Stress can trigger enduring changes in neural circuits and synapses. The behavioral and hormonal consequences of stress can also be transmitted to others, but whether this transmitted stress has similar effects on synapses is not known. We found that authentic stress and transmitted stress in mice primed paraventricular nucleus of the hypothalamus (PVN) corticotropin-releasing hormone (CRH) neurons, enabling the induction of metaplasticity at glutamate synapses. In female mice that were subjected to authentic stress, this metaplasticity was diminished following interactions with a naive partner. Transmission from the stressed subject to the naive partner required the activation of PVN CRH neurons in both subject and partner to drive and detect the release of a putative alarm pheromone from the stressed mouse. Finally, metaplasticity could be transmitted sequentially from the stressed subject to multiple partners. Our findings demonstrate that transmitted stress has the same lasting effects on glutamate synapses as authentic stress and reveal an unexpected role for PVN CRH neurons in transmitting distress signals among individuals.

中文翻译：

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压力后的社会传播和突触变化的缓冲。

压力会触发神经回路和突触的持久变化。压力的行为和荷尔蒙后果也可以传播给其他人，但是尚不清楚这种传递的压力是否对突触具有类似的作用。我们发现，在小鼠中，真实的应激和传导性应激引发了下丘脑（PVN）促肾上腺皮质激素释放激素（CRH）神经元的室旁核，从而在谷氨酸突触中诱导了可塑性。在遭受真实压力的雌性小鼠中，与幼稚的伴侣相互作用后，这种可塑性降低。从应激对象向幼稚伴侣的传播需要激活对象和伴侣中的PVN CRH神经元，以驱动和检测从应激小鼠释放假定的警报信息素。最后，可以将可塑性从压力对象顺次传递给多个伴侣。我们的发现表明，传递的压力对谷氨酸突触具有与真实压力相同的持久作用，并且揭示了PVN CRH神经元在个体之间传递求救信号中具有意想不到的作用。