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GABA is resitent to the toxicity of the excitory amino acids because it can promote the conduct of Cl-, prevent the depolarization of the postsynaptic inhibition effectively and the open of Ca2+-gated channel, reduce the metabolic rate of the ischemic nurons.

GABA可以拮抗兴奋性氨基酸的毒性作用,它主要通过促进氯离子的传导,有效的阻断突触后去极化及电压依赖性Ca2+通道的开放,降低正常灌注/缺血性神经元的代谢率和氧的消耗,从而使神经元易耐受缺血性损伤[9]。

SP can make a myenteric cholinergic neuron depolarization, i. e. SP has an important role of regulating intestinal motility.

SP可以使ChAc-IR神经元去极化,即在胃肠动力的调控中具有重要作用。

Results Sodium azide (25-100 mmol/L, after 4 h of incubation) depolarized the membrane potential and increased the Aβ production, but it showed no effect on the expression of APP.

结果叠氮钠在浓度25~100 mmol/L时,与细胞共孵育4 h,可使细胞膜电位去极化程度明显增高,并引起胞内Aβ表达显著增高,但对胞内APP表达水平影响不明显。

In the course of capacitation, the membrane potential might be depolarized resulting from K〓 or Na〓 influx.

获得精子由于阳离子内流和膜电位的去极化,Ca〓通道开放,此时Ca〓通道阻断剂使通道关闭。

Results Leptin depolarized the most neurons of the three model animal groups and hyperpolarized the minor neurons, but there had no significant difference among the three groups.

结果 瘦素使三组动物大部分神经元去极化,各组间比较差异无显著性。

These results suggest that in the central nervous system of small mammals, AP waveforms mature rapidly in many types of neurons, thus, coordinated activities in neuronal circuits may occur. In early postnatal development, GABA receptor mainly mediates an excitation effect, depolarizes P6 MGBv neurons and dramatically increases the frequency of AP firing. Inhibition of GABA receptor matures slowly along with increment of postnatal days.

结论大鼠MGBv神经元的AP波形成熟较快,可在中枢神经系统的神经元环路中产生协调性的活动;在MGBv神经元发育早期,GABA主要作为兴奋性神经递质而发挥作用,它可使P6的MGBv神经元产生去极化,AP发放频率显著增加,随着出生后日龄的增加,GABA受体的抑制作用才逐渐发育成熟。

Hypoxia inhibits a variety of K+ channels in the type Ⅰ cells of the carotid body, in a seemingly species-dependent manner, and the resultant membrane depolarisation is sufficient to activate voltage-gated Ca2+ entry leading to neurosecretion and afferent discharge.

低氧可抑制颈动脉体Ⅰ型细胞中的多种K+通道,这种作用可能有种属差异;K+通道的抑制使膜电位去极化,启动电压依赖性Ca2+内流,最后导致神经分泌和传入放电。

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