Myers A C
The Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224-6821, USA.
Am J Physiol. 1998 Aug;275(2):L357-64. doi: 10.1152/ajplung.1998.275.2.L357.
Intracellular microelectrode recordings were obtained from neurons located in adult guinea pig bronchial parasympathetic ganglia in situ to determine the calcium and potassium currents regulating repetitive action potential activity and firing rates by these neurons. Neurons in these ganglia respond to prolonged suprathreshold depolarizing current steps with either a burst of action potentials at the onset of the stimulus (accommodating or phasic neurons) or repetitive action potentials throughout the stimulus (nonaccommodating or tonic neurons). Instantaneous and adapted firing rates during prolonged threshold and suprathreshold stimuli were lower in tonic than in phasic neurons, indicating a longer interspike interval between repetitive action potentials in tonic neurons. In tonic neurons, blockade of A-type current with 4-aminopyridine increased accommodation; 4-aminopyridine or apamin decreased the interspike interval in tonic neurons. Calcium-free buffer, cadmium ions, or omega-conotoxin GVIA also increased accommodation in tonic neurons but did not affect the interspike interval; nifedipine or verapamil did not affect the tonic firing pattern. Accommodation in phasic neurons could be decreased by a conditioning hyperpolarization step of the resting potential, which could be subsequently blocked by 4-aminopyridine or calcium-free buffer. Accommodation in phasic neurons could also be decreased by apamin or barium ions: the repetitive action potentials observed during these treatments could be reversed by cadmium ions or calcium-free buffer. These results indicate that tonic and phasic neurons in guinea pig bronchial parasympathetic ganglia have similar types of calcium currents, but potassium channels may ultimately regulate the accommodation pattern, the firing rate, and, consequently, the output from these neurons.
采用细胞内微电极记录技术，从成年豚鼠原位支气管副交感神经节中的神经元获取数据，以确定调节这些神经元重复性动作电位活动和放电频率的钙电流和钾电流。这些神经节中的神经元对长时间的阈上 depolarizing 电流阶跃的反应，要么是在刺激开始时出现一阵动作电位（适应性或相位性神经元），要么是在整个刺激过程中出现重复性动作电位（非适应性或紧张性神经元）。在长时间的阈刺激和阈上刺激期间，紧张性神经元的瞬时放电频率和适应性放电频率低于相位性神经元，这表明紧张性神经元的重复性动作电位之间的峰间期更长。在紧张性神经元中，用 4-氨基吡啶阻断 A 型电流会增加适应性；4-氨基吡啶或蜂毒明肽会缩短紧张性神经元的峰间期。无钙缓冲液、镉离子或 ω-芋螺毒素 GVIA 也会增加紧张性神经元的适应性，但不影响峰间期；硝苯地平或维拉帕米不影响紧张性放电模式。相位性神经元的适应性可通过静息电位的预处理超极化步骤降低，随后该步骤可被 4-氨基吡啶或无钙缓冲液阻断。相位性神经元的适应性也可被蜂毒明肽或钡离子降低：在这些处理过程中观察到的重复性动作电位可被镉离子或无钙缓冲液逆转。这些结果表明，豚鼠支气管副交感神经节中的紧张性神经元和相位性神经元具有相似类型的钙电流，但钾通道可能最终调节适应性模式、放电频率，从而调节这些神经元的输出。
