Corticosterone and stress reduce synaptic potentiation in mouse hippocampal slices with mild stimulation

被引:112
作者
Alfarez, DN [1 ]
Wiegert, O [1 ]
Joëls, M [1 ]
Krugers, HJ [1 ]
机构
[1] Swammerdam Inst Life Sci, Neurol Sect, NL-1098 SM Amsterdam, Netherlands
关键词
glucocorticoid receptor; psychosocial stress; CA1; area; synaptic plasticity; primed burst potentiation;
D O I
10.1016/S0306-4522(02)00483-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Elevation of circulating corticosterone levels, either through exogenous administration of the hormone or following stress exposure, is known to reduce hippocampal synaptic potentiation in rodents. It is presently debated whether this reduction is due to activation of hippocampal glucocorticoid receptors or is primarily caused in other brain structures projecting to the hippocampus. To address this issue, we examined whether synaptic potentiation in hippocampal slices from mice with low basal corticosterone levels was altered 1-4 It after a brief in vitro administration of 100 nM corticosterone. Population spike and field excitatory postsynaptic potential (fEPSP) were recorded in the cell and dendritic layers, respectively, of the CA1 area, in response to Schaffer collateral/commissural fiber stimulation. Basal characteristics of the stimulus-response relationship were not affected by corticosterone treatment, except that after corticosterone treatment the maximal fEPSP slope was reduced while the excitability ratio was increased. For studies on potentiation of the fEPSP and population spike, stimulus intensities were chosen to evoke half maximal responses before potentiation; this intensity was significantly lower for the fEPSP than for the population spike. Primed burst potentiation of the fEPSP but not population spike was significantly attenuated after corticosterone treatment. When using a more rigorous stimulation paradigm, i.e. theta burst potentiation, synaptic potentiation was not affected by corticosterone. Raising corticosterone levels in mice by exposure to a psychosocial stressor led to comparable results in subsequent in vitro experiments; stress reduced primed burst potentiation only of the fEPSP. These data support that corticosterone affects synaptic potentiation in the mouse via direct activation of hippocampal glucocorticoid receptors but only when using mild stimulation conditions. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1119 / 1126
页数:8
相关论文
共 31 条
  • [1] Akirav I, 1999, J NEUROSCI, V19, P10530
  • [2] Blank T, 2002, J NEUROSCI, V22, P3788
  • [3] BODNOFF SR, 1995, J NEUROSCI, V15, P61
  • [4] DEKLOET ER, 1991, FRONT NEUROENDOCRIN, V12, P95
  • [5] DIAMOND DM, 1990, PSYCHOBIOLOGY, V18, P273
  • [6] PSYCHOLOGICAL STRESS REPEATEDLY BLOCKS HIPPOCAMPAL PRIMED BURST POTENTIATION IN BEHAVING RATS
    DIAMOND, DM
    FLESHNER, M
    ROSE, GM
    [J]. BEHAVIOURAL BRAIN RESEARCH, 1994, 62 (01) : 1 - 9
  • [7] INVERTED-U RELATIONSHIP BETWEEN THE LEVEL OF PERIPHERAL CORTICOSTERONE AND THE MAGNITUDE OF HIPPOCAMPAL PRIMED BURST POTENTIATION
    DIAMOND, DM
    BENNETT, MC
    FLESHNER, M
    ROSE, GM
    [J]. HIPPOCAMPUS, 1992, 2 (04) : 421 - 430
  • [8] Domenici MR, 1996, NEUROSCI LETT, V218, P72, DOI 10.1016/S0304-3940(96)13126-8
  • [9] BEHAVIORAL STRESS IMPAIRS LONG-TERM POTENTIATION IN RODENT HIPPOCAMPUS
    FOY, MR
    STANTON, ME
    LEVINE, S
    THOMPSON, RF
    [J]. BEHAVIORAL AND NEURAL BIOLOGY, 1987, 48 (01): : 138 - 149
  • [10] EFFECTS OF GLUCOCORTICOIDS AND NOREPINEPHRINE ON THE EXCITABILITY IN THE HIPPOCAMPUS
    JOELS, M
    DEKLOET, ER
    [J]. SCIENCE, 1989, 245 (4925) : 1502 - 1505