Abstract
The neuromodulator oxytocin, since its first synthesis by du Vigneaud in 1953, has mainly been associated with beneficial physiological effects, as well as positive social and emotional behaviors. This overall positive picture of oxytocin as the “love-, cuddle-, or bonding-hormone” has repeatedly been challenged since then. Oxytocin-induced effects that would be perceived as negative by the individual, such as increased anxiety or potentiation of stress-induced ACTH release, as well as the regulation of negative approach-related emotions, such as envy and schadenfreude (gloating) have been described. The general consent is that oxytocin, instead of acting unidirectional, induces changes in the salience network to shift the emphasis of emotional contexts, and therefore can, e.g., produce both anxiolytic as well as anxiogenic behavioral outcomes. However, the underlying mechanisms leading to alterations in the salience network are still unclear. With the aim to understand the manifold effects of oxytocin on a cellular/molecular level, a set of oxytocin receptor-coupled signaling cascades and downstream effectors regulating transcription and translation has been identified. Those oxytocin-driven effectors, such as MEF2 and CREB, are known modulators of the neuronal and glial cytoarchitecture. We hypothesize that, by determining cellular morphology and connectivity, MEF2 is one of the key factors that might contribute to the diverse behavioral effects of oxytocin.
Highlights
The neuropeptide oxytocin is mainly produced in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON), it is released from magnocellular cells by axonal and somatodendritic release, and into the periphery via axonal projections [1]
In addition to the SON and caudate nucleus, the salience network consists of other brain regions that have already been associated with oxytocinergic effects and that express the oxytocin receptor, like the anterior cingulate cortex, lateral septum, striatum, medial prefrontal cortex, hippocampus, amygdala, nucleus accumbens, and PVN [42]
While we have identified a myocyte enhancer factor 2 (MEF2) binding sequence in the oxytocin receptor promoter with in silico prediction tools, there is no recent evidence available, whether activated MEF2 alters the transcription of the Oxtr gene
Summary
The neuropeptide oxytocin is mainly produced in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON), it is released from magnocellular cells by axonal and somatodendritic release, and into the periphery via axonal projections [1]. Intra-PVN infusions of oxytocin reduce anxiety-like behavior by activating local GABAergic neurons, which dampen the stress-induced activity of CRF-positive neurons and subsequent corticosterone release [17].
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