Modulation of endogenous firing patterns by osmolarity in rat hippocampal neurones
Modulation of endogenous firing patterns by osmolarity in rat hippocampal neurones
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DOI：
10.1111/j.1469-7793.1997.175bl.x
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发表时间：
1997-07-01
影响因子：
5.5
通讯作者：
Yaari, Y
中科院分区：
文献类型：
--
作者：
Azouz, R;Alroy, G;Yaari, Y
1.用成年大鼠海马脑片的细胞内记录来研究细胞外渗透压（pi（o））的适度变化（+/-13%）对内源性神经元放电模式的调制。CA 1锥体细胞对分级去极化电流脉冲的反应被用来区分规则和爆发放电模式，并表征诱发内源性爆发放电的刺激要求.降低或增加pi（o）对静息膜电位和输入电阻、峰电位阈值和峰电位幅度以及快、中、慢峰电位后超极化（AHPs）的幅度均无显著影响。表观膜时间常数（tau（m））在低pi（o）时增加，在高pi（o）时减小.降低pi（o）将非爆发神经元（非爆发神经元）转化为爆发神经元（爆发神经元），并降低了在本地爆发神经元中唤起爆发放电的刺激要求。增加pi（o）抑制内源性爆发放电。降低pi（o）增加了尖峰后去极化（ADP）的“活性”（即再去极化）分量的大小。相反，增加pi（o）抑制活性ADP成分。锥体细胞的峰电位和放电模式对pi（o）变化的敏感性在无Ca 2+的盐水中也持续存在，表明渗透效应不是通过调节Ca 2+和/或Ca 2+激活的K+电流来赋予的。阻断大多数K+电流与Ca 2+的，TEA含有盐水诱导大的和长期的（长达1秒），TTX敏感的平台电位后的首要快速尖峰。这些电位被低pi（o）增强，并被高pi（o）减弱。当在无钙盐水中注入阈下去极化电流脉冲时，锥体细胞显示出明显的TTX敏感性内向整流。这种校正通过低pi（o）来增强，并通过高pi（o）来减少。低pi（o）和高pi（o）盐水溶液的各种影响在用渗压正常的盐水洗涤后是可逆的。我们的结论是，pi（o）是一个关键的决定因素的内源性放电模式的CA 1锥体细胞。这些数据表明，渗透效应是最有可能介导的持续Na+电流，这是积极的穗ADP和爆发电位在CA 1锥体神经元的变化。这些影响的可能贡献在各种异常的渗透状态的大脑兴奋性的变化进行了讨论。
1. Intracellular recordings in adult rat hippocampal slices were used to investigate the modulation of endogenous neuronal firing patterns by moderate changes (+/-13%) in the extracellular osmotic pressure (pi(o)). The responses of CA1 pyramidal cells to graded depolarizing current pulses were used to differentiate between regular and burst-firing patterns and to characterize the stimulus requirements for evoking endogenous burst discharge.2. Decreasing or increasing pi(o) had no significant effects on resting membrane potential and input resistance, spike threshold and amplitude, and the amplitudes of the fast, medium and slow spike after-hyperpolarizations (AHPs). The apparent membrane time constant (tau(m)) increased in low pi(o) and decreased in high pi(o).3. Reducing pi(o) converted non-bursting neurones (non-bursters) to bursting neurones (bursters) and decreased the stimulus requirements for evoking burst firing in native bursters. Increasing pi(o) suppressed endogenous burst firing.4. Lowering pi(o) increased the size of the 'active' (i.e. re-depolarizing) component of the spike after-depolarization (ADP). Conversely, increasing pi(o) suppressed the active ADP component.5. The sensitivity of spike ADPs and firing patterns of pyramidal cells to the changes in pi(o) persisted also in Ca2+-free saline, indicating that the osmotic effects are not imparted by modulation of Ca2+ and/or Ca2+-activated K+ currents.6. Blocking most K+ currents with Ca2+-free, TEA-containing saline induced large and prolonged (up to 1 s), TTX-sensitive plateau potentials following the primacy fast spikes. These potentials were augmented by low pi(o) and abated by high pi(o).7. When injected with subthreshold depolarizing current pulses in Ca2+-free saline, pyramidal cells displayed a distinct TTX-sensitive inward rectification. This rectification was augmented by low pi(o) and reduced by high pi(o).8. The various effects of low-pi(o) and high-pi(o) saline solutions were reversible upon washing with normosmotic saline.9. We conclude that pi(o) is a critical determinant of the endogenous firing patterns of CA1 pyramidal cells. The data suggest that the osmotic effects are most likely to be mediated by changes in the persistent Na+ current, which underlies the active spike ADP and the burst potential in CA1 pyramidal neurones. The possible contribution of these effects to changes in brain excitability in various abnormal osmotic states is discussed.