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Electrophysiological characteristics of feeding-related neurons after taste avoidance Pavlovian conditioning in Lymnaea stagnalis

机译:避免唇taste裂后巴甫洛夫条件下进食相关神经元的电生理特性

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摘要

Taste avoidance conditioning (TAC) was carried out on the pond snail, Lymnaea stagnalis. The conditional stimulus (CS) was sucrose which elicits feeding behavior; while the unconditional stimulus (US) was a tactile stimulus to the head which causes feeding to be suppressed. The neuronal circuit that drives feeding behavior in Lymnaea is well worked out. We therefore compared the physiological characteristics on 3 classes of neurons involved with feeding behavior especially in response to the CS in conditioned vs. control snails. The cerebral giant cell (CGC) modulates feeding behavior, N1 medial neuron (N1M) is one of the central pattern generator neurons that organizes feeding behavior, while B3 is a motor neuron active during the rasp phase of feeding. We found the resting membrane potential in CGC was hyperpolarized significantly in conditioned snails but impulse activity remained the same between conditioned vs. control snails. There was, however, a significant increase in spontaneous activity and a significant depolarization of N1M’s resting membrane potential in conditioned snails. These changes in N1M activity as a result of training are thought to be due to withdrawal interneuron RPeD11 altering the activity of the CGCs. Finally, in B3 there was: 1) a significant decrease in the amplitude and the frequency of the post-synaptic potentials; 2) a significant hyperpolarization of resting membrane potential in conditioned snails; and 3) a disappearance of bursting activity typically initiated by the CS. These neuronal modifications are consistent with the behavioral phenotype elicited by the CS following conditioning.
机译:在池塘蜗牛,Lymnaea stagnalis上进行味觉避免调理(TAC)。有条件的刺激(CS)是蔗糖,引起进食行为。而无条件刺激(US)是对头部的触觉刺激,导致进食受到抑制。可以很好地解决引起淋巴瘤进食行为的神经元回路。因此,我们比较了与进食行为有关的3类神经元的生理特性,特别是对条件蜗牛与对照蜗牛的CS反应。脑巨细胞(CGC)调节进食行为,N1内侧神经元(N1M)是组织进食行为的中央模式生成器神经元之一,而B3是在进食粗锉阶段活跃的运动神经元。我们发现条件蜗牛的CGC静息膜电位显着超极化,但是条件蜗牛与对照蜗牛之间的冲动活性保持相同。但是,条件蜗牛的自发活动显着增加,N1M的静止膜电位显着去极化。训练导致的N1M活性的这些变化被认为是由于戒断中间神经元RPeD11改变了CGC的活性所致。最后,在B3中:1)突触后电位的幅度和频率显着降低; 2)条件化蜗牛的静息膜电位明显超极化; 3)通常由CS发起的爆发活动的消失。这些神经元的修饰与条件调节后CS引起的行为表型一致。

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