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脂多糖对γ-丁内酯致大鼠失神发作皮层脑电图的影响

Influence of electrocorticogram (ECoG) in rats following absence seizures induced by γ-Butyrolactone
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摘要 目的:观察脂多糖(LPS)对γ-丁内酯(GBL)诱导大鼠失神发作皮层脑电图棘慢波(SWDs)的影响,并推测其可能的机制。方法:40只SD大鼠随机分为4组:实验1、2、3组及对照组,每组10只。分别腹腔注射LPS50μg/kg、100μg/kg、200μg/kg及NS1ml,1h后每组随机取5只大鼠处死取海马用RT-PCR方法检测IL-1βmRNA表达的变化;另外5只大鼠腹腔注射GBL200mg/kg诱发失神发作,观察皮层脑电图(ECoG)SWDs潜伏时间、持续时间的改变。结果:LPS腹腔注射后1h大鼠海马组织IL-1βmRNA表达:50μg/kg组0.196±0.04、100μg/kg组0.285±0.057、200μg/kg组0.404±0.072,与对照组(0.131±0.034)比较均有显著差异(P<0.05);另外,LPS不同剂量组大鼠失神发作SWDs放电潜伏时间均较对照组缩短、持续时间延长,两者有显著差异(P<0.05)。其中实验2、3组SWDs潜伏时间与持续时间较实验1组潜伏时间更为缩短,持续时间更为延长(P<0.05);但实验3组SWDs潜伏时间和持续时间与实验2组比较没有差异(P>0.05)。结论:LPS能影响GBL诱导大鼠失神发作的SWDs发放,缩短其潜伏时间、延长持续时间,并且有剂量依赖性及饱和性,其机制可能与LPS刺激机体引起的免疫异常有关。 Objective:To investigate the influence of bacterial lipopolysaccharides on SWDs on ECoG in rats following γ-Butyro- lactone-induced absence seizures, and speculate on its possible mechanism. Method: Forty adult SD rats were randomly divided into four groups, intraperitoneally and injected with 50μg/kg, 100 mg/kg, and 200μg/kg of LPS, and 1 ml of saline respectively. One hour later, five rats randomly selected from each group were sacrificed and changes of IL-1βmRNA in the hippocampi were detected by RT-PCR, while the other five rats were intraperitoneally injected with 200μg/kg of GBL to induce absence seizures and variations of latency and endurance time of SWD on ECG were recorded. Results:The expression of IL-1βmRNA in the hippocampi of rats one hour after intraperitoneal injection in the 50μg/kg group was 0.196 ± 0.04, while in the 100μg/kg and 200μg/kg group was 0.285 ± 0.057 and 0.404 ± 0.072,respectively, all significantly different from the control group, which was 0.131 ± 0.034 (P 〈 0.05). Besides, The SWDs latency time of discharge in absence seizure rats in the experiment groups was significantly shorter than that of the control group, while the duration time was longer(P 〈 0.05). Though the latency time the 50μg/kg and 100 μg/mg group was shorter while the durance time longer compared with that of the 50 μg/kg group (P 〈 0.05), there was no significant difference in the 50μg/kg and 100μg/kg group (P 〉 0.05). Conclusion:LPS could affect the SWDs of GBL-induced absence seizure in rats by shortening the latency time and elongating the duration time with dose dependence and saturation, the mechanism of which is probably related to the abnormal immunity stimulated by LPS.
出处 《南京医科大学学报(自然科学版)》 CAS CSCD 北大核心 2009年第2期182-185,共4页 Journal of Nanjing Medical University(Natural Sciences)
基金 南京市医学科技发展项目(YKK0784)
关键词 Γ-丁内酯 脂多糖 SD大鼠 失神癫痫 脑电图 γ-Butyrolactone lipopolysaccharide rat absence seizure electrocorticogram
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参考文献13

  • 1Maroder M, Bellavia D, Vacca A, et al. The thymus at the crossroad of neuroimmune interactions [J]. Ann N Y Acad sci, 2000,917 (12) : 741-774
  • 2Schiffelholz T, Lancel M. Sleep changes induced by lipopolysaccharide in the rat are influenced by age [J]. Am J Physiol Regul Integr Comp Physiol ,2001,280(2): 398-403
  • 3Steriade M. Sleep, epilepsy and thalamic reticular inhibitory neurons[J]. Trends Neurosci,2005,28(6) :317-324
  • 4Emmanuelle Hetier, Jesus Ayala, Anne Bousseau, et al. Ameboid microglia cells and not astrocytes synthesize TNFα in Swiss mouse brain cultures[J]. Eur J Neurosci, 1990,2(9) : 762-768
  • 5周峰,王小姗,李继民.γ-羟基丁酸致大鼠失神发作的行为学及皮层电图的对比研究[J].临床神经电生理学杂志,2008,17(1):10-13. 被引量:2
  • 6Turrin NP, Gayle D, llyin SE, et al. Pro-inflammatory and anti-inflammatory cytokine mRNA induction in the periphery and brain following intraperitoneal administration of bacterial lipopolysaccharide [J]. Brain Res Bull, 2001,54(4) :443-453
  • 7Iliev A, Traykov V, Stoykov I, et al. Estradiol inhibits astrocytic GFAP expression in an animal model of neuroinflammation [J]. Methods Find Exp Clin Pharmacol, 2001,23 ( 1 ) : 29-35
  • 8Kovacs, Kekesi KA, Szilagyi N, et al. Facilitation of spikewave discharge activity by lipopolysaccharides in Wistar Albino Glaxo/Rijswijk rats [J]. Neuroscience,2006,140 (2) :731-742
  • 9Ban E, Haour F, Lenstra R. Brain interleukin 1 gene expression induced by peripheral lipopolysaccharide administration[J]. Cytokine, 1992,4( 1 ) :48-54
  • 10Liya Qin,Jun He,Richard NH,et al. Increased systemic and brain cytokine production and neuroinflammation by endotoxin following ethanol treatment[J]. Journal of Neuroinflammation, 2008,5 (6) : 10

二级参考文献10

  • 1Gervasi N, Monnier Z, Vincent P, et al. Pathway-Specific Action of γ-Hydroxybutyric Acid in Sensory Thalamus and Its Relevance to Absence Seizures[J]. J Neurosci, 200:3, 2:3(36) : 11 469-11 478
  • 2Galloway GP, Frederick SI, Staggers FE, et al. Gammahydroxybutyrate : an emerging drug of abuse that causes phys iealdependence[J]. Addiction, 1997, 92(1): 89-96.
  • 3Bearden LJ, Snead OC, Healy CT, et al. Antagonism of gam ma-hydroxybutyrate induced frequency shifts in the cortical EEG of rats by dipropylacetate[J]. EEG Clin Neurophysiol, 1980, 49: 181-183.
  • 4Tenney JR . Duong TQ, King JA, et al. Corticothalamic Modulation during Absence Seizures in Rats: A Functional MRI Assessment[J]. Epilepsia, 2003, 14(9): 1 133-1 140.
  • 5Snead OC. Ontogeny of gamma hydroxybutyric acid. II. Electroencephalographic effects[J]. Brain Res, 1984, 317(1): 89 -96.
  • 6Crunelliv, Emri Z, Leresche N. Unraveling the brain targets ofγ-hydroxybutyric acid[J]. Current Opin Pharmacol, 2006, 6 : 44-52.
  • 7Hu RQ, Baneriee PK, Snead OC et al. Regulation of gammaaminobutyric acid (GABA) release in cerebral cortex in the gamma-hydroxybutyric acid (GHB) model of absence seizures in rat[J]. Neuropharmacology, 2000, 39(3) :427-439.
  • 8Lingenhoehl K, Brom R, Heid J, et al. Gamma hydroxybutyrate is a weak agonist at recombinant GABA (B) receptors [J]. Neuropharmacology, 1999 , 38(11): 1 667-1 673.
  • 9Feigenbaum J J, Howard SG. Gamma hydroxybutyrate is not a GABA agonist[J]. ProgNeurobiol, 1996, 50(1): 1-7.
  • 10Snead OC. Evidence of G protein-coupled gamma hydroxybutyric acid receptor[J]. J Neurochemist, 2000 , 75(5): 1 986-1 996.

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