Neuroplasticity and dysplasticity processes in schizophrenia.

Neuroplasticity and dysplasticity processes in schizophrenia.
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精神分裂症的神经可塑性和发育不良过程。

DOI:
10.1016/j.schres.2019.03.008
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发表时间:
2019
影响因子:
4.5
通讯作者:
Vinogradov,Sophia
Vinogradov,Sophia
中科院分区:
医学2区
文献类型:
--
作者:
Morishita,Hirofumi;Vinogradov,Sophia

文献摘要

相似文献

精神分裂症和其他精神病现在被认为是大脑神经回路功能的病理,其中神经元结构内生成并由神经振荡耦合支持的表征和计算过程被扭曲。神经振荡活动涵盖了广泛的生理过程,从具有毫秒周期的神经元间锥体神经元微电路,到柱状中观电路中数百毫秒的信息流,再到支持高阶认知和行动的数秒内的远程大脑宏电路相互作用(Mathalon 和 Sohal,2015)。虽然所有这些过程中的扭曲都在精神障碍中得到了充分研究,但不幸的是,常常存在一种(隐含地)概念化和研究这些不同的电路扭曲的倾向,就好像它们是静态的一样。然而,神经活动源于神经元胶质支架,并与之相互作用,其内在特性是可塑性——包括发育性和经验性。事实上,大脑回路通过依赖突触强度、膜电导、拓扑和结构体系的可塑性来表示、存储、更新和作用于信息(并执行计算)(Sejnowski 和 Paulsen,2006)。因此,正常可塑性操作的损伤——和/或试图适应其他潜在回路病理学的适应不良代偿可塑性过程——是精神分裂症和相关疾病研究的一个重要焦点。由此可见,对这些过程的更深入了解可能会带来疾病预防和治疗的新方法。我们很高兴在本期精神分裂症研究特刊中为您带来一系列数据驱动的观点,探讨这种可塑性和“发育不良”机制如何在精神障碍的表达和治疗中发挥作用。
Schizophrenia and other psychotic disorders are now understood to be pathologies of brain neural circuit function, in which representational and computational processes generated within neuronal architecture and supported by neural oscillatory coupling are distorted. Neural oscillatory activity spans a broad range of physiologic processes, extending from interneuron-pyramidal neuron microcircuits with their millisecond cycles, to flows of information over hundreds of milliseconds in columnar mesocircuits, to long-range brain macrocircuit interactions over seconds that support higher order cognitions and actions (Mathalon and Sohal, 2015). While distortions in all of these processes have been wellstudied in psychotic disorders, there is often an unfortunate tendency to (implicitly) conceptualize and study these various circuit distortions as if they were static. And yet, neural activity arises from, and interacts with, a neuronal-glial scaffold whose intrinsic property is plasticity–both developmental and experiential.Indeed, brain circuits represent, store, update, and act upon information (and execute computations) by relying on plasticity in their synaptic strength, membrane conductance, topology, and structural architecture (Sejnowski and Paulsen, 2006). It follows then, that impairments in normal plasticity operations–and/or maladaptive compensatory plasticity processes that attempt to adapt to other underlying circuit pathology–are an important focus of study in schizophrenia and related disorders. It also follows that a deeper understanding of these processes could lead to novel approaches for illness prevention and treatment. We are excited–in this Special Issue of Schizophrenia Research–to bring you a broad array of data-driven perspectives on how such plasticity and “dysplasticity” mechanisms could play a role in the expression and treatment of psychotic disorders.