电压门控性Ca2+通道阻滞剂、ω-芋螺毒素AgaIVA和Ni2+可抑制豚鼠海马CA1神经元中θ波刺激诱导的长时程增强的诱导。
Voltage-gated Ca2+ channel blockers, omega-AgaIVA and Ni2+, suppress the induction of theta-burst induced long-term potentiation in guinea-pig hippocampal CA1 neurons.
作者信息
Ito K, Miura M, Furuse H, Zhixiong C, Kato H, Yasutomi D, Inoue T, Mikoshiba K, Kimura T, Sakakibara S
机构信息
Department of Physiology, Yamagata University School of Medicine, Japan.
出版信息
Neurosci Lett. 1995 Jan 2;183(1-2):112-5. doi: 10.1016/0304-3940(94)11127-5.
It is widely believed that a rise in post-synaptic calcium concentration ([Ca2+]i) is a necessary step in the induction of long-term potentiation (LTP) (Bliss and Collingridge, Nature, 361 (1993) 31-39). In this experiment, we examine the involvement of voltage-gated Ca2+ channels (VGCC) in the induction of AP5-sensitive LTP induced by theta-burst stimulation in guinea-pig hippocampal CA1 neurons. The VGCC blockers, Ni2+ (25 microM, T-channel blocker) or omega-AgaIVA (60 nM, P-channel blocker), which have no effect on synaptic transmission, suppress 60% or 78% of the theta-burst induced LTP, respectively. This implies that Ca2+ entry through VGCC is an important step in this form of LTP.
人们普遍认为，突触后钙浓度（[Ca2+]i）的升高是诱导长时程增强（LTP）的必要步骤（布利斯和科林格里奇，《自然》，361（1993年）31 - 39）。在本实验中，我们研究了电压门控钙通道（VGCC）在豚鼠海马CA1神经元中由θ波爆发刺激诱导的AP5敏感型LTP诱导过程中的作用。对突触传递无影响的VGCC阻滞剂Ni2+（25微摩尔，T型通道阻滞剂）或ω - AgaIVA（60纳摩尔，P型通道阻滞剂）分别抑制了60%或78%的θ波爆发诱导的LTP。这表明通过VGCC的Ca2+内流是这种形式的LTP的一个重要步骤。
Zotero 插件