氟桂嗪对沙鼠脑缺血再灌注损伤后行为及海马形态学改变的影响

目的研究氟桂嗪(FNZ)对沙鼠脑缺血再灌注损伤后行为及海马区形态学改变的影响.方法取沙土鼠30只,随机分为假手术组、缺血再灌注组、FNZ治疗组.术前3d训练沙鼠跳台实验,采用双侧颈总动脉夹闭法复制脑缺血模型.术后7d重复跳台实验,观察其记忆能力及空间定向能力及海马CA1区神经细胞形态学的改变.结果FNZ能明显减轻脑缺血再灌注所致CA1区神经细胞形态的损伤,并促进沙鼠记忆能力及空间定向能力的恢复(P<0.05).结论FNZ对血管性痴呆有防治作用.     

强迫游泳大鼠海马组织5-羟色胺受体mRNA的表达

目的探讨强迫游泳大鼠海马组织中5-羟色胺（5-HT1A）受体激活物抑制因子-1（1mRNA）的表达。方法随机将雄性Wistar大鼠分为对照组、1d应激组、14d应激组和28d应激组,建立强迫游泳应激模型。用化学发光法测定血清皮质醇浓度,用逆转录聚合酶链式反应（RT-PCR）方法检测海马5-HT1A受体mRNA的变化。结果（1）对照组、1d应激组、14d应激组和28d应激组血清皮质醇浓度分别为（0．64±0．09）μg／dL、（1．14±0．19）μg／dL（1．98±0．40）μg／dL、（0．95±0．14）μg／dL。（2）强迫游泳大鼠海马5HT1A受体mRNA表达相对水平分剐为1．501±0．257、1．141±0．120、0．681±0．056,与对照组相比较,差异具有统计学意义（P〈0．05）。结论强迫游泳大鼠海马中5-HT1A受体mRNA表达降低。     

Localization and quantitation of dynorphin B in the rat hippocampus

The present study measures the content of dynorphin B in the rat hippocampus, and localizes the dynorphins within the intrinsic hippocampal neuronal circuitry. The level of dynorphin B, which is representative of the prodynorphin-derived peptides, was markedly depleted by intrahippocampal injection of colchice, which destroyed the great majority of the hippocampal granule cells and the associated mossy fiber pathway. The hippocampus contralateral to the injection demonstrated a slight, non-significant rise in dynorphin B levels after colchicine. Entorhinal cortical lesions ablating the perforant pathway input to the hippocampus did not significantly alter dynorphin B levels in the hippocampus. Unilateral fimbrial transection caused a small but significant increase in dynorphin B on the side of the lesion relative to the unlesioned side, but neither side was significantly different from control.     

Ventromedial nucleus of the hypothalamus: convergent excitatory and inhibitory responses to fimbria and stria terminalis stimulation

Field and extracellular unitary potentials were recorded in the ventromedial nucleus of the hypothalamus (VMH) of urethane-anesthetized rabbits after stimulation of the fimbria and stria terminalis. Stimulation of the lateral portion of the fimbria, which carries fibers from the ventral subiculum of the hippocampal formation, evoked a two-component response. An early excitatory response, with an average latency of 10 msec, predominated along the lateral margins of the VMH. A later inhibitory potential with an average latency of 15 msec was seen predominantly within the central portions of the VMH. Stimulation of the dorsal component of the stria terminalis produced two similar response patterns: an early excitatory response with an average latency of 16 msec, followed by an inhibitory potential with an average latency of 25 msec. The topographical distribution of these two components of the response was nearly identical to that produced by lateral fimbria stimulation. In contrast, stimulation of the ventral component of the stria terminalis evoked a simple excitatory response with an average latency of 10 msec which was maximal within the core of the VMH. Extracellular unitary recordings showed that the early negativity associated with stimulation of each of these three pathways reflects a monosynaptic excitation of VMH cells and that there was convergence of the three excitatory inputs at the single cell level.     

穹窿海马伞切割侧海马对植入神经干细胞分化为神经元的影响

为观察成鼠神经干细胞移植入切割穹窿海马伞侧海马和正常侧海马后存活和分化为神经元的状况 ,用无血清培养和单细胞克隆技术获取成年 SD大鼠前脑室下带神经干细胞 ,进行 Brd U标记和扩增。切割 SD大鼠右侧穹窿海马伞 ,术后 2周将标记有 Brd U的神经干细胞植入双侧海马齿状回。 2月后 ,行 Nissl染色、Brd U免疫荧光、NF -2 0 0 / Brd U免疫荧光、β-tubulin- / Brd U免疫组织化学染色和 ACh E组织化学染色。结果发现 ,移植的神经干细胞在海马齿状回中存活并沿颗粒下层迁移 ,切割侧海马齿状回中有较多的 Nissl深染的大胞体神经元样细胞 ,而正常侧多为小胞体胶质样细胞。切割侧海马齿状回颗粒下层中见有数个NF-2 0 0 / Brd U、β-tubulin- / Brd U双标神经元和 ACh E阳性神经元 ,而正常侧海马中则未能见到。上述结果提示 ,移植到海马中的神经干细胞能存活、迁移 ,穹窿海马伞切割侧海马中某些物质的表达增强 ,可诱导植入其内的神经干细胞向神经元或 ACh E阳性神经元分化。     

神经生长因子对痴呆模型鼠海马突触素的影响

切断SD老年鼠(24月龄)左侧穹窿海马伞.造成隔海马胆碱能系统损害的痴呆模型. 用免疫组化和图像分析技术分析神经生长因子对痴呆鼠海马突触素的影响.实验证明损伤一个月后.损伤对照组损伤侧海马CAI区多形层、辐射层、腔隙分子层和齿状回分子层突触素含量分别是减少了28.17% 、32.15%、17.36%和35.22%:NGF治疗组、损伤侧海马CAI区多形层、辐射层、腔隙分子层和齿状回分子层突触素含量只减少了6.17%、5.52%、13.50%和3.81%.提示神经生长因子能够促使痴呆鼠海马内突触素含量的增多.     

切割穹窿海马伞大鼠海马内Lhx8 mRNA表达的变化

目的:探讨切割穹窿海马伞大鼠切割侧与正常侧海马内Lhx8 mRNA表达的差异。方法:切割SD大鼠右侧穹窿海马伞。切割后7d制备海马冰冻切片,用体外转录法制备地高辛标记的Lhx8 RNA探针进行原位杂交,分析切割侧和正常侧海马锥体细胞层和齿状回颗粒层中及齿状回门区和颗粒下层中的Lhx8 mRNA阳性细胞的数量和平均光密度值。结果:切割侧和正常侧海马锥体细胞层和齿状回颗粒层Lhx8 mRNA阳性细胞数量无明显差异,但切割侧平均光密度值较正常侧明显增加;在齿状回的门区和颗粒下层,切割侧Lhx8 mRNA阳性细胞数和平均光密度值均较正常侧升高。结论:切割穹窿海马伞后海马中Lhx8 mRNA表达上调,可能与其中的神经干细胞向胆碱能神经元分化的神经再生机制有关。     

Habituation of the acoustic startle response following lesion of the medial septal nucleus

Adult male rats were subjected to one of three surgical procedures: total lesions of the medial septal nuclei (TMS), partial lesions of the medial septal nuclei (PMS), and lesions of the dorsal fimbria (FM), as an attempt to determine the role of the septo-hippocampal relationship in habituation of the acoustic startle response. The initial startle amplitude of the TMS group was approximately three times that of the other groups, but rapidly decreased to the level of the other experimental groups and thereafter habituated at similar slow rates. Unlike animals with hippocampal lesions, all animals with hippocampal afferent damage displayed overdays savings of habituation. Following nine days without startle stimulation, startle amplitudes of the TMS groups had returned to their initial level while the PMS, FM and Control groups exhibited nonsignificant recovery. Differences in rates of habituation and amplitude of startle responses were attributed to loss of hippocampal input, and increased hippocampal output over intact pathways, respectively.     

利血平脾虚证模型海马基因表达谱变化的研究

目的　应用基因芯片技术研究利血平脾虚证大鼠模型海马基因表达谱的变化。方法　雌性Wistar大鼠 3 0只 ,按体质量均衡随机分为实验组和对照组 ,实验组用利血平注射液背部皮下注射 ,造模第 1～ 9天 0 .15mg/ (kg·d) ,第 10～ 12天 0 .2 5mg/ (kg·d) ,第 13天 0 .5mg/(kg·d)。对照组同法注射同量注射用水。两组均第 14天处死 ,取海马 ,提取总RNA ,逆转录为cDNA ,用Cy3和Cy5两种荧光物质分别标记两组大鼠海马组织的cDNA ,制成探针以备检测。选用 2张BioDoorChip 40 96基因表达谱芯片 ,将探针与芯片杂交 ,计算机扫描后 ,用GenePixPro3 .0软件进行分析。结果　筛选出 2张芯片上 40 96条靶基因中 ,与脾虚证模型基因差异表达一致的基因 51条 ,占检测基因的 1.2 5% ,其中表达下调的基因 3 7条 ,已知基因 8条 ;表达上调的基因 14条 ,已知基因6条。模型大鼠海马的基因表达改变涉及免疫、炎症反应、蛋白聚糖、细胞骨架、离子通道、信号传导等多方面。结论脾虚证实质涉及海马的基因表达谱改变 ,但与大脑皮质比较基因表达改变少     

Involuntary,unreinforced (pure) spatial learning is impaired by fimbria-fornix but not by dorsal hippocampus lesions

Pure spatial learning occurs when rats acquire information about an environment while exploring it in the absence of reinforcers. We previously reported that voluntary, unreinforced exploration of a radial maze retards subsequent reinforced conditioned cue preference (CCP) learning in the same maze. In the present experiment, we examined the effects of involuntary, unreinforced pre-exposure to a radial maze. During pre-exposure, rats were moved by an experimenter between the ends of two arms of a radial maze five times in 30 min. This form of pre-exposure retarded CCP learning, whereas rats that were not pre-exposed and rats that were pre-exposed to a maze in a different room displayed normal CCP learning. These findings suggest that some information specific to the maze environment was acquired during involuntary unreinforced pre-exposure to it. In experiment 2, the retardation of reinforced CCP learning by involuntary unreinforced pre-exposure was eliminated by fimbria-fornix lesions made before pre-exposure but was unaffected by fimbria-fornix lesions made after pre-exposure but before training. Large neurotoxic lesions of the dorsal hippocampus made before pre-exposure had no effect on the retardation of CCP learning, but the rats with these lesions were impaired on a standard test of reinforced spatial learning in a water maze. The lesion effects in experiment 2 are similar to those previously reported for voluntary exploration and suggest that pure spatial learning may occur during both voluntary exploration of and involuntary exposure to an environment in the absence of reinforcers. Pure spatial learning can apparently occur with exposure to two different locations within an environment, but the rats do not have to move between the locations voluntarily. An intact fimbria-fornix is required for acquisition but not expression of this form of learning. The hippocampus is not involved in this form of learning.