Walters E T, Byrne J H, Carew T J, Kandel E R
J Neurophysiol. 1983 Dec;50(6):1543-59. doi: 10.1152/jn.1983.50.6.1543.
The tail-withdrawal reflex of Aplysia can be sensitized by weak stimulation of a site outside the site used to test the reflex or by repeatedly stimulating the test site itself. The sensitization of tail-withdrawal responses is associated with enhanced activation of the tail motor neurons and heterosynaptic facilitation of the monosynaptic connections between the tail sensory neurons and tail motor neurons. This synaptic facilitation can occur under conditions in which neither posttetanic potentiation nor generalized changes in postsynaptic input resistance contribute to the facilitation. In addition to producing monosynaptic excitatory postsynaptic potentials (EPSPs), action potentials in tail sensory neurons often recruit longer latency polysynaptic input to the tail motor neurons during sensitization. Strong, noxious tail shock similar in intensity to that used previously for sensitization and aversive classical conditioning of other responses in Aplysia produces more heterosynaptic facilitation than does weak sensitizing stimulation. Heterosynaptic facilitation builds up progressively with multiple trials and lasts for hours. Very strong shocks to the tail can change the response characteristics of tail sensory neurons so that a prolonged, regenerative burst of spikes is elicited by a brief intracellular depolarizing pulse. This bursting response produced by sensitizing stimulation has not been described previously in Aplysia sensory neurons and can greatly amplify the synaptic input to tail motor neurons from the sensory neurons. In addition, strong shocks to the tail increase the duration and magnitude of individual sensory neuron action potentials. Sensitizing tail stimulation usually produces long-lasting depolarization of the tail motor neurons and often long-lasting hyperpolarization of the tail sensory neurons. The tail motor and sensory neurons show both increases and decreases of input resistance following sensitizing stimulation. However, the small, occasional increases in input resistance of the motor neuron are insufficient to explain the heterosynaptic facilitation produced by sensitizing stimulation. Serotonin (5-HT) application can mimic many of the effects of sensitizing tail shock, including facilitation of both tail withdrawal and the monosynaptic connections between tail sensory and motor neurons, hyperpolarizing and depolarizing responses in the tail sensory neurons, and an increase in the duration and magnitude of the sensory neuron action potential. In the nearly isolated sensory neuron soma, 5-HT usually produces a slow, decreased conductance depolarizing response, suggesting that the 5-HT-induced hyperpolarizing response see
海兔的缩尾反射可通过对用于测试反射部位之外的位点进行微弱刺激，或通过反复刺激测试位点本身而被致敏。缩尾反应的致敏与尾部运动神经元的激活增强以及尾部感觉神经元和尾部运动神经元之间单突触连接的异突触易化有关。这种突触易化可以在强直后增强和突触后输入电阻的普遍变化均未对易化产生作用的条件下发生。除了产生单突触兴奋性突触后电位（EPSP）外，尾部感觉神经元的动作电位在致敏过程中通常还会募集到潜伏期更长的多突触输入至尾部运动神经元。强度与先前用于致敏及对海兔其他反应进行厌恶经典条件反射的尾部电击相似的强烈有害尾部电击，比微弱的致敏刺激产生更多的异突触易化。异突触易化在多次试验中逐渐增强，并持续数小时。对尾部的极强电击可改变尾部感觉神经元的反应特性，以至于短暂的细胞内去极化脉冲可引发持续时间长的再生性动作电位爆发。致敏刺激产生的这种爆发性反应此前在海兔感觉神经元中未曾被描述过，并且可极大地放大感觉神经元向尾部运动神经元的突触输入。此外，对尾部的强烈电击会增加单个感觉神经元动作电位的持续时间和幅度。致敏性尾部刺激通常会使尾部运动神经元产生持久的去极化，并且常常使尾部感觉神经元产生持久的超极化。致敏刺激后，尾部运动神经元和感觉神经元的输入电阻均表现出增加和减少。然而，运动神经元输入电阻偶尔出现的小幅增加不足以解释致敏刺激所产生的异突触易化。应用5-羟色胺（5-HT）可模拟致敏性尾部电击的许多效应，包括促进缩尾以及尾部感觉和运动神经元之间的单突触连接、尾部感觉神经元中的超极化和去极化反应，以及感觉神经元动作电位持续时间和幅度的增加。在几乎分离的感觉神经元胞体中，5-HT通常会产生缓慢的、电导降低的去极化反应，这表明5-HT诱导的超极化反应可见
