Rocher Cyril, Spedding Michael, Munoz Carmen, Jay Thérèse M
NAMC, CNRS UMR 8620, Bat. 446, Université Paris-Sud, 91405 Orsay, France.
Cereb Cortex. 2004 Feb;14(2):224-9. doi: 10.1093/cercor/bhg122.
Acute stress inhibits long-term potentiation (LTP) at synapses from the hippocampus to prefrontal cortex in the rat, a model of the dysfunction in the anterior cingulate/orbitofrontal cortices which has been observed in human depression. We demonstrate that the antidepressants tianeptine and, to a lesser extent, fluoxetine, are able to reverse the impairment in LTP, a measure of frontal synaptic plasticity, caused by stress on an elevated platform. LTP was induced by stimulation of hippocampal outflow. Beneficial effects on neuronal plasticity, defined as a reversal of the effects of stress in this paradigm, can be considered as a new animal model for the impact of stress on hippocampal/frontal circuits, a key target in psychiatric diseases.
急性应激会抑制大鼠海马体到前额叶皮质突触处的长时程增强(LTP),这是一种在人类抑郁症中观察到的前扣带回/眶额叶皮质功能障碍模型。我们证明,抗抑郁药噻奈普汀以及在较小程度上的氟西汀,能够逆转由高架平台应激引起的LTP损伤,LTP是额叶突触可塑性的一种指标。通过刺激海马体传出纤维诱导LTP。对神经元可塑性的有益影响,定义为在该范式中应激效应的逆转,可被视为应激对海马体/额叶回路影响的一种新动物模型,而海马体/额叶回路是精神疾病的关键靶点。