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相似文献

1
Dentate granule cells are essential for kainic acid-induced wet dog shakes but not for seizures.齿状颗粒细胞对于海藻酸诱导的湿狗样抖动至关重要,但对于癫痫发作并非如此。
J Neurosci. 1988 Jan;8(1):256-64. doi: 10.1523/JNEUROSCI.08-01-00256.1988.
2
Kainic acid as a tool to study the regulation and function of opioid peptides in the hippocampus.红藻氨酸作为研究海马体中阿片肽调节与功能的工具。
Toxicology. 1987 Oct 30;46(2):141-57. doi: 10.1016/0300-483x(87)90124-7.
3
Enkephalin contained in dentate granule cells is important for kainic acid-induced wet dog shakes.齿状颗粒细胞中含有的脑啡肽对 kainic 酸诱导的湿狗样抖动很重要。
NIDA Res Monogr. 1986;75:481-4.
4
Kainic acid alters the metabolism of Met5-enkephalin and the level of dynorphin A in the rat hippocampus.海人酸可改变大鼠海马中蛋氨酸脑啡肽的代谢及强啡肽A的水平。
J Neurosci. 1986 Oct;6(10):3094-102. doi: 10.1523/JNEUROSCI.06-10-03094.1986.
5
Granule cells in the ventral, but not dorsal, dentate gyrus are essential for kainic acid-induced wet dog shakes.
Brain Res. 1990 Apr 23;514(1):167-70. doi: 10.1016/0006-8993(90)90453-i.
6
Ventral hippocampal dentate granule cell lesions enhance motor seizures but reduce wet dog shakes induced by mu opioid receptor agonist.腹侧海马齿状颗粒细胞损伤会增强运动性癫痫发作,但会减少由μ阿片受体激动剂诱导的湿狗样抖动。
Neuroscience. 1990;35(1):71-7. doi: 10.1016/0306-4522(90)90121-j.
7
Dynorphin is contained within hippocampal mossy fibers: immunochemical alterations after kainic acid administration and colchicine-induced neurotoxicity.强啡肽存在于海马苔藓纤维中:给予 kainic 酸和秋水仙碱诱导神经毒性后的免疫化学改变。
Proc Natl Acad Sci U S A. 1983 Jan;80(2):589-93. doi: 10.1073/pnas.80.2.589.
8
Administration of kainic acid and colchicine alters mu and lambda opiate binding in rat hippocampus.
Brain Res. 1989 Jan 16;477(1-2):100-8. doi: 10.1016/0006-8993(89)91397-8.
9
[The effect of hippocampal dentate granule cell lesions upon the limbic seizure model of rats].[海马齿状颗粒细胞损伤对大鼠边缘性癫痫模型的影响]
No To Shinkei. 1998 Jul;50(7):643-9.
10
[Neurogenesis of dentate granule cells following kainic acid induced seizures in immature rats].[幼鼠海人酸诱导癫痫发作后齿状颗粒细胞的神经发生]
Zhonghua Er Ke Za Zhi. 2004 Aug;42(8):621-4.

齿状颗粒细胞对于海藻酸诱导的湿狗样抖动至关重要,但对于癫痫发作并非如此。

Dentate granule cells are essential for kainic acid-induced wet dog shakes but not for seizures.

作者信息

Grimes L, McGinty J, McLain P, Mitchell C, Tilson H, Hong J

机构信息

Curriculum in Toxicology, University of North Carolina, Chapel Hill 27514.

出版信息

J Neurosci. 1988 Jan;8(1):256-64. doi: 10.1523/JNEUROSCI.08-01-00256.1988.

DOI:10.1523/JNEUROSCI.08-01-00256.1988
PMID:2892898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6569377/
Abstract

The purpose of this study was to determine the role that dentate granule cells play in wet dog shakes (WDS), behavioral seizures, and hippocampal cell loss caused by systemic administration of kainic acid (KA). Rats were given bilateral injections of colchicine (COL) into the hippocampal formation to selectively lesion dentate granule cells. Two weeks later, they were injected subcutaneously with KA and were observed for WDS and seizures. Seizures were terminated with pentobarbital 2.5 hr after KA injection, and the rats were killed 48 hr later. The integrity of hippocampal cell populations and projections to the hippocampal formation from entorhinal cortex was assessed with radioimmunoassay and immunostaining for methionine-enkephalin (ME) and dynorphin (DYN) A, as well as with Timm and Nissl staining. Results indicate that COL injections eliminated KA-induced WDS, did not affect the latency to onset of seizures, and potentiated KA-induced cell loss in the CA3 region of hippocampus. COL lesions eliminated ME and DYN immunostaining of granule cells, but not ME immunostaining of entorhinal afferents to the dentate gyrus or Ammon's horn. These findings indicate that granule cells are an essential neuronal link in the expression of KA-induced WDS, but that seizures propagate along other pathways in the limbic system.

摘要

本研究的目的是确定齿状颗粒细胞在湿狗颤抖(WDS)、行为性癫痫发作以及由全身注射 kainic 酸(KA)引起的海马细胞丢失中所起的作用。给大鼠双侧海马结构注射秋水仙碱(COL)以选择性损伤齿状颗粒细胞。两周后,给它们皮下注射 KA,并观察其 WDS 和癫痫发作情况。注射 KA 后 2.5 小时用戊巴比妥终止癫痫发作,48 小时后处死大鼠。用放射免疫测定法以及对甲硫氨酸脑啡肽(ME)和强啡肽(DYN)A 进行免疫染色,同时结合 Timm 和 Nissl 染色,评估海马细胞群的完整性以及内嗅皮质向海马结构的投射。结果表明,注射 COL 消除了 KA 诱导的 WDS,不影响癫痫发作的起始潜伏期,并且增强了 KA 诱导的海马 CA3 区细胞丢失。COL 损伤消除了颗粒细胞的 ME 和 DYN 免疫染色,但未消除内嗅传入齿状回或海马角的 ME 免疫染色。这些发现表明,颗粒细胞是 KA 诱导的 WDS 表达中必不可少的神经元环节,但癫痫发作沿边缘系统的其他途径传播。