Rutecki P A
Department of Neurology, Baylor College of Medicine, Houston, Texas 77030.
J Clin Neurophysiol. 1992 Apr;9(2):195-211.
Neuronal membrane excitability and the synaptic connections among neurons produce behavior and cognition. The intracellular compartment of neurons is negatively charged relative to the extracellular space, and this charge, as well as current flow, is produced by ions. From the perspective of charged ions, the lipid bilayer of the neuronal membrane acts as a capacitor, and transmembrane glycoprotein pores or channels act as resistors. The open and closed states of ionic channels determine the membrane potential. At equilibrium, the lowest resistance or greatest permeability is for potassium, and the resting membrane potential is close to the equilibrium potential for potassium. When a channel is opened, permeable ions diffuse down their electrochemical gradients and the membrane potential is changed. Channels are gated (opened or closed) by voltage, neurotransmitters, and second messengers. The neuron integrates synaptic potentials produced by transmitter-gated channel activity and either generates a subthreshold potential, or a suprathreshold depolarization that generates an action potential or a burst of action potentials. Action potential generation is mediated by a large, brief sodium influx that is followed by activation of a voltage-dependent potassium eflux. The pattern of action potential firing is dependent on the interaction of a repertoire of voltage-dependent ion conductances. The action potential is the main signaling mechanism to activate synaptic transmission at axon terminals. Synaptic transmission is graded depending on the amount of calcium entering the presynaptic terminal. The number of action potentials, or the shape of the action potential, will determine the amount of calcium entering the terminal and the efficacy of synaptic transmission. Presynaptic ion channels may also be controlled by neurotransmitters or modulators and affect synaptic transmission by altering the amount of calcium influx.
神经元膜兴奋性以及神经元之间的突触连接产生行为和认知。神经元的细胞内区相对于细胞外空间带负电荷，这种电荷以及电流由离子产生。从带电离子的角度来看，神经元膜的脂质双层起电容器的作用，跨膜糖蛋白孔或通道起电阻器的作用。离子通道的开放和关闭状态决定膜电位。在平衡状态下，钾离子的电阻最低或通透性最大，静息膜电位接近钾离子的平衡电位。当通道打开时，可渗透离子沿其电化学梯度扩散，膜电位发生变化。通道由电压、神经递质和第二信使门控（打开或关闭）。神经元整合由递质门控通道活动产生的突触电位，要么产生阈下电位，要么产生阈上去极化，进而产生动作电位或一连串动作电位。动作电位的产生由大量短暂的钠离子内流介导，随后是电压依赖性钾离子外流的激活。动作电位发放模式取决于一系列电压依赖性离子电导的相互作用。动作电位是激活轴突终末突触传递的主要信号机制。突触传递根据进入突触前终末的钙量进行分级。动作电位的数量或动作电位的形状将决定进入终末的钙量以及突触传递的效能。突触前离子通道也可能受神经递质或调节剂控制，并通过改变钙内流的量来影响突触传递。
