Effects of Early Life Stress on Synaptic Plasticity in the Developing Hippocampus of Male and Female Rats.
Effects of Early Life Stress on Synaptic Plasticity in the Developing Hippocampus of Male and Female Rats.
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DOI：
10.1371/journal.pone.0164551
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Sarabdjitsingh RA
中科院分区：
文献类型：
--
作者：
Derks NA;Krugers HJ;Hoogenraad CC;Joëls M;Sarabdjitsingh RA
早期生活压力（ELS）会增加成年后患精神病理学的风险。这些影响何时发生很大程度上是未知的。我们在啮齿动物 ELS 模型中研究了从生命早期到成年期 ELS 在发育过程中的哪个时间段影响海马突触可塑性。此外，我们还研究了暴露于 ELS 是否会改变突触可塑性对应激激素皮质酮的敏感性。雄性和雌性 Wistar 大鼠在出生后第 3 天 (P) 被暴露于母体剥夺 (MD) 24 小时，或与母亲一起不受干扰（对照）。在 P8-9、22-24 和 P85-95 时，测定血浆皮质酮 (CORT) 水平、体重、胸腺和肾上腺重量，以验证 MD 的神经内分泌作用。在体外记录高频刺激前后 CA1 海马的场电位。在高频刺激前 1-4 小时，将脑切片与 100nM CORT 或载体一起孵育 20 分钟，以模拟体外高应激条件。仅在 P4 时 MD 使体重下降（p = 0.02）。对 P8-9、22-24 或 85-95 胸腺、肾上腺重量和基础 CORT 水平的影响很小。谷氨酸传输经历了强烈的发育变化：半最大信号大小强烈增加（p<0.0001），而所需的半最大刺激强度随着年龄的增长而降低（p = 0.04）。突触可塑性从 P8-9 的长期抑制发展到后期长期增强水平的增加 (p = 0.0001)。 MD 导致 P22-24 雄性 (p = 0.03) 和 P85-95 雌性 (p = 0.04) 的长期增强显着增加。贝叶斯模型强烈支持年龄依赖性发育，一些证据表明男性 MD 后加速成熟（贝叶斯因子 1.23）。 CORT 抑制成年男性的 LTP；其他年龄段和女性的突触可塑性不受影响。因此，MD 以性别依赖性方式影响 CA1 海马突触可塑性的发育，这也支持了 MD 男性成熟加速的观点。
Early life stress (ELS) increases the risk for developing psychopathology in adulthood. When these effects occur is largely unknown. We here studied at which time during development ELS affects hippocampal synaptic plasticity, from early life to adulthood, in a rodent ELS model. Moreover, we investigated whether the sensitivity of synaptic plasticity to the stress-hormone corticosterone is altered by exposure to ELS. Male and female Wistar rats were exposed to maternal deprivation (MD) for 24h on postnatal day (P)3 or left undisturbed with their mother (control). On P8-9, 22–24 and P85-95, plasma corticosterone (CORT) levels, body weight, and thymus and adrenal weights were determined to validate the neuroendocrine effects of MD. Field potentials in the CA1 hippocampus were recorded in vitro before and after high frequency stimulation. Brain slices were incubated for 20 min with 100nM CORT or vehicle 1-4h prior to high frequency stimulation, to mimic high-stress conditions in vitro. Body weight was decreased by MD only at P4 (p = 0.02). There were minimal effects on P8-9, 22–24 or 85–95 thymus and adrenal weight and basal CORT levels. Glutamate transmission underwent strong developmental changes: half-maximal signal size strongly increased (p<0.0001) while the required half-maximal stimulation intensity concomitantly decreased with age (p = 0.04). Synaptic plasticity developed from long-term depression at P8-9 to increasing levels of long-term potentiation at later ages (p = 0.0001). MD caused a significant increase in long-term potentiation of P22-24 males (p = 0.03) and P85-95 females (p = 0.04). Bayesian modeling strongly supported the age-dependent development, with some evidence for accelerated maturation after MD in males (Bayes factor 1.23). CORT suppressed LTP in adult males; synaptic plasticity at other ages and in females remained unaffected. Thus, MD affects the development of synaptic plasticity in the CA1 hippocampus in a sex-dependent manner, with some support for the notion that maturation is accelerated in MD males.
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