Rosen A S, Andrew R D
Department of Anatomy, Queen's University, Kingston, Ontario, Canada.
Neuroscience. 1990;38(3):579-90. doi: 10.1016/0306-4522(90)90052-6.
Acute osmotic disturbances can lead to profound neurological problems, yet there has been little experimentation at a cellular level to assess if neurophysiological changes are induced by altered osmolality. Using extra- and intracellular recording in the rat neocortical slice preparation, we examined pyramidal neurons of layers II-III under changing osmotic conditions. Single cell properties, field potentials, synaptic transmission and epileptiform discharges were studied in control saline (295 mOsm) and compared with corresponding data collected during exposure to osmolalities between 245 and 375 mOsm. Single cell properties (resting membrane potential, cell input resistance, action potential threshold and duration) did not change significantly, but neuronal interactions were considerably influenced by osmotic change within minutes. Hyposmolality increased the amplitude of evoked field potentials and of excitatory postsynaptic potentials recorded intracellularly. Hyperosmolality, induced with mannitol, decreased these parameters. Electrotonic coupling, as gauged by the degree of dye coupling and by cell input resistance, was not influenced by shifts in osmolality. The clinical finding that overhydration promotes seizure onset was examined in slices made epileptogenic in Mg2(+)-free saline. Hyposmolality increased the frequency and decreased the duration of interictal bursts, whereas raising osmolality with mannitol had opposite effects. None of the aforementioned effects occurred when osmolality was increased with a freely permeable substance such as dimethylsulfoxide, nor could they be ascribed to changes in saline Na+ or Ca2+ concentrations. The results are consistent with hyposmotic solutions reducing extracellular space by causing cells to swell. Theoretically, during population discharge, this should both concentrate K+ released extracellularly and possibly increase field (ephaptic) interactions. How lowered osmolality strengthens spontaneous and evoked excitatory synaptic transmission in neocortex is not yet clear. However, it may be an important mechanism underlying the increased seizure susceptibility of patients and experimental animals with lowered plasma osmolality. Conversely, suppression of excitatory postsynaptic potentials by osmotically active substances may be involved in the lowered seizure susceptibility observed clinically.
急性渗透紊乱可导致严重的神经问题，但在细胞水平上几乎没有实验来评估渗透压改变是否会引起神经生理变化。利用大鼠新皮质脑片制备中的细胞外和细胞内记录，我们在不断变化的渗透条件下检查了II-III层的锥体神经元。在对照生理盐水（295 mOsm）中研究了单细胞特性、场电位、突触传递和癫痫样放电，并与在渗透压为245至375 mOsm期间收集的相应数据进行了比较。单细胞特性（静息膜电位、细胞输入电阻、动作电位阈值和持续时间）没有显著变化，但神经元相互作用在数分钟内就受到渗透变化的显著影响。低渗增加了诱发场电位和细胞内记录的兴奋性突触后电位的幅度。用甘露醇诱导的高渗降低了这些参数。通过染料偶联程度和细胞输入电阻测量的电紧张耦合不受渗透压变化的影响。在无镁盐生理盐水中制成癫痫源的脑片中，研究了临床发现的水合过度促进癫痫发作的现象。低渗增加了发作间期爆发的频率并缩短了其持续时间，而用甘露醇提高渗透压则产生相反的效果。当用可自由通透的物质如二甲基亚砜增加渗透压时，上述效应均未出现，也不能将其归因于盐水中Na+或Ca2+浓度的变化。结果与低渗溶液通过使细胞肿胀来减少细胞外空间一致。从理论上讲，在群体放电期间，这既会使细胞外释放的K+浓度增加，也可能增加场（电突触）相互作用。低渗透压如何增强新皮质中的自发和诱发兴奋性突触传递尚不清楚。然而，这可能是血浆渗透压降低的患者和实验动物癫痫易感性增加的重要机制。相反，渗透活性物质对兴奋性突触后电位的抑制可能与临床上观察到的癫痫易感性降低有关。
