Modeling socially anhedonic syndromes: genetic and pharmacological manipulation of opioid neurotransmission in mice.
Modeling socially anhedonic syndromes: genetic and pharmacological manipulation of opioid neurotransmission in mice.
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DOI:
10.1038/tp.2012.83
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发表时间:
2012-08-28
影响因子:
6.8
通讯作者:
D'Amato FR
中科院分区:
文献类型:
--
作者:
Cinque C;Pondiki S;Oddi D;Di Certo MG;Marinelli S;Troisi A;Moles A;D'Amato FR
Social anhedonia, or the diminished capacity to experience pleasure and reward from social affiliation, is a major symptom of different psychiatric disorders, including some forms of infantile autism and schizophrenia spectrum disorders. The brain opioid hypothesis of social attachment is a promising model for achieving insights into how neurobiological and developmental factors contribute to the regulation of social reward. In this study, genetic knocking-out and naltrexone (NTRX) treatment during the first 4 days of life were used to disrupt opioid neurotransmission in mouse pups and their attachment relationships with the mother. Both permanent (genetic) and transient (pharmacological) manipulations of opioid neurotransmission exerted long-term effects on social affiliation. When juveniles, both μ-opioid receptor knockout mice and NTRX-treated pups showed reduced interest in peers and no preference for socially rewarding environment. These results demonstrate that sociability in juvenile mice is highly dependent on the establishment during infancy of a positive affective relationship with their mothers and that opioid neurotransmission has a major role in the regulation of social hedonic capacity. If the validity of this animal model will be confirmed by future research, translational studies focusing on the interaction between early experience and opioid neurotransmission could provide useful insights for identifying endophenotypes of human psychiatric disorders associated with social anhedonia.
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DOI:
10.1111/j.1749-6632.2009.04541.x
发表时间:
2009-01-01
期刊:
VALUES, EMPATHY, AND FAIRNESS ACROSS SOCIAL BARRIERS
影响因子:
--
作者:
Ebstein, Richard P.;Israel, Salomon;Yirmiya, Nurit
通讯作者:
Yirmiya, Nurit
影响因子:
64.8
作者:
Matthes, HWD;Maldonado, R;Kieffer, BL
通讯作者:
Kieffer, BL
影响因子:
4.6
作者:
Kwapil, TR
通讯作者:
Kwapil, TR
影响因子:
8.2
作者:
Brown, Leslie H.;Silvia, Paul J.;Kwapil, Thomas R.
通讯作者:
Kwapil, Thomas R.
影响因子:
11
作者:
Harvey, P-O;Pruessner, J.;Lepage, M.
通讯作者:
Lepage, M.