Dendritic peptide release and peptide-dependent behaviours

Ludwig, Mike; Leng, Gareth

doi:10.1038/nrn1845

Cited by 872 publications

(801 citation statements)

References 110 publications

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“…As a consequence, further studies have to analyze whether the behavioral profile is indeed primarily controlled by the 'septum versus MeA balance' or the result of a downstream manifestation of altered, behaviorally relevant AVP signaling elsewhere in the brain. Therefore, it would be worth testing whether during acute stressor exposure somatic-dendritic release of AVP from the SON versus PVN might influence the behavioral response in addition to local signaling (Ebner et al, 2002, Ludwig andLeng, 2006). Anhedonia was suggested to be one of the core symptoms of depression (Di Giannantonio and Martinotti, 2012, Harden et al, 2012, Hill et al, 2012, Warnock et al, 2012.…”

Section: Discussionmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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Section: Discussionmentioning

confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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“…Magnocellular neurons of the hypothalamic paraventricular nucleus (PVN) and the supraoptic nucleus , the primary sources of OT synthesis, project to the posterior pituitary, where OT is stored in large secretory vesicles, so-called large dense-core vesicles . In response to calcium influx as well as intracellular calcium release from the endoplasmic reticulum, OT is released into systemic circulation (Meyer-Lindenberg et al, 2011) from axonal terminals within the neurohypophysis (Ludwig and Leng, 2006; Ludwig et al, 2002). The most prominent peripheral OT effects via the classical hypothalamic-neurohypophyseal pathway are the induction of parturition through increased contractibility of the uterine smooth muscles and milk ejection from the mammary gland in response to suckling stimuli in lactating females (Lee et al, 2009).…”

Section: Ot and Early-life Stress (Els) – Role In Shaping Neural Cmentioning

confidence: 99%

“…First, it has been suggested that there is a slow, “unwired”, and global transmission of OT that is released mainly from neuronal dendrites, but also from axons and soma in the hypothalamus to reach extrahypothalamic brain structures, such as the amygdala or the cingulate cortex (Boccia et al, 2013). This diffuse mode of communication, referred to as volume transmission (Landgraf and Neumann, 2004; Ludwig and Leng, 2006), enables OT to act as a neuromodulator within the brain and implies a slow enzymatic degradation of OT, which in turn permits OT to travel long distances (Landgraf and Neumann, 2004). Second, it has been shown that in the rodent (Knobloch et al, 2012) and human brain (Boccia et al, 2013) there is a variety of “hard-wired” oxytocinergic nerve fibers from the hypothalamus to limbic, mesencephalic, and cortical brain regions that allow fine-tuned and fast modulation of target structures (Knobloch et al, 2012; Landgraf and Neumann, 2004; Stoop, 2012; Strathearn, 2011).…”

Section: Ot and Early-life Stress (Els) – Role In Shaping Neural Cmentioning

confidence: 99%

Oxytocin pathways in the intergenerational transmission of maternal early life stress

Toepfer

Heim

Entringer

et al. 2017

Neuroscience & Biobehavioral Reviews

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Severe stress in early life, such as childhood abuse and neglect, constitutes a major risk factor in the etiology of psychiatric disorders and somatic diseases. Importantly, these long-term effects may impact the next generation. The intergenerational transmission of maternal early life stress (ELS) may occur via pre-and postnatal pathways, such as alterations in maternal-fetal-placental stress physiology, maternal depression during pregnancy and postpartum, as well as impaired mother-offspring interactions. The neuropeptide oxytocin (OT) has gained considerable attention for its role in modulating all of these assumed transmission pathways. Moreover, central and peripheral OT signaling pathways are highly sensitive to environmental exposures and may be compromised by ELS with implications for these putative transmission mechanisms. Together, these data suggest that OT pathways play an important role in the intergenerational transmission of maternal ELS in humans. By integrating recent studies on gene-environment interactions and epigenetic modifications in OT pathway genes, the present review aims to develop a conceptual framework of intergenerational transmission of maternal ELS that emphasizes the role of OT.

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“…An interesting feature of OT action in the brain is that although OT has profound effects on social bonding that are exerted at sites that richly express oxytocin receptors, such brain regions are innervated by few, if any, oxytocin-containing projections [55]. How then does OT exert its effect in limbic and other 'socially sensitive' brain regions in the absence of apparent direct OT containing neurons?…”

Section: Dendritic Release Of Oxytocinmentioning

confidence: 99%

“…Specifically, magnocellular neurons in these two nuclei contain most of the OT and AVP in the CNS and are characterized by dendritic release, which is regulated independently of secretion into the blood. Indeed, dendrites are apparently the major source of peptides released in the brain [55]. Importantly dendritic release does not parallel axonal release and both processes are regulated independently.…”

Section: Dendritic Release Of Oxytocinmentioning

confidence: 99%

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

et al. 2011

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Edited by Sergio Papa, Gianfranco Gilardi and Wilhelm JustKeywords: Autism spectrum disorder (ASD) All-trans retinoic acid (ATRA) CD38 Oxytocin Polymorphism a b s t r a c t Increasing evidence suggests that the nonapeptide, oxytocin (OT), helps shape social and affiliative behaviors not only in lower mammals but also in humans. Recently, an essential mediator of brain OT release has been discovered, ADP-ribosyl cyclase and/or CD38. We have subsequently shown that polymorphisms across the CD38 gene are associated with autism spectrum disorders (ASD). Notably, CD38 expression in lymphoblastoid cells (LBC) is reduced in cell lines derived from ASD subjects compared to parental cell lines. Intriguingly, a correlation was observed between CD38 expression and measures of social function in ASD. Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing 'proof of principle' in a peripheral model that retinoids are potential therapeutic agents in ASD. Ó 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. OxytocinClassically, the nonapeptide oxytocin (OT) has been viewed as a hypothalamic neuropeptide that is released into the general circulation from the neural lobe of the pituitary, inducing uterine contractions during parturition and milk ejection during lactation. OT is derived from a pre-prohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary for storage and subsequent release into the bloodstream (see [1] for comprehensive review of the oxytocin receptor system). OT and social behaviorBeyond the long-known peripheral effects of OT, a wealth of animal studies have elaborated the role of OT, or their analogues such as isotocin and vasotocin [2], in molding social behavior from fish to mammals [3]. In the past few years the role of OT has also been examined in our own species, and similar to what has been learned from animal studies, it appears that this nonapeptides also influence social behaviors in humans [4,5]. Indeed, OT has been suggested as the 'great facilitator of life' in a recent review [6].In humans, intranasal administration of OT has been shown to increase trust [7], facilitate mind-reading [8], enhance human memory for social identity [9], increase positive communication between couples [10], increase gaze to the eye region [11] and increase generosity [12]. Intriguingly, OT plasma levels have been linked to individual patterns of maternal-fetal attachment [13] and salivary OT levels were associated with bonding to own parents and inversely related to psychological distress, particularly depressive symptoms [14]. Social anxiety symptom severity, adjusted for age and gender in a healthy group of subjects, was associated with higher plasma oxytocin levels [15]. Imaging studies reinforce the role of OT in influencing human social ...

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Dendritic peptide release and peptide-dependent behaviours

Cited by 872 publications

References 110 publications

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Oxytocin pathways in the intergenerational transmission of maternal early life stress

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

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