Dopamine modulates two potassium currents and inhibits the intrinsic firing properties of an identified motor neuron in a central pattern generator network
Dopamine modulates two potassium currents and inhibits the intrinsic firing properties of an identified motor neuron in a central pattern generator network
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DOI：
10.1152/jn.1999.81.1.29
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发表时间：
1999-01-01
影响因子：
2.5
通讯作者：
Harris-Warrick, RM
中科院分区：
文献类型：
--
作者：
Kloppenburg, P;Levini, RM;Harris-Warrick, RM
两个幽门扩张器(PD)神经元是断刺龙虾(Panulirus Interruptus)口胃神经节幽门网络起搏群的组成部分[与前爆发神经元一起]。多巴胺(DA)改变幽门网络产生的运动模式，部分是通过兴奋或抑制不同的神经元。DA通过使PD神经元超极化和降低其放电动作电位的速率来抑制PD神经元，从而导致PD相对于电耦合AB的相位延迟和幽门循环频率的降低。在突触分离的PD神经元中，DA减慢了超极化后恢复为峰的速度。从超极化前一步到第一动作电位的潜伏期增加，动作电位频率和动作电位总数减少。当对突触隔离的电压钳制PD神经元施加短暂的DA喷雾(1 S)时，诱发出一个小的电压依赖性外向电流，并伴随着膜电导的增加。这些反应被钾通道阻滞剂4-氨基吡啶和四乙基铵联合存在所阻断。在电压钳制的PD神经元中，DA增强了电压敏感的瞬时钾电流(I-A)的最大电导，并使其V-动作向更负的电位移动，而不影响其V-动作。这扩大了电压激活和失活曲线之间的“窗口电流”，增加了静息电位附近的音调活性I-A，并导致细胞超极化。因此，DA的作用是通过调制相同的通道来增强瞬时K+电流和静止K+电流。此外，DA可增强钙依赖性钾电流(I-O(Ca))的幅度，但对持续性钾电流(I-K(V))无影响。这些结果表明，DA至少部分地通过调节PD神经元固有的抑制后恢复特性而超极化和延迟PD神经元的活动。这种调节似乎部分是通过增加I-A和I-O(Ca)来实现的。在幽门网络中，I-A似乎是DA作用的共同靶点，但在不同的神经元中，DA可以以不同的方式增强或降低它。
The two pyloric dilator (PD) neurons are components [along with the anterior burster (AB) neuron] of the pacemaker group of the pyloric network in the stomatogastric ganglion of the spiny lobster Panulirus interruptus. Dopamine (DA) modifies the motor pattern generated by the pyloric network, in part by exciting or inhibiting different neurons. DA inhibits the PD neuron by hyperpolarizing it and reducing its rate of firing action potentials, which leads to a phase delay of PD relative to the electrically coupled AB and a reduction in the pyloric cycle frequency. In synaptically isolated PD neurons, DA slows the rate of recovery to spike after hyperpolarization. The latency from a hyperpolarizing prestep to the first action potential is increased, and the action potential frequency as well as the total number of action potentials are decreased. When a brief (1 s) puff of DA is applied to a synaptically isolated, voltage-clamped PD neuron, a small voltage-dependent outward current is evoked, accompanied by an increase in membrane conductance. These responses are occluded by the combined presence of the potassium channel blockers 4-aminopyridine and tetraethylammonium. In voltage-clamped PD neurons, DA enhances the maximal conductance of a voltage-sensitive transient potassium current (I-A) and shifts its V-act to more negative potentials without affecting its V-inact. This enlarges the "window current" between the voltage activation and inactivation curves, increasing the tonically active I-A near the resting potential and causing the cell to hyperpolarize. Thus DA's effect is to enhance both the transient and resting K+ currents by modulating the same channels. In addition, DA enhances the amplitude of a calcium-dependent potassium current (I-O(Ca)), but has no effect on a sustained potassium current (I-K(V)) These results suggest that DA hyperpolarizes and phase delays the activity of the PD neurons at least in part by modulating their intrinsic postinhibitory recovery properties. This modulation appears to be mediated in part by an increase of I-A and I-O(Ca). I-A appears to be a common target of DA action in the pyloric network, but it can be enhanced or decreased in different ways by DA in different neurons.