The Urge to Fight: Persistent Escalation by Alcohol and Role of NMDA Receptors in Mice.
The Urge to Fight: Persistent Escalation by Alcohol and Role of NMDA Receptors in Mice.
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DOI：
10.3389/fnbeh.2018.00206
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发表时间：
2018
影响因子：
3
通讯作者：
Miczek KA
中科院分区：
文献类型：
--
作者：
Covington HE 3rd;Newman EL;Tran S;Walton L;Hayek W;Leonard MZ;DeBold JF;Miczek KA
在一些人中，饮酒会导致病理性的攻击性和暴力行为。酒精会加剧打架的冲动，尽管会破坏打斗的表现。当在几种剂量条件下口服时，目前的研究在小鼠模型中检查了重复酒精是否会增强战斗的动机，执行战斗性能，或两者兼而有之。具体地说，每天服用七次酒精(0、1.8或2.2克/公斤)来确定发起攻击行为的动机是否随着战斗行为的严重程度的变化而发生变化。在固定间隔(FI)时间表的控制下做出反应，在最初的每日会话中加强攻击性，表明对酒精的镇静作用产生了耐受性。到了第7天，酒精提高了攻击性奖励的FI反应率。虽然酒精加剧了打架的动机，但在整个7天里，打架表现仍然受到抑制。低剂量酒精(1.0g/kg)对攻击奖赏的增强反应被证明是持久的，因为我们观察了酒精预处理后一个多月的敏感率。此外，动机攻击性的敏感化并不是随着运动活动的普遍增强而发生的。NMDA或AMPA受体对氯胺酮、地佐西平或NBQX的拮抗作用在随后的酒精刺激中基本上是宁静的，对酒精引起的FI反应率的表达没有任何显著影响。目前对食欲和表现指标的分离表明，控制攻击性唤醒的离散神经机制可以明显地被酒精敏化。
Alcohol drinking, in some individuals, culminates in pathologically aggressive and violent behaviors. Alcohol can escalate the urge to fight, despite causing disruptions in fighting performance. When orally administered under several dosing conditions the current study examined in a mouse model if repeated alcohol escalates the motivation to fight, the execution of fighting performance, or both. Specifically, seven daily administrations of alcohol (0, 1.8, or 2.2 g/kg) determined if changes in the motivation to initiate aggressive acts occur with, or without, shifts in the severity of fighting behavior. Responding under the control of a fixed interval (FI) schedule for aggression reinforcements across the initial daily sessions indicated the development of tolerance to alcohol’s sedative effect. By day 7, alcohol augmented FI response rates for aggression rewards. While alcohol escalated the motivation to fight, fighting performance remained suppressed across the entire 7 days. Augmented FI responding for aggression rewards in response to a low dose of alcohol (1.0 g/kg) proved to be persistent, as we observed sensitized rates of responding for more than a month after alcohol pretreatment. In addition, this sensitization of motivated aggression did not occur with a general enhancement of motor activity. Antagonism of NMDA or AMPA receptors with ketamine, dizocilpine, or NBQX during later challenges with alcohol were largely serenic without having any notable impact on the expression of alcohol-escalated rates of FI responding. The current dissociation of appetitive and performance measures indicates that discrete neural mechanisms controlling aggressive arousal can be distinctly sensitized by alcohol.
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