In many species, social networks provide benefit for both the individual and the collective. In addition to transmitting information to others, social networks provide an emotional buffer for distressed individuals. Our understanding about the cellular mechanisms that contribute to buffering is poor. Stress has consequences for the entire organism, including a robust change in synaptic plasticity at glutamate synapses onto corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVN). In females, however, this stress-induced metaplasticity is buffered by the presence of a naive partner. This buffering may be because of discrete behavioral interactions, signals in the context in which the interaction occurs (i.e., olfactory cues), or it may be influenced by local signaling events in the PVN. Here, we show that local vasopressin (VP) signaling in PVN buffers the short-term potentiation (STP) at glutamate synapses after stress. This social buffering of metaplasticity, which requires the presence of another individual, was prevented by pharmacological inhibition of the VP 1a receptor (V1aR) in female mice. Exogenous VP mimicked the effects of social buffering and reduced STP in CRH^PVN neurons from females but not males. These findings implicate VP as a potential mediator of social buffering in female mice.

SIGNIFICANCE STATEMENT In many organisms, including rodents and humans, social groups are beneficial to overall health and well-being. Moreover, it is through these social interactions that the harmful effects of stress can be mitigated, a phenomenon known as social buffering. In the present study, we describe a critical role for the neuropeptide vasopressin (VP) in social buffering of synaptic metaplasticity in stress-responsive corticotropin-releasing hormone (CRH) neurons in female mice. These effects of VP do not extend to social buffering of stress behaviors, suggesting this is a very precise and local form of sex-specific neuropeptide signaling.

在许多物种中，社交网络既为个人又为集体提供利益。除了向他人传递信息之外，社交网络还为受苦的人们提供了情感缓冲。我们对有助于缓冲的细胞机制的了解很差。压力对整个生物都有影响，包括下丘脑室旁核（PVN）中谷氨酸突触到促肾上腺皮质激素释放激素（CRH）神经元上的谷氨酸突触的突触可塑性的强烈变化。然而，在雌性中，天真伴侣的存在可缓解这种应激诱导的可塑性。该缓冲可能是由于离散的行为交互作用，交互作用发生的上下文中的信号（即嗅觉提示）引起的，或者可能受到PVN中本地信令事件的影响。这里，我们显示，PVN中的局部加压素（VP）信号可缓冲应激后谷氨酸突触的短期增强（STP）。通过药理抑制雌性小鼠中的VP 1a受体（V1aR），可以防止这种需要其他人存在的社会上的可塑性的缓冲。外源性VP模仿了CRH中的社会缓冲和STP降低的影响来自女性而非男性的^PVN神经元。这些发现暗示VP是雌性小鼠中社会缓冲的潜在媒介。

重要声明在许多生物中，包括啮齿动物和人类，社会群体对整体健康和福祉均有益。而且，通过这些社会互动，可以减轻压力的有害影响，这种现象被称为社会缓冲。在本研究中，我们描述了神经肽加压素（VP）在雌性小鼠应激反应性促肾上腺皮质激素释放激素（CRH）神经元的突触可塑性社会缓冲中的关键作用。VP的这些作用并未扩展到应激行为的社会缓冲，这表明这是性别特异性神经肽信号传导的非常精确和局部的形式。