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Front Neuroanat. 2015 Jan 20;8:164. doi: 10.3389/fnana.2014.00164. eCollection 2014.

Ontogenesis of oxytocin pathways in the mammalian brain: late maturation and psychosocial disorders.

Author information

1
Schaller Research Group on Neuropeptides, German Cancer Research Center and CellNetwork Cluster of Excellence of the University of Heidelberg Heidelberg, Germany.
2
Institute of Functional Genomics, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Université Montpellier 1, Université Montpellier 2 Montpellier, France.
3
Consiglio Nazionale delle Ricerche Institute of Neuroscience Milan, Italy.
4
Reference Centre for Prader-Willi Syndrome - Department of Pediatric Endocrinology, Hôpital des Enfants Centre Hospitalier Universitaire de Toulouse 330 Toulouse, France ; Institut National de la Santé et de la Recherche Médicale Unité Mixe de Recherche 1043, Paul Sabatier University Toulouse III Toulouse, France.
5
Institut de Neurobiologie de la Méditerranée Unité Mixe de Recherche U901, Institut National de la Santé et de la Recherche Médicale, Parc Scientifique de Luminy Marseille, France ; Aix-Marseille Université, Institut de Neurobiologie de la Méditerranée Unité Mixe de Recherche 901 Marseille, France.

Abstract

Oxytocin (OT), the main neuropeptide of sociality, is expressed in neurons exclusively localized in the hypothalamus. During the last decade, a plethora of neuroendocrine, metabolic, autonomic and behavioral effects of OT has been reported. In the urgency to find treatments to syndromes as invalidating as autism, many clinical trials have been launched in which OT is administered to patients, including adolescents and children. However, the impact of OT on the developing brain and in particular on the embryonic and early postnatal maturation of OT neurons, has been only poorly investigated. In the present review we summarize available (although limited) literature on general features of ontogenetic transformation of the OT system, including determination, migration and differentiation of OT neurons. Next, we discuss trajectories of OT receptors (OTR) in the perinatal period. Furthermore, we provide evidence that early alterations, from birth, in the central OT system lead to severe neurodevelopmental diseases such as feeding deficit in infancy and severe defects in social behavior in adulthood, as described in Prader-Willi syndrome (PWS). Our review intends to propose a hypothesis about developmental dynamics of central OT pathways, which are essential for survival right after birth and for the acquisition of social skills later on. A better understanding of the embryonic and early postnatal maturation of the OT system may lead to better OT-based treatments in PWS or autism.

KEYWORDS:

Prader-Willi syndrome; autisn; axonal release; ontogenesis; oxytocin; oxytocin receptor; somatodendritic release

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