Rationale

Delay discounting, in which an animal chooses between a small, immediate or large, delayed reinforcer, is an experimental model of impulsivity. In previous studies, d-amphetamine has both increased and decreased preference for larger-delayed reinforcers depending on experimental conditions.

Objective

Identify genotype X environment interactions responsible for these disparate findings in a single study and assess the hypothesis that baseline-dependence unifies d-amphetamine's effects.

Methods

Delay discounting by BALB/c and C57Bl/6 mice was evaluated using a choice procedure in which the six delays to the larger reinforcer were presented in a single session. Components were presented both with and without stimuli that uniquely signaled reinforcer delays. d-Amphetamine's (0.1–1.7 mg/kg) effects on delay and magnitude sensitivity were assessed when specific stimuli did or did not uniquely signal the delay to a larger reinforcer. d-Amphetamine's effects were determined using a model-comparison approach.

Results

During baseline, magnitude and delay sensitivity were identical across signal conditions for BALB/c mice and generally greater than the C57Bl/6 mice. For C57Bl/6 mice, magnitude and delay sensitivity were higher during the signaled than the unsignaled component. Amphetamine decreased delay sensitivity during both components for BALB/c mice, but this effect was attenuated by delay-specific stimuli. For C57Bl/6 mice, amphetamine decreased their high magnitude and delay sensitivity when delays were signaled and, conversely, increased the low magnitude and delay sensitivity when delays were unsignaled.

Conclusions

BALB/c mice showed high delay and magnitude sensitivity regardless of signal conditions. C57Bl/6's magnitude and delay sensitivity depended on signaling. d-Amphetamine usually decreased high baseline delay- and magnitude sensitivity and increased low sensitivities, a baseline-dependence that occurred regardless of whether delay sensitivity was driven by biological (genotype) or environmental (signaling) variables. The C57Bl/6 mouse may be a good model of environmentally-induced impulsivity while BALB/c mice could model impulsivity with a strong genetic contribution.

中文翻译：

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基线依赖性：基因型和信号延迟如何影响苯丙胺对延迟贴现的影响

基本原理

延迟贴现是动物冲动的实验模型，在延迟贴现中，动物在小的，即时的或大型的延迟加固器之间进行选择。在以前的研究中，根据实验条件，d-苯丙胺对大延迟增强剂的偏好增加或减少。

目的

在一项研究中确定导致这些不同发现的基因型X环境相互作用，并评估基线依赖性统一d-苯丙胺作用的假说。

方法

使用选择程序评估BALB / c和C57Bl / 6小鼠的延迟贴现，其中在一次会议中介绍了对较大增强剂的六个延迟。呈现有无刺激的组件，这些刺激独特地暗示了补强器的延迟。d-当特定刺激确实或不唯一地向较大的增强剂发出延迟信号时，评估了苯丙胺（0.1-1.7 mg / kg）对延迟和幅度敏感性的影响。使用模型比较方法确定d-苯丙胺的作用。

结果

在基线期间，BALB / c小鼠的信号条件在幅度和延迟敏感性上均相同，并且通常大于C57Bl / 6小鼠。对于C57Bl / 6小鼠，在信号传递期间的幅度和延迟敏感性要高于未信号传递的组分。苯丙胺降低了两种成分对BALB / c小鼠的延迟敏感性，但这种作用因延迟特异性刺激而减弱。对于C57Bl / 6小鼠，苯丙胺在发出延迟信号时会降低其高强度和延迟敏感性，反之，在未发出延迟信号时会降低其低强度和延迟敏感性。

结论

无论信号条件如何，BALB / c小鼠均表现出高延迟和幅度敏感性。C57Bl / 6的大小和延迟敏感性取决于信号传导。d-苯丙胺通常会降低高基线延迟和幅度敏感性，并增加低敏感性，无论延迟敏感性是由生物学（基因型）还是由环境（信号）变量驱动，都会出现基线依赖性。C57Bl / 6小鼠可能是环境诱导冲动的良好模型，而BALB / c小鼠可以模拟具有强烈遗传贡献的冲动。