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通过胞外记录大鼠海马颗粒细胞层诱发电位观察了皮质酮对麻醉大鼠海马神经突触可塑性的影响． 结果显示，皮质酮（１， ４ 和１０ ｍ ｇ·ｋｇ－ １， ｉｐ）有使单刺激大鼠海马颗粒细胞层基础群峰电位（ＰＳ）幅度升高的趋势，但同对照相比无显著性差异． 给予大鼠穿行通路以串刺激（６０ Ｈｚ， ３０ 次）可使海马颗粒细胞层ＰＳ幅度持续增高，增幅达７０％ － ８０％ ，说明在海马诱生长时程增强效应（ＬＴＰ）． 预先１ ｈ给予大鼠皮质酮（１， ４ 和１０ ｍ ｇ·ｋｇ－ １， ｉｐ）可剂量依赖地降低串刺激诱导的ＰＳ幅度的升高，说明皮质酮可抑制海马颗粒细胞层ＬＴＰ的诱生． 结果提示，皮质酮可损伤大鼠海马神经突触可塑性．
The effect of corticosterone on neuronal synaptic plasticity in hippocampus of anesthetized rats was observed by extracellular recording of the evoked potentials in rat granulocyte layer. The results showed that corticosterone (1, 4 and 10 m g · kg-1, ip) had the tendency to increase the basal group peak amplitude (PS) of single-stimulated rat hippocampal granular cells, but no significant difference compared with the control Sex differences. The rats were given a series of parallel routes (60 Hz, 30 times) to increase the PS amplitude of hippocampal granular cells by 70% -80%, indicating that LTP was induced in the hippocampus. Pretreatment with corticosterone (1, 4 and 10 mg · kg -1, ip) for 1 h in a dose-dependent manner reduced the amplitude of PS induced by skeletal stimulation, indicating that corticosterone inhibited LTP in hippocampal granular cells Health. The results suggest that corticosterone can damage hippocampal neuronal synaptic plasticity in rats.