Kröner Sven, Rosenkranz J Amiel, Grace Anthony A, Barrionuevo German
Center for Neural Basics Cognition, Deptartment of Neuroscience, University of Pittsburgh, Pittsburgh, Penssylvania.
J Neurophysiol. 2005 Mar;93(3):1598-610. doi: 10.1152/jn.00843.2004. Epub 2004 Nov 10.
The amygdala plays a role in affective behaviors, which are modulated by the dopamine (DA) innervation of the basolateral amygdala complex (BLA). Although in vivo studies indicate that activation of DA receptors alters BLA neuronal activity, it is unclear whether DA exerts direct effects on BLA neurons or whether it acts via indirect effects on BLA afferents. Using whole cell patch-clamp recordings in rat brain slices, we investigated the site and mechanisms through which DA regulates the excitability of BLA neurons. Dopamine enhanced the excitability of BLA projection neurons in response to somatic current injections via a postsynaptic effect. Dopamine D1 receptor activation increased excitability and evoked firing, whereas D2 receptor activation increased input resistance. Current- and voltage-clamp experiments in projection neurons showed that D1 receptor activation enhanced excitability by modulating a 4-aminopyridine- and alpha-dendrotoxin-sensitive, slowly inactivating K+ current. Furthermore, DA and D1 receptor activation increased evoked firing in fast-spiking BLA interneurons. Consistent with a postsynaptic modulation of interneuron excitability, DA also increased the frequency of spontaneous inhibitory postsynaptic currents recorded in projection neurons without changing release of GABA. These data demonstrate that DA exerts direct effects on BLA projection neurons and indirect actions via modulation of interneurons that may work in concert to enhance the neuronal response to large, suprathreshold inputs, while suppressing weaker inputs.
杏仁核在情感行为中发挥作用，而情感行为受基底外侧杏仁核复合体（BLA）的多巴胺（DA）神经支配调节。尽管体内研究表明DA受体的激活会改变BLA神经元的活动，但尚不清楚DA是直接作用于BLA神经元，还是通过对BLA传入神经的间接作用发挥作用。我们使用大鼠脑片的全细胞膜片钳记录，研究了DA调节BLA神经元兴奋性的位点和机制。多巴胺通过突触后效应增强了BLA投射神经元对体细胞电流注入的兴奋性。多巴胺D1受体激活增加了兴奋性并诱发放电，而D2受体激活增加了输入电阻。对投射神经元进行的电流钳和电压钳实验表明，D1受体激活通过调节一种对4-氨基吡啶和α-银环蛇毒素敏感、缓慢失活的钾电流来增强兴奋性。此外，DA和D1受体激活增加了快速发放的BLA中间神经元的诱发放电。与中间神经元兴奋性的突触后调制一致，DA还增加了投射神经元中记录到的自发性抑制性突触后电流的频率，而不改变GABA的释放。这些数据表明，DA对BLA投射神经元有直接作用，并通过对中间神经元的调制产生间接作用，这可能共同作用以增强神经元对大的、阈上输入的反应，同时抑制较弱的输入。
