Bishop C A, Wine J J, Nagy F, O'Shea M R
J Neurosci. 1987 Jun;7(6):1769-79. doi: 10.1523/JNEUROSCI.07-06-01769.1987.
The pentapeptide proctolin is colocalized with a conventional, conductance-increasing neurotransmitter in 3 of 5 excitatory motoneurons that innervate a posture-related tonic flexor muscle of the crayfish. It is released from these neurons in response to nerve impulses. Nanomolar concentrations of proctolin superfused on the tonic flexor muscle act postsynaptically to potentiate tension generated by a given level of depolarization. Proctolin alone has no detectable effect on muscle tension, nor does it alter the resting membrane potential of the muscle. Proctolin produces no detectable effect on the EPSPs of the 1 proctolinergic motoneuron that was examined. Neurally released proctolin can be selectively depleted from severed motor axons following prolonged, low-frequency stimulation; EPSPs reflecting conventional transmitter release are unaltered by this procedure. After proctolin depletion, tension generated by the motoneuron is greatly reduced. Taken together, these results indicate that the peptide secondary transmitter in this neuromuscular preparation is an important contributor to the magnitude of tension generated by the motoneuron, but since its effect is dependent on the depolarizing EPSPs of the conventional neurotransmitter, it does not contribute to the temporal aspects of tension generation. These aspects are controlled exclusively by the conventional neurotransmitter.
五肽促肠动素与一种传统的、能增加电导的神经递质在支配小龙虾与姿势相关的紧张性屈肌的5个兴奋性运动神经元中的3个中共同定位。它在这些神经元中响应神经冲动而释放。以纳摩尔浓度灌注在紧张性屈肌上的促肠动素在突触后起作用,增强由给定水平的去极化产生的张力。单独的促肠动素对肌肉张力没有可检测到的影响,也不会改变肌肉的静息膜电位。促肠动素对所检测的1个促肠动素能运动神经元的兴奋性突触后电位没有可检测到的影响。在长时间的低频刺激后,神经释放的促肠动素可从切断的运动轴突中被选择性耗尽;反映传统递质释放的兴奋性突触后电位不受此过程影响。促肠动素耗尽后,运动神经元产生的张力大大降低。综上所述,这些结果表明,在这种神经肌肉制剂中,肽类次要递质是运动神经元产生张力大小的重要贡献者,但由于其作用依赖于传统神经递质的去极化兴奋性突触后电位,它对张力产生的时间方面没有贡献。这些方面完全由传统神经递质控制。