单纯性脑震荡大鼠室管膜区小胶质细胞的表达变化

目的:观察单纯性脑震荡(pure cerebral concussion,PCC)模型大鼠室管膜区小胶质细胞(microglia MG)的反应和时程变化规律,探讨MG、室管膜区和PCC之间的病理关系和意义。方法:采用金属单摆闭合式脑损伤装置制备PCC模型,致伤后随机分为六个损伤组,即3 h、12 h、1 d、2 d、3 d、7 d(n=5),设正常对照组(n=5)。采用免疫组织化学SP法和免疫荧光单标染色法,观察PCC组和正常对照组大鼠脑室管膜区OX-42(MG特异性标记物)的表达变化。结果:正常对照组大鼠脑室管膜区OX-42阳性的小胶质细胞轮廓不清,数量较少,并且OX-42免疫阳性产物的表达很少。PCC组大鼠脑室管膜区OX-42阳性细胞的数量和阳性产物的表达呈现逐渐增高趋势,3 d组达高峰,7 d组有所下降,但仍高于正常对照组。各时间组与正常对照组相比均有显著性差异(P0.05)。结论:PCC损伤早期大鼠室管膜区的MG出现一系列形态学变化的激活表现,提示脑室管膜区的MG在PCC致伤后的病理变化中扮演着重要角色。     

小胶质细胞在单纯性脑震荡大鼠皮质中的变化

目的:观察单纯性脑震荡(pure cerebral concussion,PCC)大鼠前额叶皮质(prefrontal cortex,PC)、颞叶皮质(temporal cortex,TC)和梨状皮质(piriform cortex,Pir)内小胶质细胞(microglia,MG)的反应和时程变化规律,探讨小胶质细胞与脑损伤之间的病理联系。方法:采用自制金属单摆闭合式脑损伤打击装置制备清醒状态下PCC模型,随机分为伤后3 h、12 h、1 d、2 d、3 d、7 d六个损伤组(n=5),另设正常对照组(n=5)。采用OX-42单克隆抗体(MG特异性标记物)进行免疫组织化学和免疫荧光染色,观察PCC组和正常对照组大鼠PC、TC和Pir中OX-42的表达变化。结果:正常对照组大鼠PC、TC和Pir内OX-42免疫阳性产物的表达很弱,OX-42免疫阳性的小胶质细胞的数量少而轮廓不清。损伤后OX-42免疫阳性产物的表达和阳性细胞的数量逐渐增加,3 d时达高峰,7 d后有下降趋势,但仍高于正常组(P0.05)。结论:PCC损伤早期PC、TC和Pir中MG出现激活的形态学变化,提示MG可能参与了PCC致伤后的病理变化。     

单纯性脑震荡大鼠海马mPGES-1的表达

目的:观察单纯性脑震荡(pure cerebral concussion,PCC)大鼠脑内海马区膜结合型前列素E合酶1(membrane-associated prostaglandin E synthase-1,mPGES-1)的表达变化,探讨mPGES-1是否通过前列腺素代谢途径参与PCC的病理变化及其变化规律。方法:采用清醒状态下自制金属单摆闭合式脑损伤打击装置制备PCC模型,致伤后随机分为3 h、12 h、1 d、2 d、3 d、7 d组(n=5),另设正常对照组(n=5)。采用mPGES-1多克隆抗体进行免疫组织化学法和Western blot技术,检测PCC组和正常组大鼠海马CA1-4区mPGES-1的定位及定量情况。结果:正常状态下,海马CA1-4区mPGES-1阳性细胞极少,轮廓不清,致伤后3 h海马各区的mPGES-1表达水平开始增高,至3 d达高峰,与正常组比较有显著性差异(P<0.05),3 d后逐渐下降,至7 d接近正常水平。mPGES-1蛋白的变化规律和免疫组化结果相似。结论:PCC损伤早期海马区出现mPGES-1表达增强,提示mPGES-1通过前列腺素代谢途径参与PCC致伤后的病理变化。     

单纯性脑震荡对大鼠海马iNOS表达影响的实验研究

目的　观察单纯性脑震荡( pure cerebral concussion, PCC )大鼠海马脑区诱导性一氧化氮合酶( inducible nitric oxide synthase, iNOS )的表达变化,探讨iNOS表达变化规律及其与PCC之间的病理联系。 方法　采用单摆闭合式脑损伤打击装置制造PCC大鼠模型,造模后随机分为3 h、12 h、1 d、2 d、3 d、7 d 六个损伤组( n=5 ),另设正常对照组( n=5 )。采用iNOS单克隆抗体(鼠)进行免疫组织化学SP法染色和Western Blot实验,检测PCC组和正常组大鼠海马( CA1~4及上、下齿状回 ) iNOS表达的定位及定量情况。 结果　正常生理状态下,海马iNOS阳性细胞染色较浅、轮廓不清,且iNOS蛋白表达较弱,致伤后3 h组iNOS阳性表达开始增强,在3 d组出现表达高峰,iNOS蛋白表达高峰出现在2 d组,与正常组比较均有显著性差异( P<0.05 ),随后均出现下降,至7 d均仍高于正常组。 结论　PCC损伤早期海马脑区出现iNOS表达增强,提示iNOS是参与PCC继发性病理损伤的主要炎症因子之一。     

AH6809干预的单纯性脑震荡大鼠海马mPGES-1的表达变化

目的:观察单纯性脑震荡(pure cerebral concussion,PCC)致伤后大鼠海马膜结合型前列腺素E2-合酶1(membrane-associated prostaglandin E synthase-1,mPGES-1)在EP2受体抑制剂(AH6809)干预后的表达变化,探讨AH6809对mPGES-1的干预调控作用。方法:采用金属单摆闭合式脑损伤打击装置制备PCC模型,分别于致伤后即刻和12 h腹腔注射AH6809,然后随机分为1、2、3 d和7 d组(n=5),另设相应生理盐水对照组(n=5)。采用免疫组织化学染色和Western Blot方法,观察PCC+AH6809组和生理盐水对照组大鼠海马(CA1~4和上、下齿状回)内m PGES-1的表达情况。结果:免疫组化实验结果显示:在AH6809干预前后均可观察到mPGES-1阳性产物表达于海马CA1~4和上、下齿状回的神经元胞体,呈圆形或卵圆形,胞核不着色,胞浆为棕黄色。与生理盐水对照组相比,AH6809干预后2 d组均出现mPGES-1阳性表达相对减弱,染色渐浅且细胞轮廓不清,3 d组下调最为明显,其中3 d组和7 d组的差异具有显著性(P0.05)。Western Blot实验结果显示:mPGES-1蛋白出现相似的规律性变化,下降的低峰出现在7 d组,其中2、3、7 d组与对照组相比差异具有显著性(P0.05)。结论:AH6809对PCC大鼠海马mPGES-1的表达具有一定的干预抑制作用。     

慢性脑缺血大鼠海马CA_1区中的BDNF表达

为了观察慢性脑缺血时海马CA1区中BDNF的表达变化,探讨缺血性脑损伤及修复机制。我们将Wistar大鼠双侧颈总动脉结扎制成慢性脑缺血动物模型。分为三组:正常对照组、慢性脑缺血30d和120d组。分别于术后30d和120d处死动物,行BDNF免疫组化染色,计数各组大鼠海马CA1区中的阳性神经元数。结果显示:(1)在对照组的海马CA1区可见BDNF较强的表达;(2)在慢性脑缺血30d时,海马CA1区BDNF的表达高于缺血120d组及对照组(P<0.05)。而120d时,海马CA1区BDNF的表达与对照组无显著性差异(P>0.05)。结果提示:(1)在正常大鼠海马CA1区有BDNF表达,能维持神经元的存活;(2)慢性脑缺血时,BDNF在海马CA1区的表达先升后降。     

肠易激综合征内脏痛大鼠海马胶质细胞炎症反应的相关研究

目的 探讨肠易激综合征（IBS）内脏痛模型大鼠行为学和海马组织内炎症改变。方法 SD大鼠随机分为2组，即正常对照组（10只）、IBS内脏痛模型组（10只）。采用母婴分离、乙酸灌肠、卵清白蛋白腹腔注射等复合方法制备动物模型；采旷场实验评估各组大鼠的情绪心理行为；采用腹壁撤退反应(AWR)评估大鼠内脏敏感性；HE染色观察结肠黏膜组织病理改变；酶联免疫吸附法(ELISA)检测海马区IL-6、TNF-α，血清sIgE、IFN-γ、IL-4的变化；应用免疫组织化学法检测大鼠脑海马区小胶质细胞特异性标记物OX-42、星形胶质细胞特异性标记物GFAP以及P物质（SP）的表达情况。结果 相比于正常对照组，IBS内脏痛模型组大鼠行为学症状明显（P<0.01），在60、40、20 mmHg(1 mmHg=0.133 kPa)压力下AWR评分（大鼠内脏敏感性）明显上升（P<0.05），结肠组织黏膜损伤加重，海马组织内IL-6、TNF-α、SP、OX-42、GFAP均表达升高（P<0.01）。结论 IBS内脏痛大鼠同时存在海马区神经胶质细胞炎症反应加重和情绪行为活动增强。     

大鼠大脑中动脉缺血后海马星形胶质细胞反应的研究

目的:观察大鼠大脑中动脉缺血后皮层损伤侧海马星形胶质细胞反应的变化。方法:采用大鼠大脑中动脉阻塞再灌流模型,应用免疫印迹和免疫组织化学方法测定脑缺血后3 d、7 d以及30 d皮层损伤侧海马胶质纤维酸性蛋白(GFAP)以及增殖细胞核抗原(PCNA)蛋白的表达,观察星形胶质细胞增殖的变化。结果: GFAP免疫组化结果显示,脑缺血后7d皮层损伤侧海马CA1、CA2区星形胶质细胞数量较假手术组增加且胞体增大;脑缺血后30 d皮层损伤侧海马CA1、CA2区呈胶质疤痕样改变。同时,免疫印迹法显示脑缺血后7 d皮层损伤侧海马GFAP表达增强;脑缺血后30 d皮层损伤侧海马GFAP表达增高更加明显。此外,免疫印迹法显示脑缺血后3 d皮层损伤侧海马PCNA蛋白表达水平升高;脑缺血后7 d PCNA蛋白表达水平达到峰值;脑缺血后30 d,PCNA蛋白表达水平降低,但仍高于假手术组。结论: 大鼠大脑中动脉缺血后可引起其皮层损伤侧海马星形胶质细胞过度反应和增殖。     

BMP4参与海人酸损伤后成年大鼠海马齿状回颗粒细胞增殖及胶质增生

目的探讨海人酸（KA）侧脑室注射致大鼠海马损伤后骨形成蛋白-4（BMP4）的表达变化及其与颗粒细胞增殖和胶质细胞增生的关系。方法将成年大鼠分为对照组与实验组。侧脑室注射KA7d后,用尼氏染色检测海马神经元丢失,用免疫组织化学与原位杂交的方法检测海马齿状回BMP4mRNA阳性细胞与BrdU标记细胞、GFAP阳性细胞数的变化。结果正常成年大鼠BMP4mRNA阳性细胞主要分布于海马齿状回的门区、颗粒下层、CA3、CAI区。BrdU标记细胞主要分布在齿状回颗粒下层。GFAP阳性细胞主要分布在齿状回、CA3区。在KA侧脑室注射致海马损伤后7d,海马CA3、CA4区神经元丢失明显,BMP4mRNA阳性细胞与BrdU、GFAP阳性细胞均明显增加。结论KA侧脑室注射致海马损伤后,成年大鼠海马齿状回颗粒细胞增殖增强和胶质增生可能与BMP4表达增加有关。     

多重脑震荡大鼠脑神经元病理变化的研究

为探讨多重脑震荡(multiple cerebral concussion,MCC)后脑损伤的累加效应机制,本实验首次应用自制单摆式机械打击装置复制MCC大鼠模型,研究伤后大鼠脑神经元的组织病理学变化。将56只大鼠随机分为7组:对照组、伤后1、2、4、8、16和24d组(n=8),分别用Nissl染色显示神经元,并对变性神经元进行计数。结果显示:MCC后1d,大鼠大脑皮层、海马、齿状回及脑干网状结构变性神经元增加,伤后2d达到高峰,4～8d减轻,8～16d又有回升,24d基本恢复至正常水平。以上结果提示,多重脑震荡后,不同脑区的脑神经元可出现早期及迟发性的神经元变性,此病理变化可能与多次脑损伤的累积性加重有关。     

Sleep deprivation inhibits expression of NADPH-d and NOS while activating microglia and astroglia in the rat hippocampus

This study investigated the expression of nitric oxide (NO)-synthesizing enzymes and the glial reaction in the rat hippocampal formation following sleep deprivation for 5 days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas. Microglial cells were hypertrophic and showed an up-regulation of complement type 3 receptors as determined by antibody OX-42. However, expression of major histocompatibility complex class I and II antigens, and antigen of monocyte/macrophage lineage marked by OX-18, OX-6 and ED1, respectively, was undetected. Astrocytes also displayed hypertrophied processes with enhanced glial fibrillary acidic protein (GFAP) immunoreactivity. Western blots of hippocampal tissues corroborated the above-mentioned morphological findings in that expression of NO-synthase (NOS) was decreased while that of OX-42 and GFAP was increased in the sleep-deprived rats. Since NO is thought to be involved in memory consolidation processes in the hippocampus during sleep, the inhibition of NADPH-d and NOS reactivities may account for the memory decline after long-term sleep deprivation. The concomitant reactions in microglia and astrocytes suggest the involvement of these cells in the deleterious effect of prolonged sleep deprivation.     

Induction of inducible nitric oxide synthase expression in activated microglia following domoic acid (DA)-induced neurotoxicity in the rat hippocampus

Neuronal degeneration followed by glial activation (microglia and astrocytes) and nitric oxide synthase (NOS) expression in the hippocampus was investigated at 3 months after domoic acid (DA) administration and compared with DA treated rats at 5 days time interval which was reported earlier. Massive degeneration with complete absence of neurons in the hippocampal CA1 and CA3 regions and hypertrophied microglial cells showing intense immunoreaction with the antibody OX-42 was observed at 3 months after DA administration. Sparsely distributed OX-42 positive microglial cells were observed in the hippocampus of control rats at 3 months after saline treatment No apparent changes could be observed in the immunoreactivity of GFAP at 3 months after saline and DA administration. Neuronal nitric oxide synthase immunoreactive neurons were completely absent in the hippocampus at 3 months after DA administration. In contrast, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemical analysis revealed absence of NADPH-d reactivity in the neurons, but positive reactivity in the microglial cells of CA1-CA3 regions in the hippocampus after DA treatment. Double immunofluorescense revealed co-expression of inducible nitric oxide synthase with immunoreactive OX-42 positive microglial cells in the hippocampal subfields at 3 months after DA administration. The microglia-produced NO appears to be a secondary phenomenon in the prolonged inflammatory process following DA-induced neuronal degeneration.     

复方丹参对脑缺血再灌注后大鼠海马和齿状回神经细胞凋亡及Bcl-2 mRNA表达的影响

目的:探讨中药复方丹参对大鼠脑缺血再灌注后海马和齿状回神经细胞凋亡及Bcl-2 mRNA表达的影响。方法:采用大脑中动脉内栓线法建立大鼠大脑中动脉缺血再灌注模型,应用原位细胞凋亡检测和原位杂交技术检测大鼠海马和齿状回神经细胞凋亡和Bcl-2 mRNA的表达并做图像分析。结果:与假手术对照组比较,缺血再灌注组凋亡神经细胞主要位于缺血侧海马CA1、CA3区,齿状回凋亡细胞较少。3个区神经细胞Bcl-2mRNA的表达在缺血再灌注2 h后升高,随时间的延长逐渐增强。复方丹参组神经细胞Bcl-2 mRNA的表达明显强于缺血再灌组,而凋亡神经细胞数明显较低。结论:复方丹参可通过上调神经细胞Bcl-2 mRNA的表达,抑制神经细胞凋亡,从而减轻缺血再灌注对大鼠海马和齿状回的损伤。     

前脑缺血再灌流后大鼠海马 NMDA受体亚单位NR1蛋白的表达变化

目的　观察大鼠前脑缺血再灌流后海马各区域NMDA受体亚单位NR1表达的变化和差异 ,探讨NR1在缺血性脑损伤中的作用。　方法　免疫组织化学和图像处理技术。　结果　 1 在前脑缺血再灌流后早期 ,海马各区域NR1的表达水平显著下降 (P <0 0 5 )。CA1区 ,下降趋势持续存在且不可逆 ,直至再灌流后第 7d ,NR1在该区域的染色强度降至对照组的 17% (P <0 0 5 )。CA3区及齿状回 ,NR1的表达下降是可逆的 ,再灌流后 72h ,齿状回的表达恢复正常 ,再灌后第 7d ,CA3区的表达也恢复到对照组的 96 % ,两组间染色强度无显著差异。 2 在迟发性神经元坏死出现前的缺血再灌流的早期 ,NR1在CA1区、CA3区及齿状回表达下降的幅度不一致 ,再灌后 6h以前 ,CA1区的下降幅度明显小于CA3区及齿状回 (P <0 0 5 ) ,再灌后 12h ,CA1区的下降幅度仍低于CA3区 (P <0 0 5 )。结论　短暂性前脑缺血后 ,NR1在海马CA1区、CA3区及齿状回表达下降的幅度和可逆性存在显著差异 ,这种差异可能是造成CA1区缺血敏感性的重要原因。     

Ischemia-related changes of adrenocorticotropic hormone immunoreactivity and its protective effect in the gerbil hippocampus after transient forebrain ischemia

In the present study, the temporal and spatial alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the gerbil hippocampus after 5 min transient forebrain ischemia were investigated as followed up 7 days after ischemic insult, and the effects of ACTH after ischemic insult were also investigated 4 days after ischemic insult. The ectopic expression of ACTH (1-24 fragments) immunoreactive neurons in the cornus ammonis 1 (CA1) region of hippocampus and hilar region of the dentate gyrus 1 day after the ischemic insult was observed. Judging from the double immunofluorescence study, these neurons contain GABA. Four days after ischemic insult, the ACTH immunoreactivity was localized in CA1 pyramidal cells and glia near the stratum pyramidale, which normally do not express ACTH. In addition, in the saline-treated groups, the percentage of the detected Cresyl Violet positive neurons was 11.2% compared with the sham-operated group 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were detected in the strata pyramidale, oriens and radiatum. However, in the Org2766 (analog of ACTH)-treated group, 57.8% neurons compared with the sham-operated group were stained with Cresyl Violet 4 and 7 days after ischemic insult. In these groups, the OX-42 immunoreactive microglia were significantly reduced in the stratum pyramidale. These results suggest that transient forebrain ischemia may provoke selective ectopic and enhanced expression of ACTH in the hippocampus, and further suggest that ACTH plays an important role in reducing the ischemic damage.     

Regional differences in hypoxic depolarization and swelling in hippocampal slices

Pyramidal neurons in the CA1 region of the hippocampus are highly vulnerable to damage from hypoxia-ischemia, whereas neurons in the CA3 region and the dentate gyrus are more resistant. A similar pattern of vulnerability to loss of synaptic and membrane function occurs in the in vitro hippocampal slice preparation, suggesting that intrinsic factors are important in acute neuronal damage. Simultaneous recordings of DC potential and imaging of changes in light transmittance were made in slices from the middle one-third of the hippocampus to characterize the initiation and spread of depolarization and swelling during hypoxia-aglycemia. Hypoxic depolarization (HD) and associated optical changes were initiated simultaneously in the stratum oriens of the CA1 region and thereafter spread to the stratum radiatum of CA1 and later to the upper (inner) blade of the dentate gyrus. A decrease in light transmittance was associated consistently with depolarization in all regions (n = 22 slices). Investigation of the sequence of activation in intact slices showed that activation of the dentate gyrus arose independently of activation of the CA1 region. This was confirmed by recordings made from minislices in which CA1, CA3, and dentate regions were physically separated. HD and optical changes were never observed in the CA3 region, despite exposure to 40-60 min of combined hypoxia and aglycemia. In contrast, exposure to hypoxia after pretreatment of slices with altered tonicity or ion composition, which triggered episodes of spreading depolarization (SD), provoked depolarization and optical changes simultaneously in both CA1 and CA3 regions. Similarly, pretreatment with agents that cause severe metabolic impairment, such as dinitrophenol (DNP), also rendered the CA3 region vulnerable to subsequent hypoxia. This suggests that the CA3 region in hippocampal slices is normally resistant to HD and only becomes vulnerable after severe impairment of metabolic capacity. The similar order of vulnerability of in vitro and in vivo hippocampus to hypoxia-aglycemia supports the use of the hippocampal slice preparation to investigate early changes potentially contributing to hypoxic-ischemic injury.     

Kainic acid-mediated increase of preprotachykinin-A messenger RNA expression in the rat hippocampus and a region-selective attenuation by dexamethasone.

The hippocampus contains the highest number of glucocorticoid-sensitive neurons in the rat brain and excessive exposure to glucocorticoids can cause damage to hippocampal neurons and impair the capacity of the hippocampus to survive neuronal insults. In this study in situ hybridization combined with quantitative image analysis was used to study preprotachykinin-A mRNA levels after administration of a toxic dose of kainic acid in animals pretreated with glucocorticoids. Kainic acid was injected into dorsal hippocampus CA3 region in animals pretreated with the synthetic glucocorticoid receptor agonist dexamethasone and in control animals. Preprotachykinin-A mRNA was not detected in the hippocampus of untreated animals or in animals analysed 30 min after a kainic acid injection. However, 4 h after injection of kainic acid, the level of preprotachykinin-A mRNA increased to 20-times above the detection limit both in the dentate gyrus and the CA3 region of the hippocampus. Treatment of kainic acid-injected animals with dexamethasone 30 min before and 2 h after the injection attenuated the increase in the granule cells of the dentate gyrus by 50%. In contrast, dexamethasone pretreatment had no significant effect on the kainic acid-induced increase of preprotachykinin-A mRNA in pyramidal cells in regions CA3 or CA1. These results show that an excitatory stimulus within the hippocampus causes a substantial increase in the level of preprotachykinin-A mRNA in hippocampal granule and pyramidal cells and suggest that in granule cells of the dentate gyrus this increase can be modulated by glucocorticoids.     

马桑内酯致痫大鼠海马内c－fos原癌基因表达及谷氨酸免疫反应的变化

用免疫细胞化学双重染色法对马桑内酯致痫大鼠齿状回及海马回ＣＡ３区内原癌基因表达、谷氨酸免疫反应的变化及其相互关系进行了研究。一侧侧脑室内注射马桑内酯诱发癫痫后，在双重免疫细胞化学染色的切片上，齿状回及海马回ＣＡ３区内均有３种不同类型的细胞：谷氨酸（Ｇｌｕ）单标细胞、Ｆｏｓ单标细胞和Ｆｏｓ／Ｇｌｕ双标细胞。癫痫发作后１ｈ，注射侧齿状回有大量Ｆｏｓ／Ｇｌｕ双标细胞，而海马回ＣＡ３区仅有散在的双标细胞；癫痫发作后１．５ｈ，海马回ＣＡ３区双标细胞数明显增多。Ｆｏｓ单标细胞数及谷氨酸免疫反应性与双标细胞数是平行的。根据以上结果，本文对马桑内酯致痫的机制进行了讨论。     

Seizure-induced changes of mineralocorticoid and glucocorticoid receptors in the hippocampus in seizure sensitive gerbils

Abnormal corticosteroid hormone levels during stress and resultant mineralocorticoid receptor (MR)/glucocorticoid receptor (GR) imbalance enhance the vulnerability of specific hippocampal neurons. In the present study, we investigated the distribution of MR and GR in seizure resistant (SR) and seizure sensitive (SS) gerbils, and observed the seizure-induced changes of MR and GR in the hippocampus of SS gerbils using immunohistochemistry and western blot analysis. MR and GR immunoreactivities were higher in the SS pre-seizure gerbils than that in SR gerbils. In the SR gerbils, the immunodensity of GR was high compared to that of MR. The changes of MR and GR immunoreactivities were significant in the stratum pyramidale of the hippocampal CA1 region and the infrablade of the dentate gyrus after seizure on-set. MR immunoreactivity in the CA1 region was significantly increased at 12h after seizure on-set, thereafter MR immunoreactivity was decreased. MR immunoreactivity in the dentate gyrus was decreased time-dependently after seizure on-set. GR immunoreactivity was decreased in the CA1 region and dentate gyrus time-dependently after seizure on-set. At 12h after seizure on-set, differences in MR and GR immunodensity diminished in the CA1 region and dentate gyrus. This imbalance of MR and GR immunoreactivity in these regions may be associated with seizure generation in the Mongolian gerbil, which is a hereditary seizure model.