经皮三叉神经电刺激减轻戊四氮诱导的大鼠癫痫发作并抑制海马内IL-1β和TNF-α的表达

 目的:探讨经皮三叉神经电刺激预处理对戊四氮（PTZ）诱发的急性癫痫大鼠的行为学及海马致痫细胞因子白细胞介素1β(IL-1β)及肿瘤坏死因子α(TNF-α)的影响。方法:动物随机分为对照组、致痫组（PTZ组）和经皮三叉神经电刺激组,分别给予7 d、14 d和28 d的假刺激和三叉神经电刺激预处理后,腹腔注射PTZ 建立急性癫痫动物模型,观察给药后大鼠癫痫行为学表现,并分别用免疫组织化学方法及ELISA方法对海马IL-1β、TNF-α进行检测。结果:经皮三叉神经电刺激可以明显减轻大鼠的痫性发作级别,减少癫痫发作持续的时间（P<0.05）, 且海马细胞因子IL-1β及TNF-α的表达明显少于PTZ组（P<0.05或P<0.01）。结论:经皮三叉神经电刺激预处理在PTZ 急性点燃癫痫大鼠模型中不仅具有抗惊厥作用, 还可以减少海马致痫细胞因子IL-1β及TNF-α的表达,可能为癫痫的防治带来新的策略。       

癫痫发作敏感大鼠T区Bcl-2蛋白表达变化

为探讨前深梨状皮层T区中Bcl- 2蛋白的表达变化在红藻氨酸诱导的癫痫发作敏感性长期增强中的作用,本研究以免疫组化方法检测癫痫发作敏感大鼠前深梨状皮层T区Bcl- 2蛋白表达变化,以硫堇染色观察神经元脱失情况,并与经蝎毒处理后癫痫发作敏感性明显降低的大鼠进行比较。结果显示:与对照组比较,癫痫发作敏感大鼠前深梨状皮层T区Bcl 2蛋白免疫反应阳性细胞数目明显减少,染色强度明显降低(P<0. 05),神经元数量明显减少;以剂量为100mg/ (kg·d)的蝎毒给予动物连续灌胃4周,可明显降低其癫痫发作敏感性(P<0. 05),脑内前深梨状皮层神经元脱失程度减轻,Bcl- 2蛋白免疫反应产物与对照组相比无明显变化。以上结果提示,前深梨状皮层T区Bcl- 2蛋白表达减少可能是癫痫发作敏感性长期增强的重要原因之一。     

Wortmannin通过抑制癫痫大鼠海马自噬活性发挥神经保护作用

目的:探讨癫痫大鼠海马自噬活性的变化及自噬抑制剂wortmannin(WM)对致痫大鼠海马神经元的保护作用。方法:实验大鼠分为对照组、致痫2 h、8 h、16 h、24 h、72 h组和WM干预组。应用HE染色和Nissl染色观察癫痫大鼠海马神经元损伤的变化。免疫印迹检测海马组织微管相关蛋白1轻链3(LC3)Ⅱ/LC3Ⅰ的比值作为自噬活性的指标。结果:LC3Ⅱ/LC3Ⅰ比值在大鼠癫痫发作2 h时开始升高,24 h达到高峰,持续升高至少72 h。致痫24 h时海马CA1区出现明显神经元损伤和丢失。WM干预组CA1区存活神经元数目(100.88±18.73)显著高于癫痫组(70.16±5.09)(P0.05),LC3Ⅱ/LC3Ⅰ的比值低于癫痫组(P0.05)。结论:癫痫发作导致的海马损伤时存在自噬激活现象;WM通过抑制自噬活性减轻癫痫发作所致的海马损伤,具有神经保护作用。     

布洛芬通过下调环氧化酶2降低癫痫大鼠海马神经元兴奋性

目的:研究布洛芬对慢性癫痫大鼠海马区环氧化酶2(COX-2)和神经元兴奋性的影响。方法:选用雄性健康SD大鼠48只,随机分为3组,分别为对照组(control)、癫痫组(epilepsy)和治疗组(ibuprofen)。运用戊四氮(PTZ)诱导建立慢性癫痫大鼠模型并用布洛芬干预,采用行为学观察检测大鼠癫痫发作水平,运用免疫组织化学染色和Western Blot技术检测大鼠海马区COX-2的表达情况,运用全细胞膜片钳技术收集并分析大鼠海马区动作电位的变化情况。结果:与对照组相比,癫痫组大鼠癫痫发作明显,海马区COX-2表达升高,海马神经元兴奋性升高(P 0.05);治疗组大鼠癫痫发作等级降低,海马区COX-2表达明显降低,海马神经元兴奋性降低(P 0.05)。结论:布洛芬通过下调COX-2降低癫痫大鼠海马神经元的兴奋性,降低癫痫发作强度,具有一定的保护作用。     

马桑内酯致痫大鼠海马神经元丢失及化学性质的研究

为观察癫痫发作过程海马神经元丢失细胞的主要死亡方式 ,用马桑内酯建立慢性致痫大鼠模型 ,以 Nissl染色、免疫组化、TUNEL法以及后二者相结合的技术 ,对海马神经元及其中的抑制性神经元的丢失进行了分区观察、统计、分析。结果发现 :致痫组海马各区神经元较对照组明显减少 ,不同区域减少程度不同 ,以齿状回减少最为明显 ;免疫组化结果显示 ,致痫组的抑制性神经元 GABA-IR神经元、PV-IR神经元、CB-IR神经元在海马各区有不同程度的减少 ,其中 GABA-IR神经元减少最明显。在海马各区所有丢失的神经元中 ,三种抑制性神经元所占的比例不同 ;并在海马各区均可见到 TUNEL -GABA、TUNEL-PV、TU NEL-CB双重反应阳性神经元。提示 :马桑内酯所致的癫痫发作 ,可引起海马神经元丢失 ,且不同区域丢失的程度不同 ,丢失的神经元可能以凋亡方式为主 ;海马抑制性神经元 GABA-IR、PV-IR、CB-IR神经元在癫痫发作过程中也有不同程度的丢失 ,丢失很可能也是以凋亡形式为主     

转化生长因子β1降低大鼠自发性癫痫发作并抑制胶质细胞活化

 目的：观察经鼻给予转化生长因子β₁（TGF-β₁）是否能减少匹罗卡品致痫大鼠慢性自发性癫痫的发作并探讨其可能机制。方法：经鼻给予大鼠重组人TGF-β₁或等量PBS溶液,以匹罗卡品建立癫痫持续状态模型,癫痫持续状态后7 d经动态视频记录其活动,通过胶质纤维酸性蛋白(GFAP)和离子钙结合接头分子1（Iba1）免疫组化观察癫痫大鼠海马组织胶质细胞的活化,采用尼氏染色观察海马区神经元的死亡。结果：TGF-β₁有效降低自发性癫痫的平均频率、发作程度和持续时间。癫痫持续状态后14 d TGF-β₁治疗组海马区活化的胶质细胞明显少于匹罗卡品模型组（P<0.05）;TGF-β₁显著降低海马CA3区神经元的死亡(P<0.01)。结论：经鼻给予TGF-β₁可降低大鼠自发重复性癫痫发作,抑制胶质细胞活化,从而减少神经元的死亡。     

激活的星形胶质细胞分泌的TNF-α对大鼠离子型谷氨酸受体1表达的影响

目的探讨星形胶质细胞在癫痫发病中的作用。方法选用肿瘤坏死因子TNF-α(TNF-α)刺激及TNF-α反义寡核苷酸阻断后马桑内酯(CL)刺激纯化培养的海马星形胶质细胞，将这两种条件培养基提取液(ACM)10μl分别注入正常大鼠侧脑室，观察动物行为与脑电图的变化；用免疫细胞化学方法检测大脑皮质与海马中离子型谷氨酸受体(NMDARI)表达水平的改变，并做显微图像分析。结果1．侧脑室注射肿瘤坏死因子TNF-α刺激后的条件培养基提取液可引起大鼠Ⅲ级癫痫样发作及典型的尖波、棘波、棘-慢波癫痫样脑电图表现，大脑前梨状皮质和海马CA1区NMDAR1免疫反应阳性神经元数和平均光密度值均明显高于对照组；2．侧脑室注射TNF-α反义寡核苷酸阻断后由马桑内酯刺激的条件培养基提取液，大鼠无癫痫样行为发生，大脑前梨状皮质和海马CA1区NMDAR1免疫反应阳性神经元数和平均光密度值与对照组无显著性差异。结论1．激活的星形胶质细胞分泌的TNF-α可诱导大鼠癫痫发作。2．NMDAR1表达的变化可能与癫痫发作有关。     

GABA能神经成分对大鼠咀嚼肌本体觉传入进行初级整合的形态学…

本文作者普证明，三叉神经感觉主核背内侧区和三叉上核尾外侧部是大鼠三叉神经本体觉三级传入通路中继站。为证实此二处的ＧＡＢＡ能丘脑投射神经元和中间神经元是否参与三叉神经本体觉的传导和初级整合并阐明其整合机制，用ｒｉｃｉｎ毁损三叉神经中脑核神经元及其终末，ＨＲＰ逆行标记此区的丘脑投射神经元以及抗ＧＡＢＡ免疫组化三者结合的方法，在电镜下发现：（１）中脑核神经元的溃变终末与该二区神经毯中的ＧＡＢＡ能三叉－丘     

红藻氨酸诱导内质网应激模型的途径

背景:前期研究表明,海马内注射红藻氨酸海可诱发兴奋性红藻氨酸受体KA1亚受体在海马神经元的表达明显上调,内质网应激标志物磷酸化真核翻译起始因子2α表达增加并伴随细胞死亡。目的:探讨红藻氨酸海马内注射后内质网应激发生的机制。方法:取昆明小鼠32只,将0.15 nmol红藻氨酸注入海马CA1区域,注射时间为60 s。分别于红藻氨酸注射后第1,2,3,4,5,6,8,12小时灌注取脑,灌注取脑前进行Bederson体征评分,然后行全脑切片FJB染色分析与免疫荧光双标记观察。结果与结论:1红藻氨酸注射后第3,4,5,6,8小时,Bederson体征评分表明中枢神经功能出现明显损伤,FJB染色示小鼠海马内神经元死亡明显;注射后第1,2,12小时,Bederson体征评分中枢神经功能未见明显损伤,FJB染色小鼠海马神经元死亡结果不明显。2根据FJB结果,取第3,8小时的脑片做免疫组化。海马内注射红藻氨酸后导致海马神经元中KA1和磷酸化真核翻译起始因子2α在相同的时间点表达明显上调,将KA1与磷酸化真核翻译起始因子2α图片结果进行叠加处理,两者完全重合,表明KA1的表达和内质网应激发生在同一个神经细胞内。结果表明红藻氨酸首先诱导了兴奋性膜上受体KA1表达的上调,其KA1的表达上调可能引起细胞内质网功能紊乱,导致内质网应激反应,并进一步促进了神经细胞的死亡。     

高血糖加重缺血性脑损伤

目的：探讨高血糖对脑缺血损伤的影响。方法：采用大鼠高血糖全脑缺血模型,用HE和TUNEL染色,对比检测脑细胞损伤和凋亡。结果：高血糖组在缺血再灌注后与血糖正常组相比,纹状皮质脑水肿和神经元变性、死亡明显加重;海马CA1区损伤神经元计数无显著性差异;海马CA3区损伤神经细胞数明显多于血糖正常组。TUNEL染色可见,在纹状皮质、海马CA1区和CA3区高血糖组和血糖正常组阳性细胞明显多于对照组;在缺血或再灌注后,正常血糖组和高血糖组的TUNEL阳性细胞数均无显著性差异。结论：高血糖可加重缺血引起的神经元损伤。     

Protective effects of mossy fiber lesions against kainic acid-induced seizures and neuronal degeneration

The effects of a hippocampal mossy fiber lesion have been determined on neuronal degeneration and limbic seizures provoked by the subsequent intracerebroventricular administration of kainic acid to unanesthetized rats. Mossy fiber lesions were made either by transecting this pathway unilaterally or by destroying the dentate granule cells unilaterally or bilaterally with colchicine. All control rats eventually developed status epilepticus and each temporally discrete seizure that preceded status epilepticus was recorded from the hippocampus ipsilateral to the kainic acid infusion before the contralateral hippocampus. A mossy fiber lesion of the ipsilateral hippocampus prevented the development of status epilepticus in 26% of subjects and in 52% of subjects seizures were recorded from the contralateral hippocampus before the ipsilateral hippocampus. Unlike electrographic records from other treatment groups, those from rats which had received a bilateral colchicine lesion exhibited no consistent pattern indicative of seizure propagation from one limbic region to another. A bilateral, but not a unilateral, mossy fiber lesion also dramatically attenuated the behavioral expression of the seizures. Regardless of its effects on kainic acid-induced electrographic and behavioral seizures, a mossy fiber lesion always substantially reduced or completely prevented the degeneration of ipsilateral hippocampal CA3-CA4 neurons. This protective effect was specific for those hippocampal neurons deprived of mossy fiber innervation. Neurons in other regions of the brain were protected from degeneration only when the mossy fiber lesion also prevented the development of electrographic status epilepticus. These results suggest that the hippocampal mossy fibers constitute an important, though probably not an obligatory, link in the circuit responsible for the spread of kainic acid seizures. Degeneration of CA3-CA4 neurons appears to depend upon (1) the duration of hippocampal seizure activity and (2) an as yet undefined influence of or interaction with the mossy fiber projection which enhances the neurodegenerative effect of the seizures.     

Deep brain stimulation for refractory epilepsy

Deep brain stimulation (DBS) is a method of treatment utilized to control medically refractory epilepsy (RE). Patients with medically refractory epilepsy who do not achieve satisfactory control of seizures with pharmacological treatment or surgical resection of the epileptic focus and those who do not qualify for surgery could benefit from DBS. The most frequently used stereotactic targets for DBS are the anterior thalamic nucleus, subthalamic nucleus, central-medial thalamic nucleus, hippocampus, amygdala and cerebellum. The DBS is believed to be an effective method of treatment for various types of epilepsy among adults and adolescents. Side effects may be associated with implantation of electrodes and with the stimulation itself. An increasing number of publications and growing interest in DBS application for RE may result in standardization of the qualification and treatment protocol for RE with DBS.     

Damage to the amygdalo-hippocampal projection in temporal lobe epilepsy: a tract-tracing study in chronic epileptic rats

Both the amygdala and hippocampus are damaged in drug-resistant temporal lobe epilepsy (TLE), suggesting that amygdalo-hippocampal interconnectivity is compromised in TLE. Therefore, we examined one of the major projections from the amygdala to the hippocampus, the projection from the amygdala to the CA1 subfield of the hippocampus/subiculum border region, and assessed whether it is preserved in rats with spontaneous seizures. Male Wistar rats were injected with kainic acid (9 mg/kg, i.p.) to induce chronic epilepsy. The occurrence of spontaneous seizures was monitored 5 or 15 weeks later by video-recording the rats for up to 5 days. Saline-injected animals served as controls. Thereafter, the retrograde tracer Fluoro-gold was injected into the border region of the temporal CA1/subiculum. Rats were perfused for histology 1-2 weeks later and sections were immunohistochemically processed to detect Fluoro-gold-positive cells. Comparison of the labeling in control and epileptic tissue indicated that a large cluster of retrogradely labeled cells in the parvicellular division of the basal nucleus was well preserved in epilepsy, even when the neuronal damage in the amygdala was substantial. Another large cluster of retrogradely labeled cells in the lateral division of the amygdalo-hippocampal area, the posterior cortical nucleus (part of the vomeronasal amygdala), and the periamygdaloid cortex (part of the olfactory amygdala), however, had disappeared in epileptic brain in parallel to severe neuronal loss in these nuclei. These data demonstrate that a projection from the parvicellular division of the basal nucleus to the temporal CA1/subiculum region is resistant to status epilepticus-induced neuronal damage and provides a candidate pathway by which seizure activity can spread and propagate from the amygdala to the hippocampal formation.     

Interruption of supramammillohippocampal afferents prevents the genesis and spread of limbic seizures in the hippocampus via a disinhibition mechanism

In this study we describe the preventive effect of interruption of the supramammillohippocampal afferents on the Fos expression in the forebrain and epileptic discharges in the hippocampal electroencephalogram in rat model of kainic acid-induced limbic seizure. Little was known about the contribution of different degrees of neural activity of hippocampal principal cells to the genesis and spread of limbic seizures in the forebrain structures. Following kainic acid injection to the amygdala with or without concurrent injection of muscimol to the supramammillary nucleus, behavioral changes and electroencephalograms were observed in freely moving rats. The animals were processed for Fos immunocytochemical analysis at several time points. The latest expression of Fos at 2h was seen in hippocampal CA1-CA3, ventrolateral thalamic nuclei and mediodorsal caudate putamen, while the early Fos expression at 0.5h was seen in the piriform, entorhinal and other cortices, the thalamic midline nuclei and hypothalamic nuclei. Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression. This treatment also eliminated epileptic discharges and attenuated all waves in hippocampus.These findings indicate that an acute interruption of the facilitatory hypothalamic afferents by intrasupramammillary injection of muscimol may cause the inactivation of the disinhibition mechanism for hippocampal throughput at the dentate gyrus, resulting in the blockade of the genesis and spread of limbic seizures in the hippocampus.     

9602对脑缺血再灌大鼠海马CA1区诱发电位与形态学改变的影响

目的:探讨脑缺血再灌注后海马CA1区诱发群峰电位的变化与形态学改变的关系及中药9602的影响。方法:在整体脑缺血再灌注后不同时间制备的海马脑片上,记录CA1区诱发群峰电位(PS)的变化。采用TUNEL,Nissl染色法进行形态学检测。结果:脑缺血再灌组诱发PS的阈强度明显大于假手术组,波幅显著减小;加条件刺激后PS增幅显著低于假手术组,持续时间缩短。上述变化始于脑缺血再灌后8h,随再灌时间的延长而加重。海马CA1区再灌后8h起TUNEL阳性细胞明显增多,24h达高峰,异常细胞8h最多,随后降低并在低水平持续到7d,细胞总数随再灌时间的延长逐渐减少。中药9602明显降低缺血再灌脑片PS阈强度,增大PS波幅;加大条件刺激后PS增幅并延长持续时间;明显减少海马CA1区的TUNEL阳性细胞数,阻止CA1区细胞数的减少。结论:脑缺血再灌后海马CA1区神经细胞兴奋性和反应性降低,与脑缺血再灌后迟发性神经元死亡(DND)有关,细胞凋亡起重要作用。9602明显改善CA1区神经细胞的兴奋性和反应性,可能与其抑制脑缺血再灌诱导的细胞凋亡,减轻DND的发生有关。     

Selective neuronal death after transient forebrain ischemia in the Mongolian gerbil: a silver impregnation study

An important feature of ischemic brain damage is the exceptional vulnerability of specific neuronal populations and the relative resistance of others. Silver impregnation was used to delineate the extent and time-course of neuronal degeneration produced by 5 min of complete forebrain ischemia in the Mongolian gerbil. Lesions were confined to four brain regions: (1) hippocampal areas CA1, CA2-CA3a and CA4; (2) the dorsomedial portion of the lateral septal nucleus; (3) the dorsolateral portion of the striatum; and (4) the somatosensory neocortex. The ischemic lesion evolved with time in all four regions, but at different rates. Somatic argyrophilia developed rapidly in the striatum and hippocampal area CA4 (maximal in 24 h or less), at intermediate rates in the somatosensory neocortex, hippocampal areas CA1a and CA2-CA3a and the lateral septal nucleus (maximal in 2 days), and slowly in hippocampal area CA1b (maximal in 3 days). These results emphasize that the extent and rate of neuronal degeneration can vary even within a presumably homogeneous neuronal population, as evidenced by the different results in areas CA1a and CA1b. Similar results were obtained from analysis of brain sections stained with Cresyl Violet, hematoxylin-eosin or hematoxylin-eosin/Luxol Fast Blue. Terminal-like silver granules were observed in the projection fields of degenerated neurons. They also appeared, however, in the perforant path terminal zone of the hippocampal dentate molecular layer 1-2 days after transient ischemia and in stratum oriens and stratum radiatum of area CA1b prior to somatic degeneration. These granular deposits could not be clearly related to the degeneration of neuronal somata. Novel findings of this study include the degeneration of some dentate basket cells and lateral septal neurons and the appearance of terminal-like argyrophilia in the hippocampal formation without any obvious relation to somatic degeneration. Some of our results lend support to the hypothesis that ischemic neuronal cell death constitutes an excitotoxic process. Other results, however, suggest that the selective vulnerability of neurons to transient ischemia must involve factors beyond excitotoxicity.     

Excitotoxicity by kainate-induced seizure causes diacylglycerol kinase ζ to shuttle from the nucleus to the cytoplasm in hippocampal neurons

Diacylglycerol kinase (DGK), which consists of several isozymes, plays a pivotal role in lipid second-messenger diacylglycerol metabolism. A nuclear isozyme, DGKζ, which is translocated from the nucleus to the cytoplasm in hippocampal neurons under transient ischemic stress, is implicated in nuclear events of delayed neuronal death. Kainate (KA)-induced seizure is another model used to study excitotoxic stress. Therefore, we examined whether DGKζ is implicated in a different type of degenerative excitotoxicity in hippocampal neurons. We conducted immunohistochemical analysis of rat hippocampi after KA-induced seizures. DGKζ in hippocampal neurons shuttles from the nucleus to the cytoplasm. It never relocates to the nucleus during KA-induced seizures. Marked change in the immunoreactivity is first observed in CA1 pyramidal neurons 2 h after injection during stage 3 seizures. Immunoreactivity for DGKι remains unchanged in the cytoplasm. That for NeuN remains mostly unchanged in the nucleus. Results show that nucleocytoplasmic translocation of DGKζ also occurs in a different model of excitotoxicity that results in apoptotic neuronal death. Cytoplasmic translocation of DGKζ might be involved in early events of the apoptotic cell death pathway in hippocampal neurons under stressed conditions.     

大鼠血管性痴呆模型动物中海马神经元凋亡和蛋白表达的研究

目的:观察不同时点分别结扎左、右颈总动脉建立大鼠血管性痴呆模型中海马CA1区神经元凋亡和Bcl-2及Bax蛋白表达的影响,探讨其在血管性痴呆发病过程中的作用。方法:采取间隔3 d分2次结扎双侧颈总动脉建立血管性痴呆模型,术后4周用TUNEL法检测海马CA1区神经元凋亡,用免疫组织化学法检测其Bcl-2及Bax蛋白表达。结果:模型组大鼠海马CA1区可见大量凋亡神经元;模型组Bcl-2及Bax蛋白表达明显增加,与假手术组比较差异均有显著意义(P<0.05)。结论:此血管性痴呆模型大鼠中海马CA1区神经元大量凋亡丢失,可能是导致血管性痴呆的病理基础。     

Participation of NMDA-glutamatergic receptors in hippocampal neuronal damage caused by adult-onset hypothyroidism

We analyzed the participation of N-methyl-d-aspartate (NMDA) receptors in the neuronal damage caused by adult-onset hypothyroidism. Wistar rats were randomly assigned into four groups. The euthyroid group received tap water. The hypothyroid group received methimazole (60 mg/kg) in their drinking water to induce hypothyroidism. Two more groups of rats received the antithyroid treatment and were injected daily with the NMDA antagonist ketamine (15 mg/kg, sc) or MK-801 (0.5 mg/kg, ip). Treatments were administered during 4 weeks. At the end of the respective treatments rats were deeply anaesthetized and perfused intracardially with 0.9% NaCl followed by 4% paraformaldehyde. The brains were removed from the skull, and coronal brain sections (7 μm thick) were obtained. Neurons were counted in the CA1, CA2, CA3, and CA4 hippocampal regions differentiating between normal and atrophic cells by an experimenter blind to the treatment. The percentage of neuronal damage found in the MMI group was significantly greater in the hippocampal regions compared to the euthyroid group. In contrast, both NMDA antagonists were able to prevent the neuronal damage secondary to hypothyroidism in all hippocampal regions. Our results suggest that the neuronal damage caused in the hippocampus of adult-onset hypothyroid rats requires activation of NMDA channels.     

Electroacupuncture pretreatment ameliorates hypergravity-induced impairment of learning and memory and apoptosis of hippocampal neurons in rats

High-sustained positive acceleration (+Gz) exposures might lead to impairment in cognitive function. Our previous studies have shown that electroacupuncture (EA) pretreatment can attenuate transient focal cerebral ischemic injury in the rats. In this study we aimed to investigate whether EA pretreatment could ameliorate the impairment of learning and memory induced by a sustained +Gz exposure. Using the centrifuge model, rats of experimental groups were exposed to +10Gz for 5 min. Morris water maze was used for assessing the cognitive ability, and the apoptotic hippocampal CA1 pyramidal neuronal cells were evaluated by caspase-3 activity and TUNEL staining. Our results showed that +Gz exposure significantly caused pyramidal neuronal damage, increased neuronal apoptosis and caspase-3 activity in hippocampal CA1 region, as well as resulted in an impairment of spatial learning and memory, as compared to the sham group animals. Furthermore, the EA pretreatment significantly attenuated the neuronal apoptosis, preserved neuronal morphology and inhibited the caspase-3 activity in hippocampal CA1 region resulted from +Gz exposure. The EA pretreatment also ameliorated the learning and memory function in rats exposed to +Gz. These findings indicate that EA pretreatment provides a novel method to prevent the cognitive damage caused by +Gz, which could significantly protect neuronal damage and impairment of learning and memory.