Rosen S C, Weiss K R, Goldstein R S, Kupfermann I
Center for Neurobiology and Behavior, New York State Psychiatric Institute, NY 10032.
J Neurosci. 1989 May;9(5):1562-78. doi: 10.1523/JNEUROSCI.09-05-01562.1989.
Food-induced arousal in Aplysia is characterized by a progressive increase in the speed and strength of biting responses elicited by a seaweed stimulus. Data from semi-intact and dissected preparations suggest that the identified, serotonergic, metacerebral cells (MCCs) of the cerebral ganglion contribute to food-induced arousal by enhancing the strength of buccal muscle contractions, and by modulating the output of the central pattern generator for biting movements. In order to test this hypothesis in intact, free-moving animals and to determine if the MCCs play a role in satiation of feeding, the behavior of animals that had their MCCs destroyed by intracellular injection of proteases was compared with that of B Cell-Lesion and Dye injection control animals (Experiment 1) or surgical control animals (Experiment 2). Nonfeeding behaviors such as defensive withdrawal responses, locomotion, and righting reflexes were unaffected by MCC lesioning. Also unaffected by MCC lesioning were appetitive feeding behaviors and the amount of food needed to satiate animals. Significant behavioral deficits in consummatory feeding behaviors, which remained stable for periods exceeding 10 d, were observed in the MCC-lesioned animals but not in controls. Lesioned animals exhibited a slowing of rate of repetitive biting responses by 40% of controls and had reduced magnitudes of repetitive bites, particularly at the end of a testing run of 10 consecutive bites. The deficit in bite magnitude was minimally evident in food-deprived animals (Experiment 1) but became more pronounced as animals were fed to satiation (Experiment 2). MCC-lesioned animals still exhibited a residual build-up of the rate and magnitude of biting responses at the onset of feeding behavior. This suggests that, in addition to the MCCs, there are other sources of modulation that contribute to plasticity of consummatory responses during the food-induced arousal state.
海兔因食物引发的兴奋表现为，由海藻刺激引发的啃咬反应在速度和强度上逐渐增加。来自半完整和解剖标本的数据表明，已识别出的脑神经节中血清素能的大脑细胞（MCCs）通过增强颊肌收缩强度以及调节咬食运动的中央模式发生器的输出，来促成因食物引发的兴奋。为了在完整、自由活动的动物身上验证这一假设，并确定MCCs在进食饱腹感中是否起作用，将通过细胞内注射蛋白酶破坏其MCCs的动物的行为，与B细胞损伤和染料注射对照动物（实验1）或手术对照动物（实验2）的行为进行了比较。诸如防御性退缩反应、运动和翻正反射等非进食行为不受MCC损伤的影响。进食行为和使动物吃饱所需的食物量也不受MCC损伤的影响。在MCC损伤的动物中观察到了在完成性进食行为方面的显著行为缺陷，这种缺陷在超过10天的时间内保持稳定，但在对照动物中未观察到。受损动物表现出重复啃咬反应的速度比对照动物慢40%，并且重复啃咬的幅度减小，特别是在连续10次啃咬的测试过程结束时。啃咬幅度的缺陷在食物匮乏的动物中（实验1）不太明显，但随着动物进食至饱腹而变得更加明显（实验2）。MCC损伤的动物在进食行为开始时仍表现出啃咬反应的速度和幅度的残余增加。这表明，除了MCCs之外，还有其他调节来源有助于在食物引发的兴奋状态下完成性反应的可塑性。
