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Social creatures : model animal systems for studying the neuroendocrine mechanisms of social behaviour

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Robinson_et_al_2019_Journal_of_Neuroendocrinology.pdf (573.6Kb)
Date
28/11/2019
Author
Robinson, Kelly J.
Bosch, Oliver J.
Levkowitz, Gil
Busch, Karl Emanuel
Jarman, Andrew
Ludwig, Mike
Keywords
Model animals
Neuropeptides
Oxytocin
Social behaviours
QH301 Biology
RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
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Abstract
The interaction of animals with conspecifics, termed social behaviour, has a major impact on the survival of many vertebrate species. Neuropeptide hormones modulate the underlying physiology that governs social interactions, and many findings concerning the neuroendocrine mechanisms of social behaviours have been extrapolated from animal models to humans. Neurones expressing neuropeptides show similar distribution patterns within the hypothalamic nucleus, even when evolutionarily distant species are compared. During evolution, hypothalamic neuropeptides and releasing hormones have retained not only their structures, but also their biological functions, including their effects on behaviour. Here, we review the current understanding of the mechanisms of social behaviours in several classes of animals, such as worms, insects and fish, as well as laboratory, wild and domesticated mammals.
Citation
Robinson , K J , Bosch , O J , Levkowitz , G , Busch , K E , Jarman , A & Ludwig , M 2019 , ' Social creatures : model animal systems for studying the neuroendocrine mechanisms of social behaviour ' , Journal of Neuroendocrinology , vol. 31 , no. 12 , e12807 , pp. 1-12 . https://doi.org/10.1111/jne.12807
Publication
Journal of Neuroendocrinology
Status
Peer reviewed
DOI
https://doi.org/10.1111/jne.12807
ISSN
0953-8194
Type
Journal item
Rights
Copyright © 2019 The Authors. Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Description
Work was supported by grants awarded to ML (BBSRC BB/S000224/1), OJB (BO 1958/8-2, GRK 2174), KEB (Wellcome Trust 109614/Z/15/Z, MRC MR/N004574/1), AJ (BBSRC BB/S000801) and GL (Israel Science Foundation #1511/16; United States-Israel Binational Science Foundation #2017325; Nella and Leon Benoziyo Center for Neurological Diseases, Richard F. Goodman Yale/Weizmann Exchange Program and Estate of Emile Mimran).
Collections
  • University of St Andrews Research
URI
http://hdl.handle.net/10023/19050

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