Yu B, Shinnick-Gallagher P
Department of Pharmacology and Toxicology, University of Texas Medical Branch at Galveston 77555-1031, USA.
J Neurophysiol. 1997 Feb;77(2):690-701. doi: 10.1152/jn.1997.77.2.690.
The central amygdala (CeA) is an area involved in emotional learning and stress, and identification of Ca2+ currents is essential to understanding interneuronal communication through this nucleus. The purpose of this study was to separate and characterize dihydropyridine (DHP)- and neurotoxin-sensitive and -resistant components of the whole cell Ca2+ current (ICa) in acutely dissociated rat CeA neurons with the use of whole cell patch-clamp recording. Saturating concentrations of nimodipine (NIM, 5 microM), a DHP antagonist, blocked 22% of ICa: this NIM-sensitive (L-type) current was recorded in 68% of CeA neurons. The DHP agonist Bay K 8644 (5 microM) produced a 36% increase in ICa in a similar proportion of CeA neurons (70%). omega-Conotoxin GVIA (CgTx GVIA, 1 microM) in saturating concentrations inhibited 30% of ICa, whereas omega-agatoxin IVA (Aga IVA, 100 nM), in concentrations known to block P-type currents, did not affect ICa. Higher concentrations of Aga IVA (1 microM) alone reduced ICa by 34%, but in the presence of NIM (5 microM) and CgTx GVIA (1 microM) blocked only 18% of ICa. omega-Conotoxin MVIIC (CgTx MVIIC, 250 nM) reduced ICa by 13% in the presence of CgTx GVIA (1 microM). Application of NIM (5 mM), CgTx GVIA (1 microM); and Aga IVA (1 microM) blocked approximately 67% of ICa. A similar portion (63%) of Ca2+ current was blocked with CgTx MVIIC (250 nM) in the presence of NIM (5 microM) and CgTx GVIA (1 microM). The current resistant to NIM and the neurotoxins represented 37% of ICa, whereas in neurons not having L-type currents the resistant current made up approximately 53% of ICa (49 +/- 2%, mean +/- SE). The resistant current activated at around -40 mV and peaked at approximately 0 mV with half-activation and -inactivation potentials of -17 and -58 mV and slopes for activation and inactivation of -5 and 13 mV, respectively. The resistant current was sensitive to Cd2+ (IC50 = 2.5 microM) and Ni2+ (IC50 = 86 microM), was larger in Ca2+ than in Ba2+ (ratio = 1.31:1), and showed a moderate rate of decay. In summary, our results show that the high-voltage-activated calcium current in rat CeA neurons is composed of at least four pharmacologically distinct components: L-type current (NIM sensitive, 22%), N-type current (CgTx GVIA sensitive, 30%), Q-type current [Aga IVA (1 microM) and CgTx MVIIC sensitive, approximately 13-18%], and a resistant current (Non-L, -N, and -Q current, 33 approximately 37%), amounting to 37-53% of the total current. The resistant current has some electrophysiological and pharmacological characteristics in common with doe-1, alpha 1E, and R-type calcium currents, but remains unclassified.
中央杏仁核(CeA)是一个参与情绪学习和应激反应的脑区,确定Ca2+电流对于理解通过该核团的中间神经元通讯至关重要。本研究的目的是利用全细胞膜片钳记录技术,分离并鉴定急性分离的大鼠CeA神经元全细胞Ca2+电流(ICa)中对二氢吡啶(DHP)和神经毒素敏感及耐药的成分。DHP拮抗剂尼莫地平(NIM,5 microM)的饱和浓度可阻断22%的ICa:这种对NIM敏感(L型)的电流在68%的CeA神经元中被记录到。DHP激动剂Bay K 8644(5 microM)在相似比例(70%)的CeA神经元中使ICa增加了36%。饱和浓度的ω-芋螺毒素GVIA(CgTx GVIA,1 microM)可抑制30%的ICa,而ω-阿加毒素IVA(Aga IVA,100 nM)在已知可阻断P型电流的浓度下对ICa无影响。单独使用较高浓度的Aga IVA(1 microM)可使ICa降低34%,但在存在NIM(5 microM)和CgTx GVIA(1 microM)时仅阻断18%的ICa。在存在CgTx GVIA(1 microM)的情况下,ω-芋螺毒素MVIIC(CgTx MVIIC,250 nM)可使ICa降低13%。应用NIM(5 mM)、CgTx GVIA(1 microM)和Aga IVA(1 microM)可阻断约67%的ICa。在存在NIM(5 microM)和CgTx GVIA(1 microM)的情况下,用CgTx MVIIC(250 nM)可阻断相似比例(63%)的Ca2+电流。对NIM和神经毒素耐药的电流占ICa的37%,而在没有L型电流的神经元中,耐药电流约占ICa的53%(49±2%,平均值±标准误)。耐药电流在约-40 mV时激活,在约0 mV时达到峰值,半激活和半失活电位分别为-17和-58 mV,激活和失活斜率分别为-5和13 mV。耐药电流对Cd2+(IC50 = 2.5 microM)和Ni2+(IC50 = 86 microM)敏感,在Ca2+中比在Ba2+中更大(比率 = 1.31:1),并且显示出中等的衰减速率。总之,我们的结果表明,大鼠CeA神经元中的高压激活钙电流至少由四种药理学上不同的成分组成:L型电流(对NIM敏感,22%)、N型电流(对CgTx GVIA敏感,30%)、Q型电流[Aga IVA(1 microM)和CgTx MVIIC敏感,约13 - 18%]以及一种耐药电流(非L、非N和非Q电流,约33 - 37%),占总电流 的37 - 53%。耐药电流具有一些与doe-1、α1E和R型钙电流共同的电生理和药理学特征,但仍未分类。