ALPHA-BUNGAROTOXIN-SENSITIVE HIPPOCAMPAL NICOTINIC RECEPTOR-CHANNEL HAS A HIGH-CALCIUM PERMEABILITY

ALPHA-BUNGAROTOXIN-SENSITIVE HIPPOCAMPAL NICOTINIC RECEPTOR-CHANNEL HAS A HIGH-CALCIUM PERMEABILITY
复制标题

DOI:
10.1016/s0006-3495(95)80213-4
复制
发表时间:
1995-02-01
影响因子:
3.4
通讯作者:
ALBUQUERQUE, EX
ALBUQUERQUE, EX
中科院分区:
生物学3区
文献类型:
--
作者:
CASTRO, NG;ALBUQUERQUE, EX

文献摘要

被引文献

相似文献

海马烟碱乙酰胆碱受体 (nAChR) 是一种新发现的配体门控离子通道,可被蛇毒素 α-银环蛇毒素 (α-BGT) 阻断,并且其结构中可能含有 α7 nAChR 亚基。这里对其离子选择性进行了表征,并与 N-甲基-D-天冬氨酸 (NMDA) 受体通道的离子选择性进行了比较。在各种离子条件下测定乙酰胆碱和 NMDA 激活的全细胞电流的反转电位 (V-R)。使用离子活度和存在 Ca2+ 时 V-R 位移的 Goldman-Hodgkin-Katz 方程,计算渗透率比。对于 α-BGT 敏感的 nAChR,P-Na/P-Cs 接近 1,Cl- 对电流没有贡献。将 [Ca2+](0) 从 1 mM 更改为 10 mM,nAChR 和 NMDA 电流的 V(R) 分别移动 +5.6 +/- 0.4 和 +8.3 +/- 0.4 mV,并且 nAChR 电流衰减加速。这些变化使得 nAChR 通道的 P-Ca/P(Cs) 为 6.1 +/- 0.5,NMDA 通道的 P-Ca/P(Cs) 为 10.3 +/- 0.7。因此,神经元 α-BGT 敏感的 nAChR 是一种对 Ca2+ 有相当选择性的阳离子通道,并且可能介导细胞内 Ca2+ 的快速升高,其幅度会随着膜超极化而增加。
The hippocampal nicotinic acetylcholine receptor (nAChR) is a newly identified ligand-gated ion channel that is blocked by the snake toxin alpha-bungarotoxin (alpha-BGT) and that probably contains the alpha 7 nAChR subunit in its structure. Here its ion selectivity was characterized and compared with that of the N-methyl-D-aspartate (NMDA) receptor channel. The reversal potentials (V-R) of acetylcholine- and NMDA-activated whole-cell currents were determined under various ionic conditions. Using ion activities and a Goldman-Hodgkin-Katz equation for V-R shifts in the presence of Ca2+, permeability ratios were calculated. For the alpha-BGT-sensitive nAChR, P-Na/P-Cs was close to 1 and Cl- did not contribute to the currents. Changing the [Ca2+](0), from 1 to 10 mM, the V(R)s of the nAChR and NMDA currents were shifted by +5.6 +/- 0.4 and +8.3 +/- 0.4 mV, respectively, and the nAChR current decay was accelerated. These shifts yielded P-Ca/P(Cs)s of 6.1 +/- 0.5 for the nAChR channel and 10.3 +/- 0.7 for the NMDA channel. Thus, the neuronal alpha-BGT-sensitive nAChR is a cation channel considerably selective to Ca2+ and may mediate a fast rise in intracellular Ca2+ that would increase in magnitude with membrane hyperpolarization.