Vasopressin signaling at brain level controls stress hormone release: the vasopressin-deficient Brattleboro rat as a model

Abstract

The nonapeptide arginine vasopressin (AVP) has long been suggested to play an important role as a secretagogue for triggering the activity of the endocrine stress response. Most recent studies employed mutant mice for analyzing the importance of AVP for endocrine regulation under stress. However, it is difficult to compare and draw overall conclusions from all these studies as mixing the genetic material from different mouse strains has consequences on the individual's stress response. Moreover, mice are not ideal subjects for several experimental procedures. Therefore, to get more insight, we used a rather old mutant rat model: the AVP-deficient Brattleboro rat. The present short review is aimed at providing the most interesting results of these studies within the last 8 years that allowed gaining new insights in the potential signal function of AVP in stress and endocrine regulation.

Anxiety-like behavior and neuropeptide receptor expression in male and female prairie voles: The effects of stress and social buffering

“…The brain AVP system is known to be involved in stress responses as well as in social behaviors [31, 73]. For example, V1aR in the brain is altered by social defeat experience in California mice [74] and is involved in modulating behavioral reactions to a threat in rats [75].…”

Brain vasopressin signaling modulates aspects of maternal behavior in lactating rats

“…67,68 Briefly, vasopressin deriving from the parvocellular part of the PVN is an important factor in the regulation of the hypothalamo-pituitary-adrenal axis on all three levels in response to chronic 69,70 but also acute stress (for review see Refs. 71,72). Under physiological conditions, both V1 receptor subtypes are thought to be expressed in a steady state within the membrane, that is, the combination of receptor synthesis, proteolytic degradation, internalization, and recycling back to the membrane occurs until binding of the hormone or an analogue.…”

Corticosterone oscillations during mania induction in the lateral hypothalamic kindled rat—Experimental observations and mathematical modeling

“…At this stage, we have included steroid hormones in our mathematical model and not included AVP in order to keep the model concise and tractable, yet sufficiently resourceful to recapitulate the most important features of the complex real system that we are modeling. This first approximation is justifiable on factual basis–it is well established that CRH is the primary and most potent activator of the HPA axis and that AVP acts primarily as a modifier of its activity, rather than its main driver [116–118]. In addition, there are, to our best knowledge, no experimental data on the daily dynamics of AVP that are acquired with such a high temporal resolution to enable us to distinguish the contribution of CRH from the contribution of AVP and refine our model in accordance with these data.…”