γ-Aminobutyric acid (GABA) generally induces hyperpolarization and inhibition in the adult brain, but causes depolarization (and can be excitatory) in the immature brain. Depolarizing GABA actions are necessary for neurogenesis, differentiation, migration, and synaptogenesis. Additionally, the conversion of GABA responses from inhibition to excitation can be induced in adults by pathological conditions. Because GABAA receptors are Cl- channels, alternating GABA actions between hyperpolarization (Cl- influx) and depolarization (Cl- efflux) are induced by changes in the Cl- gradient, which is regulated by Cl- transporters. Thus, the dynamics of neural functions are modulated by active Cl- homeostasis (Cl- homeodynamics), alternating inhibition and excitation, and could underlie the modal shifts in cellular and network oscillations. Such a modal shift in GABA actions is required for normal development. Thus disturbances in this developmental GABA modal shift and/or the induction of excitatory GABA action could underlie the pathogenesis of diverse neurological diseases (so-called network diseases).

中文翻译：

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细胞和网络振荡模式变化的氯化物稳态

γ-氨基丁酸 (GABA) 通常在成人大脑中诱导超极化和抑制，但在未成熟大脑中会导致去极化（并且可以是兴奋性的）。去极化 GABA 作用是神经发生、分化、迁移和突触发生所必需的。此外，成人的病理条件可以诱导 GABA 反应从抑制到兴奋的转化。因为 GABAA 受体是 Cl- 通道，所以超极化（Cl-流入）和去极化（Cl-流出）之间的交替 GABA 作用是由 Cl- 梯度的变化引起的，Cl- 梯度由 Cl- 转运蛋白调节。因此，神经功能的动力学受到主动 Cl-稳态（Cl-稳态）、交替抑制和激发的调节，并且可能是细胞和网络振荡模式转变的基础。GABA 作用的这种模式转变是正常发育所必需的。因此，这种发育性 GABA 模式转变的干扰和/或兴奋性 GABA 作用的诱导可能是多种神经系统疾病（所谓的网络疾病）的发病机制的基础。