Gaĭnutdinov Kh L, Andrianov V V, Gaĭnutdinova T Kh
Group of Biophysics, Kazan Physical-Technological Institute, Russian Academy of Sciences.
Zh Vyssh Nerv Deiat Im I P Pavlova. 1999 Jan-Feb;49(1):48-58.
The influence of 5,6-dihydroxytryptamine (5,6-DHT), which selectively destroyed serotonin terminals, and p-chlorphenylalanine, which inhibited serotonin synthesis, was studied on the long-term sensitization (LTS) in a snail. The membrane mechanisms were analyzed by measuring electrical characteristics of command neurons of defensive behavior LPa3, RPa3, LPa2, and RPa2. Snails injected with saline served as an active control. It was shown that the injected drugs inhibited the LTS in certain concentrations. A significant increase was observed in the membrane potential and the threshold of the action potential generation in the command neurons after 5,6-DHT injection in the doses of 20 and 30 mg/kg (in comparison with the active control). Sensitization of snails injected with saline solution led to the LTS and decrease in the membrane and threshold potentials of the command neurons. After the LTS, changes in membrane and threshold potentials in snails injected with 5,6-DHT were negligible in comparison with those injected with 5,6-DHT but without the LTS. Neither the LTS nor subsequent learning resulted in a further decrease in membrane and threshold potentials. Thus, the neurotoxin injection led to an increase in excitability of command neurons and their depolarization, and the LDS did not elicit further excitability increase. Since the shifts of the threshold and membrane potentials were the same, it was concluded that the increase in membrane excitability was induced by the depolarizing shift of the membrane potential.
研究了选择性破坏5-羟色胺能终末的5,6-二羟基色胺(5,6-DHT)和抑制5-羟色胺合成的对氯苯丙氨酸对蜗牛长期敏感化(LTS)的影响。通过测量防御行为的指令神经元LPa3、RPa3、LPa2和RPa2的电特性来分析膜机制。注射生理盐水的蜗牛作为活性对照。结果表明,注射的药物在一定浓度下抑制了LTS。在注射20和30mg/kg剂量的5,6-DHT后,指令神经元的膜电位和动作电位产生阈值显著增加(与活性对照相比)。注射生理盐水溶液的蜗牛敏感化导致LTS以及指令神经元的膜电位和阈值电位降低。在LTS后,与注射5,6-DHT但未发生LTS的蜗牛相比,注射5,6-DHT的蜗牛的膜电位和阈值电位变化可忽略不计。LTS和随后的学习均未导致膜电位和阈值电位进一步降低。因此,注射神经毒素导致指令神经元兴奋性增加及其去极化,而LDS并未引起兴奋性进一步增加。由于阈值和膜电位的变化相同,因此得出结论,膜兴奋性的增加是由膜电位的去极化转变引起的。