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首页> 外文期刊>Progress in brain research >Glial diffusion barriers during aging and pathological states.
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Glial diffusion barriers during aging and pathological states.

机译：在衰老和病理状态期间的神经胶质扩散障碍。

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In conclusion, glial cells control not only ECS ionic composition, but also ECS size and geometry. Since ECS ionic and volume changes have been shown to play an important role in modulating the complex synaptic and extrasynaptic signal transmission in the CNS, glial cells may thus affect neuronal interaction, synchronization and neuron-glia communication. As shown in Fig. 2, a link between ionic and volume changes and signal transmission has been proposed as a model for the non-specific feedback mechanism suppressing neuronal activity (Sykova, 1997; Ransom, 2000). First, neuronal activity results in the accumulation of [K+]e, which in turn depolarizes glial cells, and this depolarization induces an alkaline shift in glial pHi. Second, the glial cells extrude acid and the resulting acid shift causes a decrease in the neuronal excitability. Because ionic transmembrane shifts are always accompanied by water, this feedback mechanism is amplified by activity-related glial swelling compensated for by ECS volume shrinkage and by increased tortuosity, presumably by the crowding of molecules of the ECS matrix and/or by the swelling of fine glial processes. This, in turn, results in a larger accumulation of ions and other neuroactive substances in the brain due to increased diffusion hinderance in the ECS. Astrocyte hypertrophy, proliferation and swelling influence the size of the ECS volume and tortuosity around neurons, slowing diffusion in the ECS. Their organization may also affect diffusion anisotropy, which could be an underlying mechanism for the specificity of extrasynaptic transmission, including 'cross-talk' between distinct synapses (Barbour and Hausser, 1997; Kullmann and Asztely, 1998). An increased concentration of transmitter released into a synapse (e.g. repetitive adequate stimuli or during high frequency electrical stimulation which induces LTP) results in a significant activation of high-affinity receptors at neighboring synapses. The efficacy of such synaptic cross-talk would be dependent on the extracellular space surrounding the synapses, i.e. on intersynaptic geometry and diffusion parameters. Other recent studies have also suggested an important role for proteoglycans, known to participate in multiple cellular processes, such as axonal outgrowth, axonal branching and synaptogenesis (Hardington and Fosang, 1992; Margolis and Margolis, 1993) that are important for the formation of memory traces. Recent observation of a decrease of fibronectin and chondroitin sulfate proteoglycan staining in the hippocampus of behaviorally impaired aged rats (Sykova et al., 1998a,b) supports this hypothesis. It is reasonable to assume that besides neuronal and glial processes, macromolecules of the extracellular matrix contribute to diffusion barriers in the ECS. It is therefore apparent that glial cells play an important role in the local architecture of the CNS and they may also be involved in the modulation of signal transmission, in plastic changes, LTP, LTD and in changes of behavior and memory formation.
机译：总之，神经胶质细胞不仅控制ECS离子组成，而且还控制ECS大小和几何形状。由于已显示ECS离子和体积变化在调节CNS中复杂的突触和突触外信号传递中起重要作用，因此神经胶质细胞可能会影响神经元的相互作用，同步和神经胶质细胞的通讯。如图2所示，已提出离子和体积变化与信号传输之间的联系，作为抑制神经元活动的非特异性反馈机制的模型（Sykova，1997; Ransom，2000）。首先，神经元活动导致[K +] e积累，进而使神经胶质细胞去极化，而这种去极化诱导神经胶质pHi发生碱性转变。第二，神经胶质细胞挤出酸，产生的酸转移导致神经元兴奋性降低。由于离子跨膜移动总是伴随着水，因此该反馈机制通过与活动相关的神经胶质肿胀得到了增强，该肿胀被ECS体积收缩和曲折性所补偿，大概是由于ECS基质分子的拥挤和/或细小颗粒的肿胀。神经胶质过程。反过来，由于ECS中扩散障碍的增加，导致大脑中离子和其他神经活性物质的积累量增加。星形胶质细胞肥大，增殖和肿胀影响ECS体积的大小和神经元周围的曲折，减慢ECS中的扩散。它们的组织也可能影响扩散各向异性，这可能是突触外传递特异性的潜在机制，包括不同突触之间的“串扰”（Barbour和Hausser，1997; Kullmann和Asztely，1998）。释放到突触中的递质浓度增加（例如重复的充分刺激或在诱导LTP的高频电刺激过程中）导致相邻突触处的高亲和力受体显着活化。这种突触串扰的功效将取决于突触周围的细胞外空间，即取决于突触间的几何形状和扩散参数。最近的其他研究也表明蛋白聚糖具有重要作用，蛋白聚糖已知参与多种细胞过程，如轴突生长，轴突分支和突触形成（Hardington和Fosang，1992; Margolis和Margolis，1993），这对记忆的形成很重要。痕迹。最近观察到行为受损的老年大鼠海马中纤连蛋白和硫酸软骨素蛋白聚糖的染色减少（Sykova等，1998a，b），支持了这一假说。可以合理地假设，除了神经元和神经胶质过程外，细胞外基质的大分子还有助于ECS中的扩散障碍。因此，很明显神经胶质细胞在中枢神经系统的局部结构中起着重要的作用，它们也可能参与信号传输的调制，塑性变化，LTP，LTD以及行为和记忆形成的变化。

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