Department of Neurobiology and Behavior, Cornell University, W 159 Seeley G. Mudd Hall, Ithaca, NY 14853, USA.
J Neurophysiol. 2011 Sep;106(3):1288-98. doi: 10.1152/jn.00456.2011. Epub 2011 Jun 15.
Endogenously bursting neurons play central roles in many aspects of nervous system function, ranging from motor control to perception. The properties and bursting patterns generated by these neurons are subject to neuromodulation, which can alter cycle frequency and amplitude by modifying the properties of the neuron's ionic currents. In the stomatogastric ganglion (STG) of the spiny lobster, Panulirus interruptus, the anterior burster (AB) neuron is a conditional oscillator in the presence of dopamine (DA) and other neuromodulators and serves as the pacemaker to drive rhythmic output from the pyloric network. We analyzed the mechanisms by which DA evokes bursting in the AB neuron. Previous work showed that DA-evoked bursting is critically dependent on external calcium (Harris-Warrick RM, Flamm RE. J Neurosci 7: 2113-2128, 1987). Using two-photon microscopy and calcium imaging, we show that DA evokes the release of calcium from intracellular stores well before the emergence of voltage oscillations. When this release from intracellular stores is blocked by antagonists of ryanodine or inositol trisphosphate (IP(3)) receptor channels, DA fails to evoke AB bursting. We further demonstrate that DA enhances the calcium-activated inward current, I(CAN), despite the fact that it significantly reduces voltage-activated calcium currents. This suggests that DA-induced release of calcium from intracellular stores activates I(CAN), which provides a depolarizing ramp current that underlies endogenous bursting in the AB neuron.
内源性爆发神经元在神经系统功能的许多方面发挥着核心作用，从运动控制到感知。这些神经元产生的特性和爆发模式受到神经调制的影响，通过改变神经元离子电流的特性，可以改变周期频率和幅度。在刺龙虾的口胃神经节（STG）中，前爆发神经元（AB）是多巴胺（DA）和其他神经调质存在时的条件振荡器，作为起搏细胞驱动从幽门网络产生节律性输出。我们分析了 DA 引发 AB 神经元爆发的机制。先前的工作表明，DA 引发的爆发严重依赖于细胞外钙（Harris-Warrick RM，Flamm RE。J Neurosci 7: 2113-2128，1987）。使用双光子显微镜和钙成像，我们显示 DA 在电压振荡出现之前很久就从细胞内储存中引发钙释放。当这种细胞内储存的释放被ryanodine 或三磷酸肌醇（IP（3））受体通道的拮抗剂阻断时，DA 无法引发 AB 爆发。我们进一步证明，DA 增强了钙激活内向电流 I（CAN），尽管它显著降低了电压激活钙电流。这表明 DA 诱导的细胞内储存钙释放激活 I（CAN），它提供了一个去极化斜坡电流，这是 AB 神经元内源性爆发的基础。
