Using an invertebrate model to investigate the mechanisms of short-term memory deficits induced by food deprivation.
Using an invertebrate model to investigate the mechanisms of short-term memory deficits induced by food deprivation.
复制标题
利用无脊椎动物模型探讨食物剥夺引起短时记忆障碍的机制。
DOI：
10.1016/j.bbr.2021.113646
复制
发表时间：
2022-02-10
影响因子：
2.7
通讯作者：
Mozzachiodi R
中科院分区：
文献类型：
--
作者：
Deng X;Mozzachiodi R
虽然长时间的食物剥夺会导致记忆缺陷，但其潜在机制只有部分了解。在这项研究中，我们开始调查的细胞基质的食物剥夺引起的记忆障碍的无脊椎动物。在一次伤害性刺激试验后，失智症同时表现出短期敏化（一种初级学习形式，其中退缩反射增强）和短期摄食抑制至少15分钟。敏化和摄食抑制的细胞相关性包括控制退缩反射的尾感觉神经元（TSN）的兴奋性增加，和摄食决策神经元B51的兴奋性降低，分别最近，据报道，14天的食物剥夺（14DFD）打破了致敏和摄食抑制的共同表达，而没有健康恶化。具体而言，在14DFD下，完全防止了致敏，同时存在摄食抑制，尽管减弱。本研究探讨了14DFD下缺乏敏化和降低摄食抑制的细胞机制。使用简化的制备物来评估通过在体外递送令人厌恶的训练方案诱导的短期细胞修饰。在14DFD下进行体外训练后，TSN兴奋性未能增加，这表明缺乏致敏性可能是TSN兴奋性未能增加的结果。在体外训练后，B51兴奋性也未能降低，这表明额外的神经元可能有助于14 DFD动物中保守但降低的摄食抑制。本研究为进一步利用失智症模型系统研究长时间食物剥夺引起的记忆障碍的机制奠定了基础。
Although prolonged food deprivation is known to cause memory deficits, the underlying mechanisms are only partially understood. In this study, we began to investigate the cellular substrates of food deprivation-induced memory impairments in the invertebrate Aplysia. Following a single trial of noxious stimuli, Aplysia concurrently express short-term sensitization (an elementary form of learning in which withdrawal reflexes are enhanced) and short-term feeding suppression for at least 15 min. Cellular correlates of sensitization and feeding suppression include increased excitability of the tail sensory neurons (TSNs) controlling the withdrawal reflexes, and decreased excitability of feeding decision-making neuron B51, respectively. Recently, 14 days of food deprivation (14DFD) was reported to break the co-expression of sensitization and feeding suppression in Aplysia without health deterioration. Specifically, under 14DFD, sensitization was completely prevented while feeding suppression was present albeit attenuated. This study explored the cellular mechanisms underlying the absent sensitization and reduced feeding suppression under 14DFD. A reduced preparation was used to evaluate the short-term cellular modifications induced by delivering an aversive training protocol in vitro. TSN excitability failed to increase following in vitro training under 14DFD, suggesting that the lack of sensitization may be a consequence of the fact that TSNs excitability failed to increase. B51 excitability also failed to decrease following in vitro training, indicating that additional neurons may contribute to the conserved albeit reduced feeding suppression in 14DFD animals. This study lays the foundations for the future use of the Aplysia model system to investigate the mechanisms underlying the memory impairments induced by prolonged food deprivation.
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DOI：
10.1523/jneurosci.1256-11.2011
发表时间：
2011-10-12
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Lorenzetti FD;Baxter DA;Byrne JH
通讯作者：
Byrne JH
影响因子：
7.2
作者：
Byrne, John H.;Hawkins, Robert D.
通讯作者：
Hawkins, Robert D.
影响因子：
5.5
作者：
GOLDMAN, JE;SCHWARTZ, JH
通讯作者：
SCHWARTZ, JH
影响因子：
5.3
作者：
Watkins, Amanda J.;Goldstein, Daniel A.;Wright, William G.
通讯作者：
Wright, William G.
影响因子：
3.3
作者：
ZAKHAROV, IS;BALABAN, PM
通讯作者：
BALABAN, PM