糖尿病脑病突触可塑性损伤的研究进展

尹华静, 王伟平, 王晓良

中国药学杂志 ›› 2018, Vol. 53 ›› Issue (21) : 1805-1809.

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中国药学杂志 ›› 2018, Vol. 53 ›› Issue (21) : 1805-1809. DOI: 10.11669/cpj.2018.21.001
综述

糖尿病脑病突触可塑性损伤的研究进展

  • 尹华静1, 王伟平2, 王晓良2*
作者信息 +

Research Progress in Synaptic Plasticity Impairment of Diabetic Encephalopathy

  • YIN Hua-jing1, WANG Wei-ping2, WANG Xiao-liang2*
Author information +
文章历史 +

摘要

糖尿病可引起认知障碍,形成糖尿病脑病(diabetic encephalopathy, DE)。大量研究提示,糖尿病脑病与海马突触可塑性的变化密切相关,包括突触结构和功能的可塑性损伤。结构方面表现为突触变性,功能方面主要体现在长时程增强(long-term potentiation, LTP)的损伤,包括N-甲基-D-天冬氨酸受体(NMDARs)、α-氨基-3-羟基-5-甲基-4-异恶口坐丙酸受体(AMPARs)和钾离子通道的构成及功能性病变。突触可塑性异常可能是糖尿病脑病的关键性病理机制,本文将对此进行综述。

Abstract

Previous studies demonstrate that diabetes mellitus induces cognitive impairment,leading to diabetic encephalopathy(DE), which is closely related with hippocampal synaptic plasticity impairment,including synaptic structural and functional damage. Structural damage mainly embodied in the synapse degeneration.Functional damage mainly reflects in the LTP damage, including the composition variation and functional lesions of N-methyl-D-aspartate receptors(NMDARs), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) and patassium channels.Abnormal synaptic plasticity may be critical in the pathogenesis of diabetic encephalopathy. In this review, we summarized the relationship between DE and synaptic plasticity impairment.

关键词

糖尿病脑病 / 突触可塑性 / 长时程增强/长时程抑制 / N-甲基-D-天冬氨酸受体 / α-氨基-3-羟基-5-甲基-4-异恶口坐丙酸受体 / 钾通道

Key words

diabetic encephalopathy / synaptic plasticity / LTP/LTD / NMDARs / AMPARs / potassium channels

引用本文

导出引用
尹华静, 王伟平, 王晓良. 糖尿病脑病突触可塑性损伤的研究进展[J]. 中国药学杂志, 2018, 53(21): 1805-1809 https://doi.org/10.11669/cpj.2018.21.001
YIN Hua-jing, WANG Wei-ping, WANG Xiao-liang. Research Progress in Synaptic Plasticity Impairment of Diabetic Encephalopathy[J]. Chinese Pharmaceutical Journal, 2018, 53(21): 1805-1809 https://doi.org/10.11669/cpj.2018.21.001
中图分类号: R964    R969   

参考文献

[1] RESKE-NIELSEN E, LUNDBK K. Diabetic encephalopathy: diffuse and focal lesions of the brain in long-term diabetes[J]. Acta Neurol Scandin, 1963, 39(S4):273-290.
[2] YIN H, WANG W, YU W, et al. Changes in Synaptic Plasticity and Glutamate Receptors in Type 2 Diabetic KK-Ay Mice[J]. J Alzheimer's Dis, 2017, 57(4):1207-1220.
[3] MILES W R, ROOT H F. Psychologic tests applied to diabetic patients[J]. Arch Int Med, 1922, 30(6):767-777.
[4] SINGH-MANOUX A, SCHMIDT R. Diabetes A risk factor for cognitive impairment and dementia?[J]. Neurology, 2015, 84 (23):2300-2301.
[5] WESSELS A M, SIMSEK S, REMIJNSE P L, et al. Voxel-based morphometry demonstrates reduced grey matter density on brain MRI in patients with diabetic retinopathy[J]. Diabetologia, 2006, 49(10):2474-2480.
[6] FERGUSON S O, BLANE A, WARDLAW J, et al. Influence of an early-on-set age of type 1 diabetes on cerebral structure and cognitive function[J]. Diabetes Care, 2005, 28(6):1431-1437.
[7] MANSCHOT SM, BRANDS AM, VAN DER GROND J, et al. Brain magnetic resonance imaging correlates of impaired cognition in patients with type 2 diabetes[J]. Diabetes, 2006, 55(4):1106-1113.
[8] LI W, HUANG E. An update on type 2 diabetes mellitus as a risk factor for dementia[J]. J Alzheimer's Dis, 2016, 53(2):393-402.
[9] BIESSELS G J, GISPEN W H. The impact of diabetes on cognition: what can be learned from rodent models?[J]. Neurobiolaging, 2005, 26(1):36-41.
[10] AKISAKI T, SAKURAI T, TAKATA T, et al. Cognitive dysfunction associates with white matter hyperintensities and subcortical atrophy on magnetic resonance imaging of the elderly diabetes mellitus Japanese elderly diabetes intervention trial (J-EDIT)[J]. Diabetes Metab Res Rev, 2006, 22(5):376-384.
[11] LI Z, ZHANG W, SIMA A A F. Alzheimer-like changes in rat models of spontaneous diabetes[J]. Diabetes, 2007, 56(7):1817-1824.
[12] ARTOLA A. Diabetes mellitus-and ageing-induced changes in the capacity for long-term depression and long-term potentiation inductions: toward a unified mechanism[J]. Eur J Pharmacol, 2013, 719(1-3):161-169.
[13] TEKKK S, KRNJEVIC′ K.Diabetes mellitus preserves synaptic plasticity in hippocampal slices from middle-aged rats[J]. Neuroscience, 1999, 91(1):185-191.
[14] SASAKI-HAMADA S, SACAI H, OKA J I. Diabetes onset influences hippocampal synaptic plasticity in streptozotocin-treated rats[J]. Neuroscience, 2012, 227: 293-304.
[15] CANDY S M, SZATKOWSKI M S. Neuronal excitability and conduction velocity changes in hippocampal slices from streptozotocin-treated diabetic rats[J]. Brain Res, 2000, 863(1):298-301.
[16] SHIMIZU E, TANG Y P, RAMPON C, et al. NMDA receptor-dependent synaptic reinforcement as a crucial process for memory consolidation[J]. Science, 2000, 290(5494):1170-1174.
[17] LAU W K, YEUNG C W, LUI P W, et al. Different trends in modulation of NMDAR1 and NMDAR2B gene expression in cultured cortical and hippocampal neurons after lead exposure[J]. Brain Res, 2002, 932(1):10-24.
[18] SOBCZYK A, SVOBODA K. Activity-dependent plasticity of the NMDA-receptor fractional Ca 2+ current[J]. Neuron, 2007, 53(1):17-24.
[19] BAUDRY M, LYNCH G. Remembrance of arguments past: how well is the glutamate receptor hypothesis of LTP holding up after 20 years?[J]. Neurobiol Learn Memory, 2001, 76(3):284-297.
[20] VALASTRO B, COSSETTE J, LAVOIE N, et al. Up-regulation of glutamate receptors is associated with LTP defects in the early stages of diabetes mellitus[J]. Diabetologia, 2002, 45(5):642-650.
[21] DI LUCA M, RUTS L, GARDONI F, et al. NMDA receptor subunits are modified transcriptionally and post-translationally in the brain of streptozotocin-diabetic rats[J]. Diabetologia, 1999, 42(6):693-701.
[22] SACAI H, SASAKI-HAMADA S, SUGIYAMA A, et al. The impairment in spatial learning and hippocampal LTD induced through the PKA pathway in juvenile-onset diabetes rats are rescued by modulating NMDA receptor function[J]. Neurosci Res, 2014, 81-82: 55-63.
[23] HARDT O, NADER K, WANG Y T. GluA2-dependent AMPA receptor endocytosis and the decay of early and late long-term potentiation: possible mechanisms for forgetting of short-and long-term memories[J]. Phil Trans R Soc B, 2014, 369(1633):20130141.
[24] MATSUO N, REIJMERS L, MAYFORD M. Spine-type-specific recruitment of newly synthesized AMPA receptors with learning[J]. Science, 2008, 319(5866):1104-1107.
[25] MAMELI M, BALLAND B, LUJáN R, et al. Rapid synthesis and synaptic insertion of GluR2 for mGluR-LTD in the ventral tegmental area[J]. Science, 2007, 317(5837):530-533.
[26] JO?L G, MILOT M, GLINAS S, et al. Binding properties of glutamate receptors in streptozotocin-induced diabetes in rats[J]. Diabetes, 1997, 46(5):841-846.
[27] LAUVER A, YUAN L L, JEROMIN A, et al. Manipulating Kv4. 2 identifies a specific component of hippocampal pyramidal neuron A‐current that depends upon Kv4. 2 expression[J]. J Neurochem, 2006, 99(4):1207-1223.
[28] LEI Z, ZHANG H, LIANG Y, et al. Reduced expression of IA channels is associated with postischemic seizures in hyperglycemic rats[J]. J Neurosci Res, 2014, 92(12):1775-1784.
[29] QIN D, HUANG B, DENG L, et al. Downregulation of K+ channel genes expression in type I diabetic cardiomyopathy[J]. Biochem Biophys Res Commun, 2001, 283(3):549-553.
[30] YAO X, CHEN F, LI P, et al. Natural product vindoline stimulates insulin secretion and efficiently ameliorates glucose homeostasis in diabetic murine models[J]. J Ethnopharmacol, 2013, 150(1):285-297.
[31] LI X N, HERRINGTON J, PETROV A, et al. The role of voltage-gated potassium channels Kv2. 1 and Kv2. 2 in the regulation of insulin and somatostatin release from pancreatic islets[J]. J Pharmacol Exp Ther, 2013, 344(2):407-416.
[32] SUKMA RITA R, DEZAKI K, KURASHINA T, et al. Partial blockade of Kv2. 1 channel potentiates GLP-1's insulinotropic effects in islets and reduces its dose required for improving glucose tolerance in type 2 diabetic male mice[J]. Endocrinology, 2014, 156(1):114-123.
[33] YASUDA T, CUNY H, ADAMS D J. Kv3. 1 channels stimulate adult neural precursor cell proliferation and neuronal differentiation[J]. J Physiol, 2013, 591(10):2579-2591.
[34] YAN L, FIGUEROA D J, AUSTIN C P, et al. Expression of voltage-gated potassium channels in human and rhesus pancreatic islets[J]. Diabetes, 2004, 53(3):597-607.
[35] TZOUNOPOULOS T, STACKMAN R. Enhancing synaptic plasticity and memory: A role for small-conductance Ca2+-activated K+ channels[J]. Neuroscientist, 2003, 9(6):434-439.
[36] HAMMOND R S, BOND C T, STRASSMAIER T, et al. Small-conductance Ca2+-activated K+ channel type 2 (SK2) modulates hippocampal learning, memory, and synaptic plasticity[J]. J Neurosci, 2006, 26(6):1844-1853.
[37] BLANK T, NIJHOLT I, KYE M J, et al. Small-conductance, Ca2+-activated K+ channel SK3 generates age-related memory and LTP deficits[J]. Nat Neurosci, 2003, 6(9):911-912.
[38] NGO-ANH T J, BLOODGOOD B L, LIN M, et al. SK channels and NMDA receptors form a Ca2+-mediated feedback loop in dendritic spines[J]. Nat Neurosci, 2005, 8(5):642-649.
[39] GLOYN A L, SIDDIQUI J, ELLARD S. Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism[J]. Human Mut, 2006, 27(3):220-231.
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