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Objective To evaluate the effect of hypoxemia factor on hippocampal long-term potentiation(LTP)in newborn rats undergoing propofol anesthesia. Methods Forty-two pathogen-free healthy Sprague-Dawley rats(21 males,21 females),aged 7 days,weighing 14-18 g,were divided into 3 groups(n=14 each)using a random number table:propofol plus air group(group PA),propofol plus pure oxygen group(group PO)and intralipid plus pure oxygen group(group IO).Propofol 50 mg/kg was injected intraperitoneally once a day for 7 consecutive days in PA and PO groups. Intralipid 5.0 ml/kg was injected intraperitoneally once a day for 7 consecutive days in IO group. The rats were exposed to air or pure oxygen for 6 h after the end of each injection. The arterial oxygen saturation and respiratory rate were determined after administration. The rats were returned to the cage after recovery of righting reflex. Six rats in each group were selected for preparation of hippocampal slices at 24 h after the last injection on 7th day,and the electric stimulation-induced field excitatory post synaptic potential(fEPSP)and success rate of LTP induction were recorded. Morris water maze test was performed in the other rats at 2 weeks after administration to assess the cognitive function. Results Compared with group IO,the respiratory rate,amplitude of fEPSP and success rate of LTP induction were significantly decreased,and the escape latency was prolonged in group PO(P<0.05).Compared with group PO,the arterial oxygen saturation,amplitude of fEPSP and success rate of LTP induction were significantly decreased,the escape latency was prolonged,and the number of crossing the original platform was decreased in group PA(P<0.05).Conclusion Hypoxemia factor increases propofol-induced neurotoxicity in the central nervous system of newborn rats.
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Objective To observe the phosphorylation level and nuclear translocation of signal transducer and activator of transcription factor-3 (STAT3) in hippocampal neurons induced by oxygen and glucose deprivation in vitro and discuss the dynamic changes of STAT3 signal pathway in an in vitro cell model of brain hypoxia and ischemia.Methods Hippocampal neurons from newly born SD rats (within 24 hours from birth) were cultured with DMEM/F12 for nine days,and then were transferred to oxygen and glucose deprivation environment for four hours to establish experimental cell models.The distribution of phosphorylated STAT3 (p-STAT3) in the hippocampal neurons in different groups was observed under laser scanning confocal microscope after immunofluorescence staining.Expression intensity of p-STAT3 at different time points after oxygen and glucose deprivation in the hippocampal neurons was detected by Western blotting.Results Expression of p-STAT3 was unobvious in the nucleus of the control group,but it was observed in the nucleus of the model group one hour after modeling,and peaked at three hour.Expression levels of p-STAT3 in the hippocampal neurons at each time point between the two groups showed significant difference (P ＜ 0.05).Conclusion Oxygen and glucose deprivation induces noticeable up-regulation of p-STAT3 in the hippocampal neuronal nucleus,which indicates the overactivation of signal transduction pathway of STAT3.
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Objective To develop experimental animal model of the brain stem myoclonus,which more closely replicate clinic features of mechanism, behavior, neuroelectrophysiology and pharmacodynamics.Methods L-5-HTP (the precursor of L-5-HT)was microinjected into the dorsal pons of young guinea pig to induce myoclonus (electromyogram burst of myoclonus≤400 ms by synchronous recording).Some animals were pretreated with anticonvulsant VPA,CZP or CBZ at effective dose 50 (EC_(50)).Myoclonus was induced when the drug level was within their effective anticonvulsion concentration.The neuroelectrophysiological characteristics of myoclonus including latency,time of reaching its peak,duration of seizure peak,the maximum seizure frequency and total duration were detected.EMG and ictal electroencephalogram(EEG)were recorded synchronously.The origin of myoclonus and its correlation with epileptic discharges were further confirmed by jerk-locked back averaging(JLA).Results (1)L-5-HTP induced pure myoclonus from the dorsal pons of guinea pig permanently(8/every site,the rate of producing myoclonus is 100%).(2)The myoclonus presented bilaterally or as general myoclonus,which was sensitive to tactile and sound sensation.(3)The EMG duration of the myoclonus wag longer((208.75 ± 81.42)ms),and ictal EEG showed scattered and irregular spikes and sharp waves without time-locked correlation with EMG activities.(4)The synchronous ictal EEG of the myoclonus showed spike and sharp waves,but there was no time-locked EEG activity in JLA.(5)In the animals treated with anticonvulsant at EC_(50) concentrations:VPA and CZP decreased the maximum seizure frequency(there are 28.13±3.79 per minutes in VPA group and 37.17±4.67 perminutes in CZP group)and shortened the duration of peak time ((55.00±14.14)minutes in VPA group and(50.00±11.73)minutes in CZP group respectively)and total time(VPA group was(124.17±40.04)minutes and CZP group was(156.88±30.71)minutes)of myoclonus(F value were between 23.41 and 35.44,P＜0.01 or P＜0.05).CBZ increased duration of peak time((98.75±13.86)minutes)and total time((257.50±14.79)minutes)of myoclonus(P＜0.05 and 0.01).Conclusions The new model generates pure myoclonus originating from brain stem and also has a shorter duration of muscle construction(≤400 ms)and more sensitivity to tactile and sound sensation.Therefore,the model presents characteristics closer to the brain stem myoclonus in the clinic phenotype in respect of seizure behavior,pharmacodynamics and neuroelectrophysiology.
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Objective To study the changes of the transient outward K+ current (Ito),delayed rectifier K+ current(IkDR) and the inward rectifier K+ current(Ik1) of the rat bone mesenchymal stem cells (MSCs) induced by 5-Azacytidine(5-Aza) during proliferating and differentiating process in vitro. Methods MSCs were cultured according to related articles for two weeks and then some of the cells were induced by 5-Azacytidine.The experiment was divided into uninduced(cultured for 6w) and induced(1,2,3 and 4w) cell groups. Each week had twenty cells random tested by the whole-cell patch clamp technology and the K+ currents were identified by corresponding ionic blockers.Results The detection rate of the same type of K+ current during test weeks had no significant deviation;The three types of K+ current intensity were gradually augmented after being inducing cultured for 1,2,3 and 4 weeks(P
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<p><b>OBJECTIVE</b>To investigate the therapeutic effect of nerve growth factor (NGF) on changes of myelin basic protein (MBP) and functional repair of sensory and motor nerve following sciatic nerve injury.</p><p><b>METHODS</b>The sciatic nerves of rats were injured by sectioning with shaver,and divided into 3 groups: NGF group (Group A), group of normal saline solution (Group B), untreated group (Group C). The time point of observation was at the 4th week after operation. Sensory evoked potential (SEP) and motor evoked potential (MEP) were detected by Model WD-4000 nerve potential working diagnosis system. Immunohistochemical analysis was used for identification of MBP.</p><p><b>RESULTS</b>The latency of SEP in the Group A at the 4th week after operation was shorter than that in the Group B (P<0.05). The MEP was elicited in 76% of the Group A and was higher than that in the Group B. Results of immunohistochemistry showed that there were less MBP-positive cells in the Group A than in the Group B in one and four weeks respectively.</p><p><b>CONCLUSIONS</b>NGF can improve the conductive function of injured peripheral nerve and facilitate regeneration of nerve.</p>
Subject(s)
Animals , Female , Rats , Evoked Potentials , Immunohistochemistry , Myelin Basic Protein , Metabolism , Nerve Growth Factor , Pharmacology , Peripheral Nerve Injuries , Peripheral Nerves , Metabolism , Rats, Wistar , Sciatic Nerve , Wounds and Injuries , MetabolismABSTRACT
The changes of the activities of succinic dehydrogenase (SDH) and acid phosphatase (ACP) in spinal motoneurons after ventral cord compression were observed with microphotometry in 15 rabbits.The first lumbar segment of the spinal cord was compressed epidurally with 50g weight for one minute.It was found that statistically significant changes of both SDH and ACP took place immediately and 2 hours after cord compression (P