Abstract
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.
Highlights
Alcohol-escalated violence inflicts serious harm and suffering on a global scale as documented over many decades (Pernanen, 1993; Bye and Rossow, 2010)
Appetitive and performance measures in the context of aggression are clearly dissected with the implementation of an fixed interval (FI) schedule of reinforcement (Skinner and Morse, 1957)
Alcohol, at both 1.8 and 2.2 g/kg/day, initially disrupted both responding during the FI and subsequent fighting performance
Summary
Alcohol-escalated violence inflicts serious harm and suffering on a global scale as documented over many decades (Pernanen, 1993; Bye and Rossow, 2010). The neural architecture supporting such maladaptive aggression remains unknown, but key epidemiological findings provide some insight into their origins, including the predictably high rate of reoccurrence and their progressive escalation in alcohol use disorders (Fergusson and Horwood, 2000; Coid et al, 2006). Preclinical data corroborate these trends, such that the proportion of alcohol-heightened aggressors in a sample increases with a history of intermittent voluntary drinking (Fish et al, 2002; Hwa et al, 2015). Our final hypothesis explored to what extent the activation of ionotropic glutamate receptors (iGluRs) is necessary for maintaining any lasting changes in aggressive reinforcement resulting from repeated oral administrations of alcohol
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