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Calcium currents and calcium-dependent potassium currents in mammalian medullary respiratory neurones.

机译:哺乳动物髓质呼吸神经元中的钙电流和钙依赖性钾电流。

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摘要

1. Respiratory neurons of mammals are rhythmically active because their membrane potential fluctuates periodically over a voltage range of -70 to -55 mV. These respiratory drive potentials lead to periodic discharges of bursts of action potentials lasting for 1-2 s. The neuronal processes stabilizing this rhythmic activity involve excitatory and inhibitory synaptic processes that interact with specific membrane properties of the postsynaptic neurones. In the present experiments, performed on dorsal and ventral groups of respiratory neurones under in vivo and in vitro conditions, we verified the modulating feature of such intrinsic neuronal properties. 2. Intrinsic neuronal properties involve Ca2+ mechanisms that lead to intracellular Ca2+ accumulation, and consequently to activation of Ca(2+)-dependent K+ currents. 3. Blockade of intracellular Ca2+ accumulation significantly changed the amplitude and pattern of respiratory drive potentials, and blocked initial hyperpolarizing shifts of the membrane potential following each period of synaptic activation. 4. The data demonstrate that postsynaptic activities and action potential discharges activate low and high voltage-activated Ca2+ currents leading to intracellular Ca2+ accumulation and to activation of Ca(2+)-dependent K+ currents that significantly modulate the voltage response of medullary respiratory neurones to on-going synaptic activation. These intrinsic membrane properties also seem to be involved in the processes controlling termination of rhythmic burst discharges.
机译:1.哺乳动物的呼吸神经元具有节律性,因为它们的膜电位在-70至-55 mV的电压范围内周期性波动。这些呼吸驱动电位导致持续1-2 s的动作电位爆发的周期性放电。稳定该节律性活动的神经元过程涉及与突触后神经元的特定膜特性相互作用的兴奋性和抑制性突触过程。在目前的实验中,在体内和体外条件下对呼吸神经元的背侧和腹侧组执行的操作,我们验证了这种内在神经元特性的调节特征。 2.本征神经元特性涉及导致细胞内Ca2 +积累并因此导致Ca(2+)依赖性K +电流激活的Ca2 +机制。 3.阻止细胞内Ca2 +积累会显着改变呼吸驱动电位的幅度和模式,并在每个突触激活周期后阻止膜电位的初始超极化移动。 4.数据表明,突触后活动和动作电位放电激活低和高电压激活的Ca2 +电流,导致细胞内Ca2 +积累,并激活Ca(2+)依赖性K +电流,从而显着调节髓质呼吸神经元的电压响应。持续的突触激活。这些固有的膜特性似乎也参与了控制节律性突发放电终止的过程。

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