发育中的大脑发生热性惊厥会导致边缘回路神经元兴奋性的持续改变。
Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits.
作者信息
Chen K, Baram T Z, Soltesz I
机构信息
Department of Anatomy and Neurobiology, University of California, Irvine 92697-1280, USA.
出版信息
Nat Med. 1999 Aug;5(8):888-94. doi: 10.1038/11330.
Abstract
Febrile (fever-induced) seizures affect 3-5% of infants and young children. Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial. Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood. The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions.
摘要
热性（发热引起的）惊厥影响3%至5%的婴幼儿。尽管热性惊厥的发病率很高，但其对日后癫痫发展的影响一直存在争议。结合一种新的复杂性热性惊厥大鼠模型和膜片钳技术，我们确定未成熟大鼠中热诱导的惊厥会导致海马体中抑制性突触传递的选择性突触前增加，这种增加会持续到成年期。热性惊厥后突触通讯中这些强烈改变的持久性质并不支持早期热性惊厥“良性”性质的普遍观点。
相似文献
1
Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits.发育中的大脑发生热性惊厥会导致边缘回路神经元兴奋性的持续改变。
Nat Med. 1999 Aug;5(8):888-94. doi: 10.1038/11330.
2
Mechanisms of hyperthermia-induced depression of GABAergic synaptic transmission in the immature rat hippocampus.未成熟大鼠海马中热疗诱导的GABA能突触传递抑制机制。
J Neurochem. 2008 Sep;106(5):2158-69. doi: 10.1111/j.1471-4159.2008.05576.x. Epub 2008 Jul 15.
3
Long-lasting modulation of synaptic plasticity in rat hippocampus after early-life complex febrile seizures.大鼠海马体早期生活复杂性热性惊厥后突触可塑性的持久调节。
Eur J Neurosci. 2010 Sep;32(5):749-58. doi: 10.1111/j.1460-9568.2010.07321.x. Epub 2010 Jul 16.
4
Long-term plasticity of endocannabinoid signaling induced by developmental febrile seizures.发育性热性惊厥诱导的内源性大麻素信号传导的长期可塑性。
Neuron. 2003 Aug 14;39(4):599-611. doi: 10.1016/s0896-6273(03)00499-9.
5
Febrile convulsions: a 'benign' condition?
Nat Med. 1999 Aug;5(8):871-2. doi: 10.1038/11308.
6
Prevention of plasticity of endocannabinoid signaling inhibits persistent limbic hyperexcitability caused by developmental seizures.抑制内源性大麻素信号的可塑性可预防发育性癫痫引起的持续性边缘系统过度兴奋。
J Neurosci. 2007 Jan 3;27(1):46-58. doi: 10.1523/JNEUROSCI.3966-06.2007.
7
N-methyl-D-aspartate, hyperpolarization-activated cation current (Ih) and gamma-aminobutyric acid conductances govern the risk of epileptogenesis following febrile seizures in rat hippocampus.N-甲基-D-天冬氨酸、超极化激活阳离子电流（Ih）和γ-氨基丁酸电导可控制大鼠海马发热性惊厥后致痫的风险。
Eur J Neurosci. 2010 Apr;31(7):1252-60. doi: 10.1111/j.1460-9568.2010.07159.x. Epub 2010 Mar 22.
8
Effects of temperature elevation on neuronal inhibition in hippocampal neurons of immature and mature rats.温度升高对未成熟和成熟大鼠海马神经元抑制的影响。
J Neurosci Res. 2009 Sep;87(12):2773-85. doi: 10.1002/jnr.22105.
9
Cell-type specific GABA synaptic transmission and activity-dependent plasticity in rat hippocampal stratum radiatum interneurons.大鼠海马辐射层中间神经元中细胞类型特异性GABA突触传递及活动依赖性可塑性
Eur J Neurosci. 2005 Jul;22(1):179-88. doi: 10.1111/j.1460-9568.2005.04207.x.
10
Ca2+-permeable AMPA receptors mediate induction of test pulse depression of naive synapses in rat visual cortical slices at early postnatal stage.在大鼠早期视觉皮层脑片上，Ca2+-通透型 AMPA 受体介导诱导测试脉冲的幼稚突触抑制。
Neuroscience. 2010 Feb 3;165(3):684-91. doi: 10.1016/j.neuroscience.2009.11.030. Epub 2009 Nov 17.
引用本文的文献
1
Animal Models of Febrile Seizures: Limitations and Recent Advances in the Field.发热性惊厥的动物模型：该领域的局限性和最新进展。
Cells. 2024 Nov 16;13(22):1895. doi: 10.3390/cells13221895.
2
Enhancing glymphatic fluid transport by pan-adrenergic inhibition suppresses epileptogenesis in male mice.通过泛肾上腺素能抑制增强糖液转运可抑制雄性小鼠的癫痫发生。
Nat Commun. 2024 Nov 6;15(1):9600. doi: 10.1038/s41467-024-53430-y.
3
Alterations in Rat Hippocampal Glutamatergic System Properties after Prolonged Febrile Seizures.大鼠海马谷氨酸能系统特性在长时间热性惊厥后的改变。
Int J Mol Sci. 2023 Nov 28;24(23):16875. doi: 10.3390/ijms242316875.
4
Febrile Seizures Cause a Rapid Depletion of Calcium-Permeable AMPA Receptors at the Synapses of Principal Neurons in the Entorhinal Cortex and Hippocampus of the Rat.发热性惊厥导致大鼠内嗅皮层和海马体主神经元突触处钙通透性 AMPA 受体迅速耗竭。
Int J Mol Sci. 2023 Aug 9;24(16):12621. doi: 10.3390/ijms241612621.
5
Investigation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in vitro inflammation model at molecular level.在分子水平上研究超极化激活环核苷酸门控（HCN）通道的体外炎症模型。
Mol Cell Biochem. 2024 May;479(5):1223-1229. doi: 10.1007/s11010-023-04788-y. Epub 2023 Jul 11.
6
The long-term neurodevelopmental outcomes of febrile seizures and underlying mechanisms.热性惊厥的长期神经发育结局及其潜在机制。
Front Cell Dev Biol. 2023 May 25;11:1186050. doi: 10.3389/fcell.2023.1186050. eCollection 2023.
7
The rearrangement of actin cytoskeleton in mossy fiber synapses in a model of experimental febrile seizures.实验性高热惊厥模型中苔藓纤维突触肌动蛋白细胞骨架的重排
Front Neurol. 2023 Apr 20;14:1107538. doi: 10.3389/fneur.2023.1107538. eCollection 2023.
8
Temperature-dependent structural plasticity of hippocampal synapses.海马体突触的温度依赖性结构可塑性
Front Cell Neurosci. 2022 Oct 19;16:1009970. doi: 10.3389/fncel.2022.1009970. eCollection 2022.
9
Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury.创伤性脑损伤中的超急性兴奋毒性机制与突触功能障碍
Front Mol Neurosci. 2022 Feb 24;15:831825. doi: 10.3389/fnmol.2022.831825. eCollection 2022.
10
Adenosine Kinase Isoforms in the Developing Rat Hippocampus after LiCl/Pilocarpine Status Epilepticus.氯化锂/匹罗卡品癫痫持续状态后发育大鼠海马中的腺苷激酶同工型。
Int J Mol Sci. 2022 Feb 24;23(5):2510. doi: 10.3390/ijms23052510.
本文引用的文献
1
A molecular correlate of memory and amnesia in the hippocampus.
Nat Neurosci. 1999 Apr;2(4):309-10. doi: 10.1038/7217.
2
Seizures in the developing brain: perhaps not so benign after all.
Neuron. 1998 Dec;21(6):1231-4. doi: 10.1016/s0896-6273(00)80642-x.
3
The in vivo proconvulsant effects of corticotropin releasing hormone in the developing rat are independent of ionotropic glutamate receptor activation.促肾上腺皮质激素释放激素在发育中大鼠体内的惊厥前效应与离子型谷氨酸受体激活无关。
Brain Res Dev Brain Res. 1998 Nov 1;111(1):119-28. doi: 10.1016/s0165-3806(98)00130-8.
4
Selective changes in single cell GABA(A) receptor subunit expression and function in temporal lobe epilepsy.颞叶癫痫中单个细胞GABA(A)受体亚基表达和功能的选择性变化。
Nat Med. 1998 Oct;4(10):1166-72. doi: 10.1038/2661.
5
Increased number of synaptic GABA(A) receptors underlies potentiation at hippocampal inhibitory synapses.海马体抑制性突触处的增强作用源于突触GABA(A)受体数量的增加。
Nature. 1998 Sep 10;395(6698):172-7. doi: 10.1038/25999.
6
Seizure-induced neuronal injury: vulnerability to febrile seizures in an immature rat model.癫痫发作诱导的神经元损伤：未成熟大鼠模型中对热性惊厥的易感性
J Neurosci. 1998 Jun 1;18(11):4285-94. doi: 10.1523/JNEUROSCI.18-11-04285.1998.
7
Magnetic resonance imaging evidence of hippocampal injury after prolonged focal febrile convulsions.长时间局灶性热性惊厥后海马损伤的磁共振成像证据。
Ann Neurol. 1998 Apr;43(4):413-26. doi: 10.1002/ana.410430403.
8
Prolonged febrile seizures and mesial temporal sclerosis.
Ann Neurol. 1998 Apr;43(4):411-2. doi: 10.1002/ana.410430402.
9
The absence of a major Ca2+ signaling pathway in GABAergic neurons of the hippocampus.海马体GABA能神经元中主要钙离子信号通路的缺失。
Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3245-50. doi: 10.1073/pnas.95.6.3245.
10
Local circuit abnormalities in chronically epileptic rats after intrahippocampal tetanus toxin injection in infancy.幼年海马内注射破伤风毒素后慢性癫痫大鼠的局部回路异常
J Neurophysiol. 1998 Jan;79(1):106-16. doi: 10.1152/jn.1998.79.1.106.
Zotero 插件