Opendak Maya, Offit Lily, Monari Patrick, Schoenfeld Timothy J, Sonti Anup N, Cameron Heather A, Gould Elizabeth
Princeton Neuroscience Institute and.
Princeton Neuroscience Institute and Department of Psychology, Princeton University, Princeton, New Jersey 08540, and.
J Neurosci. 2016 Jun 29;36(26):7027-38. doi: 10.1523/JNEUROSCI.4435-15.2016.
Research on social instability has focused on its detrimental consequences, but most people are resilient and respond by invoking various coping strategies. To investigate cellular processes underlying such strategies, a dominance hierarchy of rats was formed and then destabilized. Regardless of social position, rats from disrupted hierarchies had fewer new neurons in the hippocampus compared with rats from control cages and those from stable hierarchies. Social disruption produced a preference for familiar over novel conspecifics, a change that did not involve global memory impairments or increased anxiety. Using the neuropeptide oxytocin as a tool to increase neurogenesis in the hippocampus of disrupted rats restored preference for novel conspecifics to predisruption levels. Conversely, reducing the number of new neurons by limited inhibition of adult neurogenesis in naive transgenic GFAP-thymidine kinase rats resulted in social behavior similar to disrupted rats. Together, these results provide novel mechanistic evidence that social disruption shapes behavior in a potentially adaptive way, possibly by reducing adult neurogenesis in the hippocampus.
To investigate cellular processes underlying adaptation to social instability, a dominance hierarchy of rats was formed and then destabilized. Regardless of social position, rats from disrupted hierarchies had fewer new neurons in the hippocampus compared with rats from control cages and those from stable hierarchies. Unexpectedly, these changes were accompanied by changes in social strategies without evidence of impairments in cognition or anxiety regulation. Restoring adult neurogenesis in disrupted rats using oxytocin and conditionally suppressing the production of new neurons in socially naive GFAP-thymidine kinase rats showed that loss of 6-week-old neurons may be responsible for adaptive changes in social behavior.
关于社会不稳定的研究主要聚焦于其有害后果，但大多数人具有恢复力，并通过运用各种应对策略做出反应。为了探究这些策略背后的细胞过程，构建了大鼠的优势等级制度，然后使其不稳定。无论社会地位如何，与来自对照笼的大鼠以及来自稳定等级制度的大鼠相比，等级制度被打乱的大鼠海马体中的新神经元较少。社会扰乱导致大鼠偏好熟悉的同种个体而非陌生的同种个体，这种变化并不涉及整体记忆损伤或焦虑增加。使用神经肽催产素作为工具来增加被打乱等级制度的大鼠海马体中的神经发生，可将对陌生同种个体的偏好恢复到扰乱前的水平。相反，在幼稚的转基因GFAP - 胸苷激酶大鼠中通过有限抑制成体神经发生来减少新神经元的数量，会导致其社会行为类似于等级制度被打乱的大鼠。总之，这些结果提供了新的机制证据，表明社会扰乱可能通过减少海马体中的成体神经发生，以一种潜在的适应性方式塑造行为。
为了探究适应社会不稳定背后的细胞过程，构建了大鼠的优势等级制度，然后使其不稳定。无论社会地位如何，与来自对照笼的大鼠以及来自稳定等级制度的大鼠相比，等级制度被打乱的大鼠海马体中的新神经元较少。出乎意料的是，这些变化伴随着社会策略的改变，而没有认知或焦虑调节受损的证据。使用催产素恢复被打乱等级制度的大鼠的成体神经发生，并在社会上幼稚的GFAP - 胸苷激酶大鼠中有条件地抑制新神经元的产生，结果表明6周龄神经元的丧失可能是社会行为适应性变化的原因。
