the expressions of orexin receptor 2,p-AKT,p-GSK-3β proteins in hippocampus were detected;Jumping test was used to detect learning and memory abilities in rats. Results Orexin-B significantly reduced the volume of cerebral infarction in TTC staining;orexin-B group was significantly increased the expression of orexin receptor 2as well as p-AKT,which decreased p-GSK-3β (P<0.05),compared with the untreated group. Furthmore,the orexin-B treated group can improve the latency period and decline the mistakes in rat Jumping test(P<0.05). Conclusions The neuroprotective effect of orexin-B in cerebral ischemia-reperfusion injury may enhance p-AKT activity and inhibit p-GSK-3β activity,which may increase the proliferation of neurons and improve the cerebral blood glucose concentration.
ABSTRACT
Objective To provide new evidences for understanding the mechanisms of promo-tive role of orexins in anesthetic emergence and the effect of microinjection of orexin-A/orexin-B into cerebral ventricle on the release of histamine.Methods Male SD rats were randomly divided into sa-line (control ), orexin-A and orexin-B groups. The microdialysis probe was inserted into hypothalamus under stereotaxic apparatus.The perfused fluid from the area of hypothalamic tube-romammillary nucleus was collected using in vivo microdialysis at 1 h,2 h and 3 h after 1 nmol or 5 nmol orexin-A or orexin-B microinjection into the cerebral ventricle (n =5 each).The concentrations of histamine at each time point in dialysates of perfused fluid were detected by high performance liquid chromatography (HPLC)to analyze its dynamic changes.After one week,each group was microin-jected with 10 nmol,15 nmol and 20 nmol orexin-A and orexin-B (n =5)into the cerebral ventricle respectively,dialysates was collect and histamine was detected at 1 h to analyze its dosage response. After one week,each group was microinjected 0.3 μl saline orexin-A and orexin-B (n =6)into the tu-beromammillary nucleus.Results Compared with the control group,microinjection of 1 nmol orexin-A significantly increased histamine release at 1 h,but the same dose of orexin-B had no such effect,5 nmol of orexin-A or orexin-B injections significantly facilitated histamine release at 2 h and 3 h (P <0.01).Microinjection of 10 nmol,15 nmol and 20 nmol orexin-A and orexin-B into ventricle caused an significant increase of histamine release at 1 h while the effect was the strongest in 20 nmol (P <0.05).Compared with the control group,microinjection of orexin-A significantly decreased time of the righting reflex (P <0.01),but the same dose of orexin-B had no such effect.Conclusion Micro-injection of both orexin-A or orexin-B into cerebral ventricle could promote the release of histamine, while the effect of orexin-A was stronger.Microinjection orexin-A into tuberomammillary nucleus sig-nificant facilitated recovery from isoflurane.