Tripp Gail, Wickens Jeff
Human Developmental Neurobiology Unit, Okinawa Institute of Science and Technology Graduate University, Okinawa, Japan.
Neurobiology Research Unit, Okinawa Institute of Science and Technology Graduate University, Okinawa, Japan.
Personal Neurosci. 2024 Jan 31;7:e2. doi: 10.1017/pen.2023.12. eCollection 2024.
An altered behavioral response to positive reinforcement has been proposed to be a core deficit in attention deficit hyperactivity disorder (ADHD). The spontaneously hypertensive rat (SHR), a congenic animal strain, displays a similarly altered response to reinforcement. The presence of this genetically determined phenotype in a rodent model allows experimental investigation of underlying neural mechanisms. Behaviorally, the SHR displays increased preference for immediate reinforcement, increased sensitivity to individual instances of reinforcement relative to integrated reinforcement history, and a steeper delay of reinforcement gradient compared to other rat strains. The SHR also shows less development of incentive to approach sensory stimuli, or cues, that predict reward after repeated cue-reward pairing. We consider the underlying neural mechanisms for these characteristics. It is well known that midbrain dopamine neurons are initially activated by unexpected reward and gradually transfer their responses to reward-predicting cues. This finding has inspired the dopamine transfer deficit (DTD) hypothesis, which predicts certain behavioral effects that would arise from a deficient transfer of dopamine responses from actual rewards to reward-predicting cues. We argue that the DTD predicts the altered responses to reinforcement seen in the SHR and individuals with ADHD. These altered responses to reinforcement in turn predict core symptoms of ADHD. We also suggest that variations in the degree of dopamine transfer may underlie variations in personality dimensions related to altered reinforcement sensitivity. In doing so, we highlight the value of rodent models to the study of human personality.
对正强化的行为反应改变被认为是注意力缺陷多动障碍（ADHD）的核心缺陷。自发性高血压大鼠（SHR）是一种同源动物品系，对强化的反应也有类似改变。在啮齿动物模型中存在这种基因决定的表型，使得对潜在神经机制的实验研究成为可能。在行为方面，与其他大鼠品系相比，SHR对即时强化的偏好增加，相对于综合强化历史，对单个强化实例的敏感性增加，强化梯度延迟更陡峭。SHR在重复线索-奖励配对后，对预测奖励的感觉刺激或线索的接近动机发展也较少。我们考虑这些特征的潜在神经机制。众所周知，中脑多巴胺神经元最初由意外奖励激活，并逐渐将其反应转移到预测奖励的线索上。这一发现激发了多巴胺转移缺陷（DTD）假说，该假说预测了多巴胺反应从实际奖励到预测奖励线索的转移不足会产生的某些行为效应。我们认为DTD假说可以解释SHR和ADHD患者中观察到的对强化的改变反应。这些对强化的改变反应反过来又预示着ADHD的核心症状。我们还认为，多巴胺转移程度的变化可能是与强化敏感性改变相关的人格维度变化的基础。在此过程中，我们强调了啮齿动物模型对人类人格研究的价值。
