Sex-specific vasopressin signaling buffers stress-dependent synaptic changes in female mice

Abstract

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 naïve partner. This buffering may be due to 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 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 StatementIn 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 in social buffering of synaptic metaplasticity in stress-responsive corticotropin-releasing hormone neurons in female mice. These effects of vasopressin do not extend to social buffering of stress behaviors, suggesting this is a very precise and local form of sex-specific neuropeptide signaling.

Social buffering of human fear is shaped by gender, social concern and the presence of real vs virtual agents

“…Excessive fear responses are characteristic of anxiety disorders and pave the way for a variety of other psychological and psychiatric problems. There is evidence from animal models that autonomic (1,2) and neural (2)(3)(4)(5) fear responses are reduced in the presence of a conspecific, a phenomenon known as social buffering (6)(7)(8). Adapting the paradigms that were used to study social buffering in animals, recent studies have shown similar social buffering of autonomic fear responses in humans (9,10).…”