Analysis of ionic channels involved in burst generation of respiratory neurons in newborn rat medulla in vitro.

腹外侧髓质呼吸神经元有高阈值（N、L型）、中阈值（P型）和低阈值（T型）Ca^<2+>通道。利用膜片钳方法，我们研究了高阈值和中阈值Ca^<2+>通道和Ca^<2+>依赖的K^+通道，这些通道被认为是爆发产生的重要因素，以及持续的Na^<2+>通道，这些通道与膜电位的内在振荡有关。[结果]1)应用p型钙通道阻滞剂omega-Aga-IVA （0.2muM）可降低突发幅度。2) n型Ca^<2+>通道阻滞剂omega-CgTx （2muM）增加了突发幅度，导致动作电位部分失活。omega-CgTx也减少了超极化后的峰值，可能是由于间接阻断了Ca^<2+>依赖的K^+通道。3) Ca^<2+>-依赖性K^+通道阻滞剂，apamine （0.4-1muM）可引起猝发幅度增加和部分动作电位失活。4) l型Ca^<2+>通道阻滞剂，非地平（20muM）可缩短burst持续时间。5)由于Ca^<2+>通道阻断0.1 mM Cb^<2+>完全抑制突发活动后，Pre-I神经元表现出缓慢的去极化反应和去极化依赖的膜振荡。激活阈值在-45 mV左右。随后的K^+通道阻断产生自发爆发活动和去极化平台电位。这些反应被0.5muM TTX superfusion阻断。[讨论]我们认为爆发产生的离子机制如下：由于ttx敏感的持续Na^<2+>通道和p型Ca^<2+>通道的激活，在前i神经元内固有的缓慢去极化在爆发活动的上升阶段是重要的。然后，N型和l型Ca^<2+>通道被激活以增强突发。Ca^<2+>依赖的K^+通道被认为参与了突发活动的维持和终止。[结论]揭示了脑脊液腹外侧呼吸神经元中的离子通道，并推测了这些通道在脑脊液破裂产生中的作用。少

Respiratory neurons in the ventrolateral medulla have high threshold (N,L types), intermediate threshold (P type) and low threshold (T type) Ca^<2+> channels. Using patch clamp method, we investigated high and intermediate throshold Ca^<2+> channels and Ca^<2+>-dependent K^+ channels which are thought to be important in the burst generation, and persistent Na^<2+> channels which are related to intrinsic oscillation of membrane potentials.[Result] 1) Application of P-type Ca channel blocker, omega-Aga-IVA (0.2muM), reduced the burst amplitude. 2) N-type Ca^<2+> channel blocker, omega-CgTx (2muM) increased the burst amplitude and caused partial inactivation of action potentials. omega-CgTx also reduced spike after-hyperpolarization, probably owing to indirect blockade of Ca^<2+>-dependent K^+ channels. 3) Ca^<2+>-dependent K^+ channel blocker, apamine (0.4-1muM) induced an increase in the burst amplitude and partial inactivation of action potentials. 4) L-type Ca^<2+> channel blocker, ni … More fedipine (20muM) shortened the burst duration. 5) After complete inhibition of the burst activity due to Ca^<2+> channel blockade by 0.1 mM Cb^<2+>, Pre-I neurons showed slow depolarizing responses and depolarization-dependent membrane oscillation. The activation threshold was around-45 mV.Subsequent K^+ channel blockade produced spontaneous bursting activity and depolarizing plateau potentials. These responses were blocked by 0.5muM TTX superfusion. [Discussion] We suggest ionic mechanisms of the burst generation as follows : Intrinsic slow depolarization in Pre-I neurons due to activation of TTX-sensitive persistent Na^<2+> channels and P-type Ca^<2+> channels is important in rising phase of burst activity. Then, N and L-Type Ca^<2+> channels are activated to augment the burst. Ca^<2+>-dependent K^+ channels are thought to participate in maintenance and termination of the burst activity. [Conclusion] We revealed ion channels in respiratory neurons in the ventrolateral medulla and suggested function of these channels for the burst generation. Less