To develop and validate a vasopressin (AVP) receptor knockdown strategy, we infused an antisense oligodeoxynucleotide to the V1 subtype mRNA into the septum of male rats with osmotic minipumps and measured behavioral, cellular and molecular parameters. Compared to vehicle and scrambled-sequence oligo controls, chronic antisense administration for up to 4 d diminished the ability of the animals to distinguish a previously exposed juvenile from a novel one and to respond to exogenous AVP (1 ng/5 microliters, intracerebroventricular) with an improved social memory. Furthermore, anxiety-related behavior was reduced. As measured in the behaviorally tested rats, antisense treatment resulted in a reduced binding of radiolabeled AVP in the septum, but not in other limbic brain areas (receptor autoradiography), and an increased amount of V1 receptor mRNA (reverse transcriptase PCR), indicating translational arrest and ongoing transcriptional activity. In sense oligo-treated rats, on the other hand, both the social and the anxiety-related behavior scores lay between levels obtained in control and antisense-treated animals. These sense-treated rats showed a slightly reduced V1 receptor density in the septum and reduced receptor mRNA levels, indicating hybridization of the sense oligo to the DNA. The data show the potential of antisense targeting to further reveal relationships between local gene expression, neuropeptide-receptor interactions in distinct brain areas, and behavioral performance.

https://www.jneurosci.org/content/jneuro/15/6/4250.full.pdf

V1 vasopressin receptor antisense oligodeoxynucleotide into septum reduces vasopressin binding, social discrimination abilities, and anxiety-related behavior in rats

Simultaneous microdialysis in the brain and blood was used to monitor the release of vasopressin and oxytocin within the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei and into the systemic circulation of urethane-anaesthetized male rats before and after central administration of interleukin-1β (IL-1β). Following intracerebroventricular infusion of the cytokine (200 ng/5 μl), the content of vasopressin (up to 278% compared to vehicle-treated control, P < 0.01 compared to vehicle-treated control and preinfusion baseline) but not oxytocin (up to 148%, not significant) in 30-min blood microdialysates was found to be increased. This peripheral release was accompanied by a transient rise in vasopressin (up to 163%, P < 0.05) and oxytocin (up to 182%, P < 0.05) release within the SON, the peak typically occurring during the first and second 30-min collection intervals after IL-1 β respectively. In contrast, in the simultaneously microdialysed PVN, both vasopressin and oxytocin failed to respond to intracerebroventricular IL-1 β. In another series of experiments, IL-1 β was directly infused (20 ng0.5 μl) into either the SON or PVN during microdialysis of the corresponding nucleus. The cytokine caused a significant and immediate rise in intra-SON release of both vasopressin (up to 225%, P < 0.01) and oxytocin (up to 178%, P < 0.05). Again, in the PVN, nonapeptide release, although tending to be stimulated in response to intranuclear IL-1 β, failed to reach statistical significance. The cytokine-induced central and peripheral release pattern appeared to be independent of the rise in body temperature observed after IL-1 β administration. In a third series of experiments, bilateral administration of IL-1 β into the SON (20 ng/0.5 μl) failed to alter peripheral release of both vasopressin and oxytocin into the systemic circulation. The increase in central nonapeptide release in response to IL-1 β shown in this paper supports the hypothesis that at least vasopressin might act to oppose central effects of the cytokine, including those on thermoregulation and behaviour, in this way contributing to the neuroendocrine-immune dialogue at brain level.

Interleukin-1β stimulates both central and peripheral release of vasopressin and oxytocin in the rat

Vasopressin in the septal area of the golden hamster controls scent marking and grooming.

The aim of the present study was to investigate the physiological significance of the neuropeptide arginine vasopressin (AVP) released within the septum, in the behavioural response of rats to stress. In the first experiment, rats were chronically implanted with a microdialysis probe aimed at the mediolateral or ventral septum to monitor the local release of AVP in response to 10 min of forced swimming in 20 degrees C warm water. Exposure to this stressor caused a significant increase in AVP release in both the mediolateral (174 +/- 21%, P < 0.01) and ventral septum (220 +/- 33%, P < 0.01). In contrast, microdialysates collected outside the mediolateral septum or in the lateral ventricle remained at prestress levels throughout the dialysis period. Furthermore, unstressed control animals failed to show significant alterations in vasopressin release in the mediolateral septum. In a second experiment, the introduction of the V1 receptor antagonist d(CH2)5Tyr(Me)AVP into the mediolateral septum via inverse microdialysis concomitant with stressor exposure caused the rats to spend an increased time floating and a reduced time swimming compared to vehicle-treated rats. This effect was acute and also detected 24 h after antagonist administration. Taken together, these findings demonstrate a significant activation of the septal vasopressinergic system in response to swim stress. Furthermore, our data support the view that AVP released within this brain area is involved in the generation of active behavioural strategies aimed at coping with new and challenging situations.

Vasopressin released within the septal brain area during swim stress modulates the behavioural stress response in rats

In addition to its peripheral secretion from the neurohypophysis, the neuropeptide vasopressin (VP) is released within the mammalian brain from probably all parts of the neuronal membrane. In particular the development of brain microdialysis in vivo together with blood microdialysis or blood sampling provides the advantage of being able to reliably compare the dynamic release patterns into different compartments of the organism. The central VP release within hypothalamic (e.g., supraoptic, paraventricular and suprachiasmatic nuclei) and limbic (e.g., septum, amygdala) rat brain areas is stimulated by a variety of substances and stressors, including interleukin-1β, social defeat and forced swimming. Furthermore, it is characterized by positive and negative feedback mechanisms and the capacity of the VP system for co-ordinated or independent release, the latter being observed, for example, during social defeat. This emotional stressor, in contrast to exposure to a novel cage, increased VP release within the supraoptic nucleus, but not into plasma. This failure to release VP peripherally could be observed also during forced swimming, despite a dramatic rise in plasma osmolality and a markedly stimulated central release. In another series of experiments we studied the effects of centrally-released VP on cognitive and emotional aspects of behavior using reverse microdialysis for antagonist administration during the behavioral tests and antisense targeting to downregulate either VP or its local V 1 receptor subtype. In this way, centrally (in particular septally) released VP could be shown to be causally involved in short-term memory and anxiety-related behavior. Furthermore, VP release within the hypothalamic paraventricular nucleus is likely to provide a negative tonus on the activity of the hypothalamic-pituitary-adrenocortical axis. This neuroendocrine effect together with cognitive, emotional and immunological effects of centrally released VP is thought to be essential to ensure adequate behavior of the animal during challenging situations and to contribute to the development of efficient coping strategies.

Release of vasopressin within the brain contributes to neuroendocrine and behavioral regulation.

The role of vasopressin as an antipyretic in the ventral septal area and its possible involvement in convulsive disorders.

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The role of vasopressin as an antipyretic in the ventral septal area and its possible involvement in convulsive disorders.