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1.
听源性遗传癫痫易感大鼠大脑皮层胆囊收缩素mRNA的原位杂交检测 总被引:1,自引:0,他引:1
本实验用原位杂交法,对听源性遗传癫痫易感大鼠(P77PMC)癫痫发作前,单次癫痫发作和多次发作时大脑颞皮层CCK mRNA阳性信号进行了检测,结果显示:(1)单次和多次癫痫发作后颞皮层CCK mRNA阳性神经元数量明显增加(P<0.01);(2)多次癫痫发作者上述脑区CCK mRNA阳性神经元数量较单次癫痫发作有明显的下降(P<0.01),大脑颞皮层CCK mRNA增高表明,CCK mRNA在癫痫发作过程中起了某种作用,多次癫痫发作大鼠CCK mRNA表达降低提示,单次和多次癫痫发作时大脑皮层CCK mRNAl转录的调控可能存在不同的机制。 相似文献
2.
徐珞 《中国应用生理学杂志》2000,16(1):75-78
目的和方法:采用原位杂交技术,观察遗传性听源性癫痫易感大鼠海马内CCKmRNA表达的改变及少我注射CCK3及其受体阻断剂对大鼠癫痫发作的影响。结果:(1)癫痫发作大鼠海马内CCKmRNA表达明显增强(P〈0.05-0.01),但癫痫反复发作的大嫌海马内CCKmRNA表达的较癫痫发作一次大鼠明显减少(P〈0.05),海马CA主射L365后,CCK8压抑癫痫发作的作用消失(P〈0.01)。结论:CCK 相似文献
3.
蝎毒对癫痫大鼠海马内强啡肽原mRNA表达的影响 总被引:7,自引:0,他引:7
姜春玲 《中国应用生理学杂志》2000,16(1):72-74
目的和方法:本工作用红藻氨酸癫痫模型,通过对癫痫大鼠蝎毒处理后民内哟啡肽原mRNA(KPUYNmRNA)表达的原位杂交观察,对国产蝎粗毒抗癫痫反复发作的细胞分子机制进行初步探讨。结果:原位杂交的实验显示,三周KA后,实验对照组与空白对照组相比,腹侧海马尤其是海马门区PDYNmRNA阳性数目明显减少(P〈0.01)。实验给药组大鼠8例,其中有6例腹侧海马门区PDYNmRNA阳性神经元数目未见减少且有 相似文献
4.
蝎毒诱导红藻氨酸癫痫大鼠海马内胆囊收缩素原mRNA的表达 总被引:5,自引:0,他引:5
姜春玲 《中国应用生理学杂志》2000,16(2):108-110
目的和方法:本工作用红藻氨酸(KA)癫痫模型,对用蝎毒处理住房第马内胆囊收缩素原mRNA(PCCK mRNA)表达进行原位杂交观察,并对国产东亚钳蝎粗毒抗癫痫反复发作的机制做了初步探讨。结果:原位杂交的实验显示,三周KA后,实验对照组与空白对照组相比,腹侧海马是海马门区PCCK mRNA阳性神经元数目明显减少(P〈0.05);实验给药组大鼠8例,其中有6例腹侧海马门区PCCK mRNA阳性神经元数 相似文献
5.
吗啡对福尔马林引起大鼠海马内IL-2RβmRNA表达的影响 总被引:1,自引:0,他引:1
本实验采用原位杂交法观察足底注射福尔马林(For)痛敏对海马内白细胞介素2受体βmRNA(IL-2RβmRNA)生成的影响及其与吗啡、促肾上腺皮质激素(ACTH)的关系。结果表明:正常大鼠海马有IL-2RβmRNA表达,集中分布于CA1-CA4区神经元、齿状回颗粒细胞。足底注射For后6h双侧海马IL-2RβmRNA表达均增加(P〈0.05),12h达高峰,24h仍高于正常。在6h时,腹腔注射吗啡 相似文献
6.
应激刺激对大鼠下丘脑血管升压素mRNA水平的影响 总被引:8,自引:2,他引:8
实验在给予慢性应激刺激的Sprague Dawlay雄性大鼠中进行,用核酸斑点杂交技术观察大鼠下丘脑组织中血管升压素(AVP)mRNA水平变化,用异羟基洋地黄毒甙(DIG)标记的26个碱基长寡聚核苷酸作为检测探针。结果观察到:在给予电击足底结合噪声的应激刺激之后,尾动脉收缩压逐渐升高,到刺激第5天,刺激组与对照组动物之间尾动脉收缩压差别有统计学显著意义;到刺激第9天,刺激组尾动脉收缩压达最高值;以 相似文献
7.
琥珀酰-CCK7为新合成的CCK8的一种类似物,当琥珀酰-CCK7的浓度为1×10^-11mol/L-1×10[-7]mol/L时,能促使大鼠胰腺离体腺泡细胞分泌α淀粉酶和蛋白酶,其最有效浓度为1×10^-9mol/L。在相同摩尔条件下,琥珀酰-CCK7的促分泌效应明显大于CCK8,且这种效应在3小时内随着作用时间的延长而增加,这为开发高活性CCK8的类似物提供了依据。 相似文献
8.
八肽胆囊收缩素对大鼠心功能的影响及受体机制 总被引:4,自引:0,他引:4
为探讨八肽胆囊收缩素 (CCK 8)对麻醉大鼠心功能的影响及受体机制 ,实验监测了左心室收缩压(LVP)、左心室收缩与舒张期内压变化的最大速率 (±LVdp/dtmax)、心率 (HR)和平均动脉压 (MAP)。结果如下 :小剂量CCK 8(0 4 μg/kg)可引起心动过速 ,MAP、LVP和±LVdp/dtmax轻度上升 ;中剂量CCK 8(4 μg/kg)和大剂量CCK 8(4 0 μg/kg)可引起心动过缓 ,MAP、LVP和±LVdp/dtmax显著增加 ;应用CCK 受体 (CCK R)拮抗剂丙谷胺 (1 0mg/kg)抑制以上变化 ;由逆转录 聚合酶链反应 (RT PCR)检测到心肌组织有CCK A受体 (CCK AR)和CCK B受体 (CCK BR)mRNA表达。以上结果提示 :CCK 8可激活心肌组织的CCK R ,引起剂量依赖性的心功能增加和心率改变。 相似文献
9.
大鼠杏仁核内注射八肽胆囊收缩素(CCK—8)拮抗吗啡镇痛的研究 总被引:2,自引:0,他引:2
大鼠双侧杏仁核内注射CCK-81ng(1μl),能明显降低皮下注射4mg/kg吗啡产生的镇痛作用,并在0.1-1ng范围内呈量效关系。分别向双侧仁核注射CCK-A受体拮抗剂Devazepide50ng能部分翻转,200ng则完全翻转CCK-8的抗吗啡镇痛作用,10ng无效;而CCK-B受体拮抗剂L-365,260在5-8ng时即可完全番转CCK-8的抗吗啡镇痛作用。杏仁核注射200ng的Devaz 相似文献
10.
本工作用家兔38只,麻醉并切断双侧迷走神经和三叉神经上颌支,观察连续刺激大脑皮层不同区域对呼吸的影响。结果:1.适度的电刺激:(1)对肢体运动区(L),使吸气加强,呼吸频率(RF)和潮气量(TV)均显著增加;(2)对颜面运动区(F),使RF显著增加,但呼气和吸气均被抑制,TV显著降低;(3)对咀嚼运动区(M),出现间歇性吸气或呼气加强,RF和TV均明显增加;(4)对眶后区(PO),使RF和TV均显 相似文献
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12.
Mauricio Díaz-Muñoz Jorge Suárez Rolando Hernández-Muñoz Victoria Chagoya de Sánchez 《Neurochemical research》1987,12(4):315-321
A study of the lipidic pattern of the cerebral cortex of the normal adult rat during the daynight cycle was carried out. The changes observed were the following: phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine plus phosphatidic acid showed a peak at 16:00 hr possibly due to a general increase in phospholipid biosynthesis. During the nocturanl period the variations of phosphatidylcholine and phosphatidylethanolamine were not clearly observe, they might be due to an increase in the interconversion or exchange reaction, since the ratio phosphatidylcholine/phosphatidylethanolamine showed a significative change at 04:00 hr. This occurred because small but opposite changes in both phospholipids were observed, suggesting an increase in the methylation reactions of phospholipids. Cardiolipin showed a significant peak at 04:00 hr. Plasmalogens exhibited significative changes, an important diminution at 16:00 hr and a prominent peak at 24:00 hr. Cholesterol levels were high during the light period and low in the dark one. Cerebrosides and gangliosides showed no day-night variations. The changes observed indicate a phenomenon of biological rhythmicity synchronized by the photoperiod, suggesting that these fluctuations could act as physiological modulators of the properties and functions of the nerve cell membrane. 相似文献
13.
Amila Zuko Asami Oguro-Ando Roland van Dijk Sara Gregorio-Jordan Bert van der Zwaag 《Cell Adhesion & Migration》2016,10(4):378-392
The gene encoding the neural cell adhesion molecule Contactin-6 (Cntn6 a.k.a. NB-3) has been implicated as an autism risk gene, suggesting that its mutation is deleterious to brain development. Due to its GPI-anchor at Cntn6 may exert cell adhesion/receptor functions in complex with other membrane proteins, or serve as a ligand. We aimed to uncover novel phenotypes related to Cntn6 functions during development in the cerebral cortex of adult Cntn6?/? mice. We first determined Cntn6 protein and mRNA expression in the cortex, thalamic nuclei and the hippocampus at P14, which decreased specifically in the cortex at adult stages. Neuroanatomical analysis demonstrated a significant decrease of Cux1+ projection neurons in layers II-IV and an increase of FoxP2+ projection neurons in layer VI in the visual cortex of adult Cntn6?/? mice compared to wild-type controls. Furthermore, the number of parvalbumin+ (PV) interneurons was decreased in Cntn6?/? mice, while the amount of NPY+ interneurons remained unchanged. In the hippocampus the delineation and outgrowth of mossy fibers remained largely unchanged, except for the observation of a larger suprapyramidal bundle. The observed abnormalities in the cerebral cortex and hippocampus of Cntn6?/? mice suggests that Cntn6 serves developmental functions involving cell survival, migration and fasciculation. Furthermore, these data suggest that Cntn6 engages in both trans- and cis-interactions and may be involved in larger protein interaction networks. 相似文献
14.
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15.
O. M. Tsupykov T. A. Pivneva T. N. Kovalenko I. A. Osadchenko D. A. Vasilenko G. G. Skibo 《Neurophysiology》2007,39(6):396-405
We studied changes in behavior of Mongolian gerbils (Meriones unguiculatus) after ischemia-reperfusion of the brain (7-min-long occlusion of both arteriae carotis) and structural alterations in the hippocampus of such animals. Behavioral manifestations were observed under conditions
of the open field test within 7 days of the postischemic period; immunofluorescent staining of brain sections with antibodies
against specific proteins of neurons and glial cells was used. Motor hyperactivity reaching its maximum a day after ischemization
and gradually decreasing within the postocclusion period was found in ischemized animals. On the 7th day, the level of locomotor
activity in experimental gerbils was practically equal to that in the control group. In contrast, a postischemic decrease
in the duration of episodes of resting was preserved for a longer time. A week after ischemia-reperfusion, intense delayed
neuronal death and activation of glial cells were observed in the CA1 hippocampal area. Thus, cerebral ischemia-reperfusion results in significant transient disorders of behavioral phenomena
in gerbils; at the same time, a clear correlation is observed between structural changes of neurons and the level of reactivity
of glial cells in the hippocampus. These events can be significant aspects of the dynamics of postischemic damage to the above
structure.
Neirofiziologiya/Neurophysiology, Vol. 39, No. 6, pp. 458–467, November–December, 2007. 相似文献
16.
目的:拟观察高压氧(HBO)治疗对急性创伤性颅脑损伤后皮层NOSmRNA表达的影响,探讨HBO治疗急性脑损伤的机理。方法:采用自由落体法打击模型制备SD大鼠急性脑创伤,伤后1 h、12 h采用0.25 MPaHBO治疗,伤后6 h、24 h取样皮层,应用半定量逆转录聚合酶链反应(RT-PCR)观察神经元型一氧化氮合酶(nNOS)、内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)mRNA表达量变化。结果:0.25MPaHBO治疗各时间组nNOS、eNOS和iNOSmRNA较急性颅脑损伤各时间组显著下降(P<0.01),且HBO治疗24 h组较6 h组下降更明显(P<0.05,P<0.01),0.25 MPa常氧高氮各时间组与急性颅脑损伤各时间组NOSmRNA表达量无统计学意义。结论:HBO治疗可以下调nNOSmRNA、iNOSmRNA和eNOSmRNA的表达量,可能为HBO治疗脑创伤的机理之一。 相似文献
17.
Sukhbinder Kumar Heidi M. Bonnici Sundeep Teki Trevor R. Agus Daniel Pressnitzer Eleanor A. Maguire Timothy D. Griffiths 《Proceedings. Biological sciences / The Royal Society》2014,281(1791)
Previous behavioural studies have shown that repeated presentation of a randomly chosen acoustic pattern leads to the unsupervised learning of some of its specific acoustic features. The objective of our study was to determine the neural substrate for the representation of freshly learnt acoustic patterns. Subjects first performed a behavioural task that resulted in the incidental learning of three different noise-like acoustic patterns. During subsequent high-resolution functional magnetic resonance imaging scanning, subjects were then exposed again to these three learnt patterns and to others that had not been learned. Multi-voxel pattern analysis was used to test if the learnt acoustic patterns could be ‘decoded’ from the patterns of activity in the auditory cortex and medial temporal lobe. We found that activity in planum temporale and the hippocampus reliably distinguished between the learnt acoustic patterns. Our results demonstrate that these structures are involved in the neural representation of specific acoustic patterns after they have been learnt. 相似文献
18.
Cain BM Connolly K Blum AC Vishnuvardhan D Marchand JE Zhu X Steiner DF Beinfeld MC 《Journal of neurochemistry》2004,89(2):307-313
Prohormone convertase (PC1) is found in endocrine cell lines that express cholecystokinin (CCK) mRNA and process pro CCK to biologically active products. Other studies have demonstrated that PC1 may be a one of the enzymes responsible for the endoproteolytic cleavages that occur in pro CCK during its biosynthesis and processing. Prohormone convertase 1 (PC1) has a distribution that is similar to cholecystokinin (CCK) in rat brain. A moderate to high percentage of CCK mRNA-positive neurons express PC1 mRNA. CCK levels were measured in PC1 knockout and control mice to assess the degree to which loss of PC1 changed CCK content. CCK levels were decreased 62% in hippocampus, 53% in amygdala and 57% in pons-medulla in PC1 knockout mice as compared to controls. These results are highly correlated with the colocalization of CCK and PC1. The majority of CCK mRNA-positive neurons in the pyramidal cell layer of the hippocampus express PC1 mRNA and greater than 50% of CCK mRNA-positive neurons in several nuclei of the amygdala also express PC1. These results demonstrate that PC1 is important for CCK processing. PC2 and PC5 are also widely colocalized with CCK. It may be that PC2, PC5 or another non-PC enzyme are able to substitute for PC1 and sustain production of some amidated CCK. Together these enzymes may represent a redundant system to insure the production of CCK. 相似文献
19.
Alterations of cerebral cortex and hippocampal proteasome subunit expression and function in a traumatic brain injury rat model 总被引:1,自引:0,他引:1
Following cellular stress or tissue injury, the proteasome plays a critical role in protein degradation and signal transduction. The present study examined the β-subunit expression of constitutive proteasomes (β1, β2, and β5), immunoproteasomes (β1i, β2i, and β5i) and the 11S proteasome activator, PA28α, in the rat CNS after traumatic brain injury (TBI). Concomitant measures assessed changes in proteasome activities. Quantitative real time PCR results indicated that β1 and β2 mRNA levels were not changed, while β5 mRNA levels were significantly decreased in injured CNS following TBI. However, β1i, β2i, β5i, and PA28α mRNA levels were significantly increased in the injured CNS. Western blotting studies found that β1, β2, β5, β2i, and β5i subunit protein levels remained unchanged in the injured CNS, but β1i and PA28α protein levels were significantly elevated in ipsilateral cerebral cortex and hippocampus. Proteasome activity assays found that peptidyl glutamyl peptide hydrolase-like and chymotrypsin-like activity were significantly reduced in the CNS after TBI, and that trypsin-like proteasome activity was increased in the injured cerebral cortex. Our results demonstrated that both proteasome composition and function in the CNS were affected by trauma. Treatments that preserve proteasome function following CNS injury may be beneficial as an approach to cerebral neuroprotection. 相似文献
20.
Hiroyuki Nozaki Kortaro Tanaka Shintaro Gomi Ban Mihara Shigeru Nogawa Eiichiro Nagata Taro Kondo Yasuo Fukuuchi 《Neurochemical research》1996,21(8):975-982
Alterations in ryanodine binding and local cerebral blood flow (LCBF) were examined at 30 minutes and 2 hours post-ischemia
in the gerbil brain in order to evaluate the influence of cerebral ischemia on the intracellular channels of Ca2+-induced Ca2+ release (CICR). Severe hemispheric cerebral ischemia was induced by occluding the right common carotid artery. LCBF was measured
at the end of the experiment using [14C]iodoantipyrine method, and the ryanodine binding was evaluated in vitro using [3H]ryanodine as a specific ligand for CICR channels. An autoradiographic method developed in our laboratory enabled us to determine
both parameters within the same brain. A group of gerbils who underwent a sham procedure served as controls. LCBF was found
to be significantly reduced in most of the cerebral regions on the occluded side at both 30 minutes as well as 2 hours post-ischemia.
In contrast, a significant reduction in ryanodine binding was noted only in the hippocampus CA1 on the occluded side at 30
minutes and 2 hours after the occlusion. These findings suggest that regionally specific changes of CICR may be the cause
of decreased ryanodine binding in the hippocampus CA1, and that these changes may be related to the pathophysiological mechanisms
that cause this region to be particularly vulnerable to ischemia. 相似文献