Piekarski David J, Johnson Carolyn M, Boivin Josiah R, Thomas A Wren, Lin Wan Chen, Delevich Kristen, M Galarce Ezequiel, Wilbrecht Linda
Department of Psychology, University of California, Berkeley, Berkeley CA 94720, USA.
Neuroscience Graduate Program, University of California, San Francisco, San Francisco CA 94158, USA.
Brain Res. 2017 Jan 1;1654(Pt B):123-144. doi: 10.1016/j.brainres.2016.08.042. Epub 2016 Aug 31.
Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental inputs and reorganization of cortical circuits that matches behavior with environmental contingencies. Significant headway has been achieved in characterizing and understanding sensitive period biology in primary sensory cortices, but relatively little is known about sensitive period biology in associative neocortex. One possible mediator is the onset of puberty, which marks the transition to adolescence, when animals shift their behavior toward gaining independence and exploring their social world. Puberty onset correlates with reduced behavioral plasticity in some domains and enhanced plasticity in others, and therefore may drive the transition from juvenile to adolescent brain function. Pubertal onset is also occurring earlier in developed nations, particularly in unserved populations, and earlier puberty is associated with vulnerability for substance use, depression and anxiety. In the present article we review the evidence that supports a causal role for puberty in developmental changes in the function and neurobiology of the associative neocortex. We also propose a model for how pubertal hormones may regulate sensitive period plasticity in associative neocortex. We conclude that the evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required. We argue that further work of this kind is urgently needed to determine how earlier puberty may negatively impact human health and learning potential. This article is part of a Special Issue entitled SI: Adolescent plasticity.
出生后脑发育过程中存在多个敏感期,在此期间依赖经验的可塑性增强。这使得大脑能够快速从环境输入中学习,并重组皮层回路,使行为与环境偶发事件相匹配。在表征和理解初级感觉皮层的敏感期生物学方面已经取得了重大进展,但对于联合新皮层的敏感期生物学却知之甚少。一种可能的调节因素是青春期的开始,它标志着向青春期的过渡,此时动物的行为转向寻求独立并探索其社会环境。青春期开始与某些领域行为可塑性的降低以及其他领域可塑性的增强相关,因此可能推动从幼年到青少年脑功能的转变。在发达国家,尤其是在未得到充分服务的人群中,青春期开始也出现得更早,而青春期提前与物质使用、抑郁和焦虑的易感性有关。在本文中,我们综述了支持青春期在联合新皮层功能和神经生物学发育变化中起因果作用的证据。我们还提出了一个模型,说明青春期激素可能如何调节联合新皮层的敏感期可塑性。我们得出结论,现有证据表明青春期开始可能在联合新皮层发育的某些方面起因果作用,但需要进一步开展操纵青春期并测量性腺激素的研究。我们认为迫切需要开展这类进一步的研究,以确定青春期提前可能如何对人类健康和学习潜力产生负面影响。本文是名为“SI:青少年可塑性”的特刊的一部分。