Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia

被引:13
|
作者
Gajendiran, M [1 ]
Ling, GY [1 ]
Pang, Z [1 ]
Xu, ZC [1 ]
机构
[1] Indiana Univ, Sch Med, Dept Anat & Cell Biol, Indianapolis, IN 46202 USA
关键词
excitation; inhibition; cell death; lateralization; intracellular recording; in vivo;
D O I
10.1016/S0306-4522(01)00163-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Spiny neurons in neostriatum are vulnerable to cerebral ischemia. To reveal the mechanisms underlying the postischemic neuronal damage, the spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum. were compared before and after transient forebrain ischemia using intracellular recording and staining techniques in vivo. In control animals the membrane properties of spiny neurons were about the same between the left and right neostriatum but the inhibitory synaptic transmission was stronger in the left striatum. After severe ischemia, the spontaneous firing and membrane potential fluctuation of spiny neurons dramatically reduced. The cortically evoked initial excitatory postsynaptic potentials were suppressed after ischemia indicated by the increase of stimulus threshold and the rise time of these components. The paired-pulse facilitation test indicated that such suppression might involve presynaptic, mechanisms. The inhibitory postsynaptic potentials in spiny neurons were completely abolished after ischemia and never returned to the control levels. A late depolarizing postsynaptic potential that was elicited from similar to5% of the control neurons by cortical stimulation could be evoked from similar to 30% of the neurons in the left striatum and similar to 50% in the right striatum after ischemia. The late depolarizing postsynaptic potential could not be induced after acute thalamic transection. The intrinsic excitability of spiny neurons was suppressed after ischemia evidenced by the significant increase of spike threshold and rheobase as well as the decrease of repetitive firing rate following ischemia. The membrane input resistance and time constant increased within 6 h following ischemia and the amplitude of fast afterhyperpolarization significantly increased after ischemia. These results indicate the depression of excitatory monosynaptic transmission, inhibitory synaptic transmission and excitability of spiny neurons after transient forebrain ischemia whereas the excitatory polysynaptic transmission in neostriatum was potentiated. The facilitation of excitatory polysynaptic transmission is stronger in the right neostriatum than in the left neostriatum after ischemia. The suppression of inhibitory component and the facilitation of excitatory polysynaptic transmission may contribute to the pathogenesis of neuronal injury in neostriatum after transient cerebral ischemia. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:139 / 152
页数:14
相关论文
共 50 条
  • [21] Regulation of XIAP and Smac/DIABLO in the rat hippocampus following transient forebrain ischemia
    Siegelin, MD
    Kossatz, LS
    Winckler, J
    Rami, A
    NEUROCHEMISTRY INTERNATIONAL, 2005, 46 (01) : 41 - 51
  • [22] Phosphorylation of PTEN and Akt in astrocytes of the rat hippocampus following transient forebrain ischemia
    Jeong-Sun Choi
    Hyun-Jung Park
    Ha-Young Kim
    Seong Yun Kim
    Ju Eun Lee
    Yun-Sik Choi
    Myung-Hoon Chun
    Jin-Woong Chung
    Mun-Yong Lee
    Cell and Tissue Research, 2005, 319 : 359 - 366
  • [23] Cell death in the choroid plexus following transient forebrain global ischemia in the rat
    Ferrand-Drake, M
    MICROSCOPY RESEARCH AND TECHNIQUE, 2001, 52 (01) : 130 - 136
  • [24] Induction of midkine expression in reactive astrocytes following rat transient forebrain ischemia
    Mochizuki, R
    Takeda, A
    Sato, N
    Kimpara, T
    Onodera, H
    Itoyama, Y
    Muramatsu, T
    EXPERIMENTAL NEUROLOGY, 1998, 149 (01) : 73 - 78
  • [25] Molecular correlates of delayed neuronal death following transient forebrain ischemia in the rat
    Wiessner, C
    Vogel, P
    NeumannHaefelin, T
    Hossmann, KA
    MECHANISMS OF SECONDARY BRAIN DAMAGE IN CEREBRAL ISCHEMIA AND TRAUMA, 1996, 66 : 1 - 7
  • [26] VINPOCETINE AMELIORATES HIPPOCAMPAL NEURONAL DAMAGE FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN THE RAT
    RISCHKE, R
    SAUER, D
    ROSSBERG, C
    MENNEL, HD
    KRIEGLSTEIN, J
    PHARMACOLOGY OF CEREBRAL ISCHEMIA 1988, 1989, : 295 - 298
  • [27] Phosphorylation of PTEN and Akt in astrocytes of the rat hippocampus following transient forebrain ischemia
    Choi, JS
    Park, HJ
    Kim, HY
    Kim, SY
    Lee, JE
    Choi, YS
    Chun, MH
    Chung, JW
    Lee, MY
    CELL AND TISSUE RESEARCH, 2005, 319 (03) : 359 - 366
  • [28] Coincidence detection and changes of synaptic efficacy in spiny stellate neurons in rat barrel cortex
    Veronica Egger
    Dirk Feldmeyer
    Bert Sakmann
    Nature Neuroscience, 1999, 2 : 1098 - 1105
  • [29] POSTISCHEMIC REGIONAL CHANGES IN ACETYLCHOLINE SYNTHESIS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN GERBILS
    BERTRAND, N
    BRALET, J
    BELEY, A
    NEUROCHEMICAL RESEARCH, 1992, 17 (04) : 321 - 325
  • [30] Expression and changes of galanin in neurons and microglia in the hippocampus after transient forebrain ischemia in gerbils
    Hwang, IK
    Yoo, KY
    Kim, DS
    Do, SG
    Oh, YS
    Kang, TC
    Han, YH
    Kim, JS
    Won, MH
    BRAIN RESEARCH, 2004, 1023 (02) : 193 - 199