Fung S J, Barnes C D
Arch Ital Biol. 1986 Oct;124(4):229-43.
The present study demonstrates the enhanced efficacy of impulse initiation among the hindlimb alpha motoneurons of flexor and extensor origins (n = 35) upon electrical stimulation of the locus coeruleus (LC) in decerebrate cats. When combined with the LC-evoked excitatory postsynaptic potential (EPSP), intracellular hyperpolarization-induced partial and total blocks of antidromic invasion were overcome, resulting in full-spike generation in all cells (n = 21). In three other cells, partial blocks, representing the motoneuron refractoriness resulting from double stimulation at close intervals, were relieved by the concomitant LC-EPSP. When an antidromic volley occurred at a time when the somadendritic (SD) membrane was near threshold, LC stimulation was shown to increase the probability of full-spike initiation as well as to shorten the initial segment (IS)-SD delay, suggesting a coerulospinal enhancement of the safety factor for IS-SD impulse conduction. When coincident with the LC-EPSPs, group Ia EPSPs of flexor and extensor origins were demonstrated to reach the threshold of discharging the cells (n = 4). In those cells exhibiting prominent depolarizing synaptic noise (n = 10), LC stimulation was sufficient to cause the cell to fire action potentials presumably by interacting with concomitant excitatory synaptic drive. The present results advocate that the descending LC excitatory drive has engaged in the action potential initiation process of the alpha motoneuron, facilitating its reaching the firing threshold during concurrent depressed membrane excitability as well as subthreshold converging inputs.
本研究表明,在去大脑猫中,电刺激蓝斑(LC)时,起源于屈肌和伸肌的后肢α运动神经元的冲动起始效率增强(n = 35)。当与LC诱发的兴奋性突触后电位(EPSP)相结合时,细胞内超极化诱导的逆行入侵部分和完全阻断被克服,导致所有细胞(n = 21)产生全峰电位。在另外三个细胞中,代表近距离双重刺激导致的运动神经元不应期的部分阻断,被伴随的LC-EPSP缓解。当在树突体(SD)膜接近阈值时出现逆行冲动时,LC刺激显示会增加全峰电位起始的概率,并缩短始段(IS)-SD延迟,表明蓝斑脊髓对IS-SD冲动传导安全系数的增强。当与LC-EPSP同时出现时,起源于屈肌和伸肌的Ia类EPSP被证明达到使细胞放电的阈值(n = 4)。在那些表现出明显去极化突触噪声的细胞中(n = 10),LC刺激足以通过与伴随的兴奋性突触驱动相互作用使细胞产生动作电位。目前的结果表明,下行的LC兴奋性驱动参与了α运动神经元的动作电位起始过程,在膜兴奋性同时降低以及阈下汇聚输入的情况下,促进其达到放电阈值。