Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
Eur J Neurosci. 2019 Nov;50(10):3663-3673. doi: 10.1111/ejn.14512. Epub 2019 Aug 8.
Heightened neuronal plasticity expressed during early postnatal life has been thought to permanently decline once critical periods have ended. For example, monocular deprivation is able to shift ocular dominance in the mouse visual cortex during the first months of life, but this effect is lost later in life. However, various treatments, such as the antidepressant fluoxetine, can reactivate a critical period-like plasticity in the adult brain. When monocular deprivation is supplemented with chronic fluoxetine administration, a major shift in ocular dominance is produced after the critical period has ended. In the current study, we characterized the temporal patterns of fluoxetine-induced plasticity in the adult mouse visual cortex, using in vivo optical imaging. We found that artificially induced plasticity in ocular dominance extended beyond the duration of the naturally occurring critical period and continued as long as fluoxetine was administered. However, this fluoxetine-induced plasticity period ended as soon as the drug was not given. These features of antidepressant-induced plasticity may be useful when designing treatment strategies involving long-term antidepressant treatment in humans.
在生命早期表达的增强的神经元可塑性，一旦关键期结束，就被认为会永久下降。例如，在生命的头几个月，单眼剥夺能够改变小鼠视觉皮层的眼优势，但这种效应在生命后期会消失。然而，各种治疗方法，如抗抑郁药氟西汀，可以在成年大脑中重新激活类似关键期的可塑性。当单眼剥夺与慢性氟西汀给药相结合时，在关键期结束后会产生主要的眼优势转变。在目前的研究中，我们使用活体光学成像来描述成年小鼠视觉皮层中氟西汀诱导的可塑性的时间模式。我们发现，眼优势的人工诱导可塑性超出了自然发生的关键期的持续时间，并在给予氟西汀的情况下持续存在。然而，一旦停止使用药物，这种氟西汀诱导的可塑性就会结束。这些抗抑郁药诱导的可塑性的特征在设计涉及人类长期抗抑郁治疗的治疗策略时可能是有用的。
