The nucleus accumbens (NAc) is known for its role in reward processing or motivation, but more recently it has also been linked to altered eating behaviors in disorders such as anorexia nervosa. In a study published in Nature Communications, Walle et al. investigated the subtype-specific roles of medium spiny neurons (MSNs) in the NAc in mouse feeding behaviors. The authors chemogenetically manipulated MSNs expressing either the dopamine D1 receptor (D1-MSNs) or the D2 receptor (D2-MSNs) in mice with free access to a running wheel and a high-fat diet following food restriction. Selective activation of D2-MSNs caused mice to consume more food and run less, leading to substantial fat gain. By contrast, chronic activation of D1-MSNs promoted running behavior and an initial decrease in food consumption, but with no impact on body weight or fat mass. Simultaneous activation of D1-MSNs and inhibition of D2-MSNs caused mice to prioritize wheel running activity and exhibit pathological (≥20%) weight loss. These results suggest that the activities of D1-MSNs and D2-MSNs in the NAc together balance physical exertion (or food-seeking behavior) and food consumption. Disruption of D1-MSN versus D2-MSN activity may have relevance for abnormal feeding behavior in human eating disorders.

Original reference: Nat. Commun. 15, 2543 (2024)

伏隔核 (NAc) 以其在奖励处理或动机中的作用而闻名，但最近它也与神经性厌食症等疾病的饮食行为改变有关。Walle 等人在《自然通讯》上发表的一项研究中。研究了 NAc 中中型多棘神经元 (MSN) 在小鼠进食行为中的亚型特异性作用。作者通过化学遗传学方法，在限制食物后自由使用跑步轮和高脂肪饮食的小鼠中表达多巴胺 D1 受体 (D1-MSN) 或 D2 受体 (D2-MSN) 的 MSN。 D2-MSN 的选择性激活导致小鼠消耗更多食物并减少跑步，导致脂肪大量增加。相比之下，D1-MSN 的慢性激活促进了跑步行为和食物消耗的最初减少，但对体重或脂肪量没有影响。同时激活 D1-MSN 和抑制 D2-MSN 导致小鼠优先考虑轮跑活动并表现出病理性（≥20%）体重减轻。这些结果表明，NAc 中 D1-MSN 和 D2-MSN 的活动共同平衡体力消耗（或觅食行为）和食物消耗。 D1-MSN 与 D2-MSN 活性的破坏可能与人类饮食失调中的异常喂养行为有关。

原文参考： Nat.交流。15 , 2543 (2024)