Vasopressin and Oxytocin Excite Distinct Neuronal Populations in the Central Amygdala

By D. Huber, P. Veinante, R. Stoop. Science, 2005

786 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Cognitive Neuroscience, Social Psychology

View Paper: https://www.semanticscholar.org/paper/536bcd221ae987091ae0d6c8f83e6f4196eab90b

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Citations in the corpus

Amygdala inhibitory circuits and the control of fear memory. (2009, background): “In line with the latter hypothesis, Huber and colleagues (Huber et al., 2005) demonstrated that oxytocin, a neuropeptide with strong anxiolytic effects, excites a subpopulation of GABAergic, CEm-projecting neurons in CEl.”
Oxytocin, vasopressin, and human social behavior. (2009, background): “Intracerebral OT has been shown to inhibit the stress-induced activity of the hypothalamic–pituitary–adrenal (HPA) axis responsiveness [119,123] and the activity of the amygdala in the modulation of the autonomic fear response [80].”
A common allele in the oxytocin receptor gene (OXTR) impacts prosocial temperament and human hypothalamic-limbic structure and function (2010, background): “Consistent with these findings, complex interacting and mutually inhibiting neuropeptide effects have been identified on the level of cellular physiology in the amygdala (69, 75), where distinct populations of neurons encode for the emotional and social salience of positively and negatively valenced”
Dendritic peptide release and peptide-dependent behaviours (2006, background): “For instance, the olfactory bulbs and the amygdala are important sites for oxytocin-dependent behaviours, rich in oxytocin receptors but only sparsely innervated by oxytocin fibre”
Evoked axonal oxytocin release in the central amygdala attenuates fear response. (2012, positive): “Four-to-eight weeks after injection of ChR2-mCherry rAAV into the SON, PVN, and AN of adult virgin female rats, brains were removed, cut into 400 mm horizontal slices (described in Huber et al., 2005), and kept in artificial cerebrospinal fluid in the dark to avoid ChR2 activation.”
The Challenge of Translation in Social Neuroscience: A Review of Oxytocin, Vasopressin, and Affiliative Behavior (2010, neutral): “While this finding is broadly consistent with the vole data as well as evidence for vasopressin receptors in the rat amygdala (Huber et al., 2005), the evidence in humans points to a role for OT rather than AVP on amygdala activation (Kirsch et al., 2005).”
A role for brain stress systems in addiction. (2008, positive): “Vasopressin also activated cells in the medial part of the central nucleus of the amygdala (Huber et al., 2005).”
Oxytocin Enhances Amygdala-Dependent, Socially Reinforced Learning and Emotional Empathy in Humans (2010, background): “, 1993; Hein and Singer, 2008), we have focused on the amygdala, building on previous findings showing substantial OTR expression in the rat amygdala (Insel and Shapiro, 1992; Veinante and Freund-Mercier, 1997) and where OT regulates neuronal activity (Huber et al., 2005).”
The role of oxytocin in social bonding, stress regulation and mental health: an update on the moderating effects of context and interindividual differences. (2013, background): “In rats it was shown that oxytocin-binding to its receptor in the amygdala inhibited activity of neural populations that project to hypothalamic and brainstem areas regulating peripheral stress and fear responses respectively (Huber et al., 2005; Viviani et al., 2011).”
Approach–Avoidance versus Dominance–Submissiveness: A Multilevel Neural Framework on How Testosterone Promotes Social Status (2013, background): “, 2011), is independent from vasopressin (Huber et al., 2005; Veinante & Freund-Mercier, 1997).”
Neuroendocrinology of coping styles: towards understanding the biology of individual variation. (2010, positive): “One key brain area that importantly controls behavioral and autonomic stress-coping responses, and where vasopressin and oxytocin modulate neuronal activity in opposite ways, is the central nucleus of the amygdala (CeA) [67] Stressful stimuli increase the levels of both peptides in the extracellular”