Bargas J, Galarraga E, Aceves J
Department of Physiology, Biophysics and Neurosciences, Centro de Investigación del IPN, México, D.F.
Exp Brain Res. 1989;75(1):146-56. doi: 10.1007/BF00248538.
An in vitro slice preparation was used to obtain intracellular recordings of neostriatal neurons. Indirect evidence for the presence of an early outward conductance in neostriatal neurons is presented. With near threshold stimulation neostriatal neurons fired very late during the pulse. The long firing latency was associated with a slow (ramp-like) depolarization. In the presence of TTX the slow depolarization was lost and outward-going rectification dominated the subthreshold response. This finding demonstrated that both, outward- and inward-going conductances play a role during the ramp-like depolarization. Outward-going rectification during depolarizing responses could be further augmented if the depolarizing stimulus was preceded by a conditioning hyperpolarization. A conditioning hyperpolarization prolonged the firing latency and slowed the firing frequency. A conditioning depolarization had opposite effects. After TTX treatment, the response showed a hyperpolarizing "sag" when depolarizing stimulation was preceded by conditioning hyperpolarization. 4-AP (0.5-2.5 mM) blocked the effects of the conditioning hyperpolarization on the firing latency and on the voltage trajectory. 4-AP also disclosed a slow depolarization which could produce neuronal firing very early during the pulse. This depolarization was TTX-sensitive and Co++-insensitive. In contrast to 4-AP, TEA (20 mM) did not produce a reduction in the firing latency but disclosed a membrane oscillatory behavior most probably produced by the interplay of these opposing conductances: the slow inward (probably Na+) and the transient outward (probably K+). Repetitive firing during 4-AP treatment was of the "phasic-tonic" type with an initial burst riding on the initial Co++-insensitive slow depolarization and a somehow irregular train of spikes during the remainder of the stimulation. Action potentials during 4-AP treatment were followed by an afterdepolarization which dominated the initial part of the interspike interval.
采用体外脑片制备技术获取新纹状体神经元的细胞内记录。本文提供了新纹状体神经元存在早期外向电导的间接证据。在接近阈值刺激时，新纹状体神经元在脉冲期间放电非常晚。长放电潜伏期与缓慢（斜坡样）去极化相关。在存在河豚毒素（TTX）的情况下，缓慢去极化消失，外向整流主导阈下反应。这一发现表明，外向和内向电导在斜坡样去极化过程中均起作用。如果在去极化刺激之前先进行一个条件性超极化，去极化反应期间的外向整流可进一步增强。条件性超极化延长了放电潜伏期并减慢了放电频率。条件性去极化则产生相反的效果。在TTX处理后，当去极化刺激之前先进行条件性超极化时，反应表现出一个超极化“凹陷”。4-氨基吡啶（4-AP，0.5 - 2.5 mM）阻断了条件性超极化对放电潜伏期和电压轨迹的影响。4-AP还揭示了一种缓慢去极化，其可在脉冲早期产生神经元放电。这种去极化对TTX敏感而对Co++不敏感。与4-AP不同，四乙铵（TEA，20 mM）并未使放电潜伏期缩短，但揭示了一种膜振荡行为，这很可能是由这些相反电导（缓慢内向电导，可能是Na+；瞬时外向电导，可能是K+）的相互作用产生的。4-AP处理期间的重复放电为“相位-紧张性”类型，初始爆发叠加在最初对Co++不敏感的缓慢去极化上，在刺激的其余部分有一些不规则的尖峰序列。4-AP处理期间的动作电位之后是一个后去极化，其在峰电位间隔的初始部分占主导。
