想正面记忆是否能减轻抑郁?美国麻省理工大学Susumu Tonegawa 及同事利用与一个正面的、中性的或负面的经历相关的、通过光遗传学方法标记的特定海马体记忆印迹对这一问题进行了研究。这些记忆之后可以通过光被人工激活。正面印迹的急性激活被发现会抑制暴露于慢性压力的小鼠类似抑郁症的行为，这是由 “海马体-杏仁核-伏隔核”通道介导的一个效应。重要的是，正面印迹的慢性激活也会抑制处于压力状态下的小鼠类似抑郁症的行为，即便在激活已经结束以后也是这样，说明这种抗抑郁效应并不取决于对印迹的实时人工激活。作者提出，对与一个正面记忆相关的海马体齿状回细胞的直接激活，也许能为减轻一类与抑郁相关的行为提供一个潜在的治疗节点，尽管在目前阶段还不清楚这些发现对人类是否适用。

    原文链接：Activating positive memory engrams suppresses depression-like behaviour

    原文摘要：metastatic disease remains the primary cause of death for patients with breast cancer. The different steps of the metastatic cascade rely on reciprocal interactions between cancer cells and their microenvironment. Within this local microenvironment and in distant organs, immune cells and their mediators are known to facilitate metastasis formation1, 2. However, the precise contribution of tumour-induced systemic inflammation to metastasis and the mechanisms regulating systemic inflammation are poorly understood. Here we show that tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis. We mechanistically demonstrate that interleukin (IL)-1β elicits IL-17 expression from gamma delta (γδ) T cells, resulting in systemic, granulocyte colony-stimulating factor (G-CSF)-dependent expansion and polarization of neutrophils in mice bearing mammary tumours. Tumour-induced neutrophils acquire the ability to suppress cytotoxic T lymphocytes carrying the CD8 antigen, which limit the establishment of metastases. Neutralization of IL-17 or G-CSF and absence of γδ T cells prevents neutrophil accumulation and downregulates the T-cell-suppressive phenotype of neutrophils. Moreover, the absence of γδ T cells or neutrophils profoundly reduces pulmonary and lymph node metastases without influencing primary tumour progression. Our data indicate that targeting this novel cancer-cell-initiated domino effect within the immune system—the γδ T cell/IL-17/neutrophil axis—represents a new strategy to inhibit metastatic disease.