Nikitin V P, Kozyrev S A, Shevelkin A V, Sherstnev V V
P. K. Anokhin Science Research Institute of Normal Physiology, Russian Academy of Medical Sciences, Moscow.
Neurosci Behav Physiol. 2002 Jan-Feb;32(1):25-31. doi: 10.1023/a:1012992124052.
The effects of antibodies to a total fraction of s100 proteins and protein s100b on the activity of defensive behavior command neurons LP11 and RP11 were studied in common snails, using non-sensitized animals and animals which had acquired nociceptive sensitization. In non-sensitized snails, application of antibodies against s100 or s100b (0.1 mg/ml) induced membrane depolarization, increased membrane permeability, and suppressed slow excitatory postsynaptic potentials in the responses of neurons to sensory stimulation. Acquisition of sensitization in snails in the presence of antibodies to s100 or s100b (0.1 mg/ml) led to significantly less marked facilitation of synaptic transmission and smaller increases in neuron membrane excitability than in cells of control sensitized animals. The difference in synaptic facilitation in the neurons of control sensitized snails and neurons in sensitized snails given antibody was comparable with the magnitude of synaptic depression due to antibody in non-sensitized animals. At a dose of 0.01 mg/ml, antibody had no effect on these measures of neuron activity. It is suggested that s100 proteins, particularly s100b, are involved in the mechanisms regulating excitability, the membrane potential, and synaptic transmission in command neurons in untrained snails, as well as in the mechanism of plasticity of the electrogenic membranes of nerve cells during the acquisition of nociceptive sensitization.
利用未致敏动物和已获得伤害性致敏的动物，研究了抗s100蛋白总组分和s100b蛋白的抗体对普通蜗牛防御行为指令神经元LP11和RP11活性的影响。在未致敏的蜗牛中，应用抗s100或s100b的抗体（0.1mg/ml）可诱导膜去极化、增加膜通透性，并抑制神经元对感觉刺激反应中的慢兴奋性突触后电位。在存在抗s100或s100b的抗体（0.1mg/ml）的情况下，蜗牛获得致敏后，与对照致敏动物的细胞相比，突触传递的易化作用明显减弱，神经元膜兴奋性的增加也较小。对照致敏蜗牛的神经元与给予抗体的致敏蜗牛的神经元之间突触易化的差异，与未致敏动物中抗体引起的突触抑制程度相当。在0.01mg/ml的剂量下，抗体对这些神经元活动指标没有影响。提示s100蛋白，尤其是s100b，参与了调节未训练蜗牛指令神经元兴奋性、膜电位和突触传递的机制，以及在获得伤害性致敏过程中神经细胞电生膜可塑性的机制。
