Yun A Joon, Bazar Kimberly A, Lee Patrick Y
Stanford University, 470 University Avenue, Palo Alto, CA 94301, USA.
Med Hypotheses. 2004;63(6):939-50. doi: 10.1016/j.mehy.2004.07.027.
Cognitive plasticity, a developmental trait that promotes acquisition of complex skills such as language or playing musical instruments, diminishes substantially during puberty. The loss of plasticity has been attributed to surge of sex steroids during adolescence, but the phenomenon remains poorly understood. We hypothesize that pineal involution during puberty may contribute to plasticity decay. The pineal gland produces melatonin, the level of which declines dramatically during onset of puberty. Emerging evidence suggest that melatonin may modulate cognitive plasticity, independent of the effects of sex steroids, and low sex steroids and high melatonin may be simultaneously required to maintain cognitive plasticity. Potential mechanisms by which melatonin may modulate plasticity are examined within the sleep and hippocampal long-term potentiation frameworks. Implications for psychiatric conditions that involve sleep disorders and learning dysfunctions such as schizophrenia and autism are discussed, and the potential adaptive roles of postprandial and postcoital sleep are explored. From the Darwinian perspective, development and reproductive maturity may represent distinct phases that require tailored cognitive strategies to maximize fitness. While cognitive flexibility and susceptibility to new skills may be paramount during development, reduced cognitive flexibility and increased cognitive determinism may enable more efficient responses to stimuli during adulthood. Thus, cognitive plasticity and cognitive determinism may represent trade-off adaptations and different dimensions of intelligence. The decline of plasticity and emergence of puberty during the second decade may be relics of prehistoric times when the human lifespan was short and the environment was relatively simple and static. Today, when the environment is more complex and dynamic, and humans are living far longer, the early obsolescence of plasticity during puberty may represent a Darwinian inefficiency exposed by evolutionary displacement. Regulation of plasticity may be a systemic phenomenon, as exemplified by the association of learning disability with allergic conditions, a form of immune plasticity dysfunction. Ramifications for other plastic functions that decline during puberty such as wound healing and hyaline cartilage regeneration are explored. Like the plasticity of immunity and cognition, the plasticity of hyaline cartilage during youth may enable hosts to respond to ecologic opportunities and generate the optimally adapted adult phenotype. Pineal involution may represent a potential target for therapeutic extension or restoration of plasticity after puberty. Extending plasticity may have far-reaching consequences for human evolution.
认知可塑性是一种促进语言或演奏乐器等复杂技能习得的发育特性,在青春期会大幅下降。可塑性的丧失被归因于青春期性激素的激增,但这一现象仍未得到充分理解。我们假设青春期的松果体退化可能导致可塑性衰退。松果体分泌褪黑素,在青春期开始时其水平会急剧下降。新出现的证据表明,褪黑素可能独立于性激素的作用来调节认知可塑性,并且可能需要低水平的性激素和高水平的褪黑素同时存在来维持认知可塑性。在睡眠和海马体长期增强的框架内研究了褪黑素调节可塑性的潜在机制。讨论了其对涉及睡眠障碍和学习功能障碍的精神疾病(如精神分裂症和自闭症)的影响,并探讨了餐后和性交后睡眠的潜在适应性作用。从达尔文主义的角度来看,发育和生殖成熟可能代表不同的阶段,需要量身定制的认知策略以实现适应性最大化。虽然在发育过程中认知灵活性和对新技能的敏感性可能至关重要,但在成年期,认知灵活性降低和认知确定性增加可能使个体能够更有效地应对刺激。因此,认知可塑性和认知确定性可能代表权衡性适应以及智力的不同维度。在人类寿命较短且环境相对简单和静态的史前时代,可塑性的下降和青春期的出现可能是遗留现象。如今,当环境更加复杂和动态,且人类寿命长得多时,青春期可塑性的过早衰退可能代表了进化位移所暴露的达尔文式低效。可塑性的调节可能是一种系统性现象,例如学习障碍与过敏状况(一种免疫可塑性功能障碍形式)之间的关联就证明了这一点。探讨了其对青春期其他下降的可塑性功能(如伤口愈合和透明软骨再生)的影响。与免疫和认知的可塑性一样,年轻时透明软骨的可塑性可能使个体能够应对生态机遇并产生最佳适应的成年表型。松果体退化可能是青春期后治疗性延长或恢复可塑性的潜在靶点。延长可塑性可能对人类进化产生深远影响。