Nishimura T
Department of Physiology, Kurume University School of Medicine, Japan.
J Auton Nerv Syst. 1995 Mar 2;51(3):213-22. doi: 10.1016/0165-1838(94)00134-6.
Intracellular recordings were made from neurons in rabbit and feline vesical parasympathetic ganglia in vitro. In response to cathodal current injection (0.1-1 nA for 2-20 ms) the majority of rabbit neurons (229 out of 250) exhibited a single action potential that was followed by a fast and slow after-hyperpolarization (sAHP neuron). The remainder of the cells exhibited an action potential followed by only a fast after-hyperpolarization (fAHP neuron). fAHP neurons did not exhibit anomalous rectification and a spontaneous rhythmic hyperpolarization, which were common membrane properties in sAHP neurons. In response to a train of cathodal current pulses (5-20 Hz for 0.1-10 s), fAHP neurons exhibited action potentials followed by a post-tetanic depolarization (PTD). The PTD was associated with a decrease in membrane input resistance. The amplitude and duration of the PTD were a function of the number of action potentials in the train. The amplitude of the PTD was increased by membrane hyperpolarization and its estimated reversal potential was approximately -30 mV. Low-chloride solution and intracellular injection of chloride ions augmented the amplitude and duration of the PTD, whereas low-sodium, high-potassium and low-potassium solutions did not affect them. Tetraethylammonium (5-10 mM) and barium (0.5-1 mM) increased the amplitude and duration of the PTD. Nominal calcium-free solutions and omega-conotoxin (500 nM) abolished the PTD. The data suggest that activation of chloride channels by calcium influx through omega-conotoxin-sensitive calcium channels mediates the PTD. Repetitive stimulation of the pelvic nerve evoked a train of orthodromic action potentials followed by the PTD of fAHP neurons. (+)-Tubocurarine (10 microM) and hexamethonium (200 microM), but not atropine (1 microM), abolished orthodromic action potentials and the PTD, whereas these cholinergic antagonists did not depress the PTD evoked by direct action potentials. In summary, the data suggest that the PTD may function as a slow synaptic potential in fAHP neurons. This appears likely because neither slow excitatory nor inhibitory postsynaptic potentials are present in neurons of rabbit vesical parasympathetic ganglia. In contrast, slow inhibitory and excitatory postsynaptic potentials were recorded from neurons in feline vesical parasympathetic ganglia.
在体外对兔和猫的膀胱副交感神经节中的神经元进行细胞内记录。响应阴极电流注入（0.1 - 1 nA，持续2 - 20 ms），大多数兔神经元（250个中的229个）表现出单个动作电位，随后是快速和慢速超极化后电位（sAHP神经元）。其余细胞表现出动作电位，随后仅有快速超极化后电位（fAHP神经元）。fAHP神经元未表现出反常整流和自发节律性超极化，而这是sAHP神经元常见的膜特性。响应一串阴极电流脉冲（5 - 20 Hz，持续0.1 - 10 s），fAHP神经元表现出动作电位，随后是强直后去极化（PTD）。PTD与膜输入电阻的降低有关。PTD的幅度和持续时间是脉冲串中动作电位数量的函数。PTD的幅度因膜超极化而增加，其估计的反转电位约为 -30 mV。低氯溶液和细胞内注入氯离子增加了PTD的幅度和持续时间，而低钠、高钾和低钾溶液对其无影响。四乙铵（5 - 10 mM）和钡（0.5 - 1 mM）增加了PTD的幅度和持续时间。无钙名义溶液和ω - 芋螺毒素（500 nM）消除了PTD。数据表明，通过ω - 芋螺毒素敏感的钙通道内流的钙激活氯离子通道介导了PTD。盆腔神经的重复刺激诱发一串顺向动作电位，随后是fAHP神经元的PTD。（+） - 筒箭毒碱（10 μM）和六甲铵（200 μM），但不是阿托品（1 μM）消除了顺向动作电位和PTD，而这些胆碱能拮抗剂并未抑制直接动作电位诱发的PTD。总之，数据表明PTD可能在fAHP神经元中作为一种缓慢的突触电位起作用。这似乎是可能的，因为兔膀胱副交感神经节的神经元中既不存在缓慢的兴奋性也不存在抑制性突触后电位。相反，在猫膀胱副交感神经节的神经元中记录到了缓慢的抑制性和兴奋性突触后电位。
