Intracerebrally Released Vasopressin and Oxytocin: Measurement, Mechanisms and Behavioural Consequences

Landgraf, Rainer

doi:10.1111/j.1365-2826.1995.tb00754.x

Cited by 103 publications

(40 citation statements)

References 72 publications

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“…Released centrally and interacting with V1a-R (Raggenbass et al, 1998) and V1b-R (Griebel et al, 2002), AVP is well known to be involved in multiple behavioral processes including cognition and emotionality (De Wied et al, 1988;Landgraf, 1995;Landgraf et al, 1995a;Engelmann et al, 1996;Liebsch et al, 1996;Makara et al, 1996;Young, 2002). In all the brain areas studied here, V1a-R binding failed to differentiate between the lines, suggesting that a critical involvement of this receptor subtype in trait anxiety/ depression is rather unlikely.…”

Section: Arginine-8-vasopressinmentioning

confidence: 82%

“…Since humans suffering from psychiatric disorders are not easily accessible for neurobiological studies, several animal models have been developed to mimic psychopathological conditions (Overstreet et al, 1992;Driscoll et al, 1998;Escorihuela et al, 1999). Over the past few decades, two Wistar rat lines have been bred in our laboratory for extremes in high (HAB) or low (LAB) anxiety-related behavior on the elevated plus-maze (EPM) and were now established as a novel animal model of trait anxiety/ depression (for a review, see Landgraf andWigger, 2002, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Alterations in Central Neuropeptide Expression, Release, and Receptor Binding in Rats Bred for High Anxiety: Critical Role of Vasopressin

Wigger

Sánchez

Mathys

et al. 2003

Neuropsychopharmacol

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240

152

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To model aspects of trait anxiety/depression, Wistar rats were bred for extremes in either hyper (HAB)-or hypo(LAB)-anxiety as measured on the elevated plus-maze and in a variety of additional behavioral tests. Similar to psychiatric patients, HAB rats prefer passive stress-coping strategies, indicative of depression-like behavior, show hyper-reactivity of the hypothalamo-pituitary-adrenal axis, and a pathological response to the dexamethasone/corticotropin-releasing hormone (CRH) challenge test. Here we tested central mRNA expression, release patterns, and receptor binding of neuropeptides critically involved in the regulation of both anxiety-related behavior and the HPA axis. Thus, CRH, arginine-8-vasopressin (AVP), and oxytocin (OXT) were studied in brains of HAB and LAB males both under basal conditions and after exposure to a mild emotional stressor. In HAB rats, CRH mRNA was decreased in the bed nucleus of the stria terminalis only. While no significant difference in CRH1-receptor binding was found in any brain area, CRH2-receptor binding was elevated in the hypothalamic paraventricular nucleus (PVN), the ventromedial hypothalamus, and the central amygdala of HABs compared to LABs. AVP, but not OXT, mRNA expression as well as release of the neuropeptide, were higher in the PVN of HABs, whereas AVP V1a-receptor binding failed to show significant differences in any brain region studied. Remarkably, intra-PVN treatment of HABs with the AVP V1-receptor antagonist d (CH 2 ) 5 Tyr (Me) AVP resulted in a decrease in anxiety/depression-related behavior. The elevated expression and release of AVP within the PVN of HAB rats together with the behavioral effects of the AVP V1-receptor antagonist suggest a critical involvement of this neuropeptide in neuroendocrine and behavioral phenomena associated with trait anxiety/ depression.

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Section: Arginine-8-vasopressinmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Alterations in Central Neuropeptide Expression, Release, and Receptor Binding in Rats Bred for High Anxiety: Critical Role of Vasopressin

Wigger

Sánchez

Mathys

et al. 2003

Neuropsychopharmacol

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240

152

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“…Moreover, hypothalamic expression of PRL (Emanuele et al, 1992) and PRL release from hypothalamic explants in response to depolarizing media and angiotensin II (DeVito et al, 1991;Torner et al, 1995) have been observed. This points toward the possibility of intracerebral PRL release, which may occur for example under stressful conditions, as found for various other neuropeptides such as vasopressin and oxytocin (Landgraf, 1995). In our study, to reveal receptor-mediated actions of PRL in the brain in the absence of a specific PRL-R antagonist, we used several complementary approaches.…”

Section: Discussionmentioning

confidence: 99%

Anxiolytic and Anti-Stress Effects of Brain Prolactin: Improved Efficacy of Antisense Targeting of the Prolactin Receptor by Molecular Modeling

et al. 2001

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We provide the first evidence that prolactin is a neuromodulator of behavioral and neuroendocrine stress coping in the rat. In virgin female and male rats, intracerebral infusion of ovine prolactin (oPRL) into the lateral cerebral ventricle (intracerebroventricular) exerted an anxiolytic effect on the elevated plusmaze in a dose-dependent manner (0.1 and 1.0 g/5 l; p Ͻ 0.01). In contrast, downregulation of the expression of the long form of brain prolactin receptors by chronic intracerebroventricular infusion of an antisense oligodeoxynucleotide (ODN) (osmotic minipump, 0.5 g ⅐ 0.5 l Ϫ1 ⅐ hr Ϫ1 ; 5 d) increased anxiety-related behavior on the plus-maze compared with mixed bases-treated and vehicle-treated rats ( p Ͻ 0.01), again demonstrating an anxiolytic effect of PRL acting at brain level. Furthermore, in jugular vein-catheterized female rats, the stress-induced increase of corticotropin secretion was decreased after chronic intracerebroventricular infusion of oPRL (osmotic minipump, 1.0 g ⅐ 0.5 l Ϫ1 ⅐ hr Ϫ1 ; p Ͻ 0.05) and, in contrast, was further elevated by antisense targeting of the brain prolactin receptors ( p Ͻ 0.01). This provides evidence for a receptor-mediated attenuation of the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis by prolactin. The antisense ODN sequence was selected on the basis of secondary structure molecular modeling of the target mRNA to improve antisense ODN-mRNA hybridization. Receptor autoradiography confirmed the expected improvement in the efficacy of downregulation of prolactin receptor expression [empirically designed antisense, 30%; p Ͼ 0.05, not significant; adjustment of target position after mRNA modeling, 72%; p Ͻ 0.05). Taken together, prolactin acting at brain level has to be considered as a novel regulator of both emotionality and HPA axis reactivity.

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“…Tissue measurements of neuropeptides are determined by a number of variables (e.g., synthesis, transport, storage, release, and degradation) and thus do not necessarily reflect the dynamics of local release (for review, see ref. 35). Because neuropeptides such as SP become biologically active only after their release into the extracellular space, attempts to measure intracerebral release focus on approaches that are able to reflect concentrations and their fluctuations in the extracellular fluid.…”

Section: Discussionmentioning

confidence: 99%

Substance P in the medial amygdala: Emotional stress-sensitive release and modulation of anxiety-related behavior in rats

Ebner

Rupniak

Saria

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

200

178

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Increasing evidence implicates the substance P (SP)͞neurokinin-1 receptor system in anxiety and depression. However, it is not known whether emotional stimulation alters endogenous extracellular SP levels in brain areas important for processing of anxiety and mood, a prerequisite for a contribution of this neuropeptide system in modulating these behaviors. Therefore, we examined in rats whether the release of SP is sensitive to emotional stressors in distinct subregions of the amygdala, a key area in processing of emotions. By using in vivo micropush-pull superfusion and microdialysis techniques, we found a pronounced and long-lasting increase (150%) in SP release in the medial nucleus of the amygdala (MeA), but not in the central nucleus of the amygdala, in response to immobilization stress. SP release in the MeA was transiently enhanced (40%) in response to elevated platform exposure, which is regarded as a mild emotional stressor. T he neuropeptide substance P (SP) and its preferred neurokinin-1 (NK 1 ) receptor have been proposed as possible targets for new antidepressant and anxiolytic therapies. Several preclinical studies have demonstrated a range of anxiety-related behaviors and defensive cardiovascular changes in response to central administration of SP agonists (1-6). Conversely, NK 1 receptor antagonists have been shown to produce anxiolytic-like effects after intracerebroventricular (4) or systemic administration (5,7,8). In addition, mice with selective deletion of the gene encoding the NK 1 receptor or the peptide itself also showed decreased anxiety-related behaviors (9-11). Thus, these findings suggest that SP acting as neurotransmitter͞neuromodulator (for review, see ref. 12) may be of relevance in the regulation of emotional states including anxiety-related behavior. Confirmation of this proposal was obtained by using a highly selective NK 1 receptor antagonist MK-0869, which relieved the symptoms of depression and anxiety in patients with major depressive disorder and a significant degree of anxiety (5). Although it has been shown that emotional and physical stressors modulate SP tissue levels or SP immunoreactivity in brain areas that are implicated in fear and anxiety (13-17), a change in extracellular SP levels, which is a direct and dynamic marker of SP neurotransmission, cannot be reliably predicted from these studies. Hence, at present it is not clear whether emotional stimuli actually do alter the in vivo release of SP, which is a prerequisite for a contribution of this neuropeptide system in modulating emotional states. Since stressful life experiences are thought to play a role in precipitating episodes of neuropsychiatric disorders including anxiety and depression (18,19), and laboratory stressors can produce behavioral and physiological changes resembling these mental disorders (20), it is of particular interest to examine the effect of emotional stressors on SP neurotransmission.The amygdala is critical for the processing of emotions including fear and anxiety (21, 22), and SP-cont...

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Intracerebrally Released Vasopressin and Oxytocin: Measurement, Mechanisms and Behavioural Consequences

Cited by 103 publications

References 72 publications

Alterations in Central Neuropeptide Expression, Release, and Receptor Binding in Rats Bred for High Anxiety: Critical Role of Vasopressin

Alterations in Central Neuropeptide Expression, Release, and Receptor Binding in Rats Bred for High Anxiety: Critical Role of Vasopressin

Anxiolytic and Anti-Stress Effects of Brain Prolactin: Improved Efficacy of Antisense Targeting of the Prolactin Receptor by Molecular Modeling

Substance P in the medial amygdala: Emotional stress-sensitive release and modulation of anxiety-related behavior in rats

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