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小鼠体内的黑皮质素-5受体缺陷阻断了一条影响信息素诱导攻击行为的新途径。

Melanocortin-5 receptor deficiency in mice blocks a novel pathway influencing pheromone-induced aggression.

作者信息

Morgan Caurnel, Cone Roger D

机构信息

Vollum Institute for Advanced Biomedical Research, Oregon Health and Science University, Portland, 97239, USA.

出版信息

Behav Genet. 2006 Mar;36(2):291-300. doi: 10.1007/s10519-005-9024-9. Epub 2006 Jan 12.

DOI:10.1007/s10519-005-9024-9
PMID:16408249
Abstract

The rodent preputial gland secretes aggression-promoting pheromones and expresses melanocortin-5 receptor (MC5R), but the functional relationship is poorly understood. We investigated whether MC5R deficiency in male mice alters stimulatory melanocortin influences on preputial growth and pheromone-induced aggression. In wild-type (MC5R(+/+)) pairs, repeated NDP-MSH injection decreased attack latency and increased aggression in initial attackers. Similar NDP-MSH treatment in MC5R-deficient (MC5R(-/-)) pairs failed to alter attack latency or aggression frequency, but aggression increased in vehicle-injected opponents. NDP-MSH treatment promoted preputial hypertrophy, and in MC5R(+/+) mice paired against non-aggressive stimulus opponents it decreased attack latency and increased aggression. MC5R(-/-) mice were insensitive to behavioral and physiological effects of NDP-MSH, and preputialectomized mice were insensitive to behavioral effects of NDP-MSH. The results suggest that MC5R inactivation reduced a pheromonal signal for aggression that acts on donors, rather than their opponents.

摘要

啮齿动物的包皮腺分泌促进攻击行为的信息素并表达黑皮质素-5受体(MC5R),但其功能关系尚不清楚。我们研究了雄性小鼠中MC5R缺乏是否会改变黑皮质素对包皮生长和信息素诱导攻击行为的刺激作用。在野生型(MC5R(+/+))小鼠对中,重复注射NDP-MSH可缩短攻击潜伏期并增加初始攻击者的攻击性。在MC5R缺陷型(MC5R(-/-))小鼠对中进行类似的NDP-MSH处理未能改变攻击潜伏期或攻击频率,但注射溶剂的对手的攻击性增加。NDP-MSH处理促进了包皮肥大,在与无攻击性刺激对手配对的MC5R(+/+)小鼠中,它缩短了攻击潜伏期并增加了攻击性。MC5R(-/-)小鼠对NDP-MSH的行为和生理作用不敏感,而包皮切除的小鼠对NDP-MSH的行为作用不敏感。结果表明,MC5R失活减少了一种作用于供体而非其对手的攻击性信息素信号。

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