Faber E S Louise, Sah Pankaj
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia.
J Neurosci. 2004 Mar 24;24(12):3031-9. doi: 10.1523/JNEUROSCI.4496-03.2004.
Pyramidal neurons in the lateral amygdala discharge trains of action potentials that show marked spike frequency adaptation, which is primarily mediated by activation of a slow calcium-activated potassium current. We show here that these neurons also express an alpha-dendrotoxin- and tityustoxin-Kalpha-sensitive voltage-dependent potassium current that plays a key role in the control of spike discharge frequency. This current is selectively targeted to the primary apical dendrite of these neurons. Activation of micro-opioid receptors by application of morphine or d-Ala(2)-N-Me-Phe(4)-Glycol(5)-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the alpha-dendrotoxin-sensitive potassium current. The effects of micro-opioid agonists on spike frequency adaptation were blocked by inhibiting G-proteins with N-ethylmaleimide (NEM) and by blocking phospholipase A(2). Application of arachidonic acid mimicked the actions of DAMGO or morphine. These results show that micro-opioid receptor activation enhances spike frequency adaptation in lateral amygdala neurons by modulating a voltage-dependent potassium channel containing Kv1.2 subunits, through activation of the phospholipase A(2)-arachidonic acid-lipoxygenases cascade.
外侧杏仁核中的锥体神经元发放动作电位序列，这些动作电位表现出明显的放电频率适应性，这主要由一种缓慢的钙激活钾电流的激活介导。我们在此表明，这些神经元还表达一种对α-树眼镜蛇毒素和美洲毒蜘蛛毒素-Kα敏感的电压依赖性钾电流，该电流在控制放电频率中起关键作用。这种电流选择性地靶向这些神经元的主要顶端树突。通过应用吗啡或D-Ala(2)-N-Me-Phe(4)-Glycol(5)-脑啡肽（DAMGO）激活微阿片受体，可通过增强对α-树眼镜蛇毒素敏感的钾电流来增强放电频率适应性。微阿片激动剂对放电频率适应性的影响可通过用N-乙基马来酰亚胺（NEM）抑制G蛋白和通过阻断磷脂酶A2来阻断。应用花生四烯酸可模拟DAMGO或吗啡的作用。这些结果表明，微阿片受体激活通过磷脂酶A2-花生四烯酸-脂氧合酶级联反应调节含有Kv1.2亚基的电压依赖性钾通道，从而增强外侧杏仁核神经元的放电频率适应性。
