Methamphetamine enhances memory of operantly conditioned respiratory behavior in the snail Lymnaea stagnalis
Methamphetamine enhances memory of operantly conditioned respiratory behavior in the snail Lymnaea stagnalis
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DOI：
10.1242/jeb.042820
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发表时间：
2010-06-15
影响因子：
2.8
通讯作者：
Sorg, Barbara A.
中科院分区：
文献类型：
--
作者：
Kennedy, Colin D.;Houmes, Stephen W.;Sorg, Barbara A.
安非他明已被用作认知增强剂，以促进学习和记忆。安非他明也是一种滥用药物，可能会促使人们产生强烈的记忆，最终导致上瘾。为了了解甲基苯丙胺（Methe）是如何增强学习和记忆的，我们选择了一个相对简单的系统，池塘蜗牛，Stagnalis。研究了甲基苯丙胺暴露对灰蝶长时记忆（LTM）、操作性条件呼吸行为的消退和恢复的影响。我们首先确定了会剧烈改变呼吸行为的甲基苯丙胺剂量。接下来，我们使用在对照条件下产生LTM（>6小时）的训练程序测量了在甲基溶液或水中训练蜗牛（对照组）的影响。两次训练后21小时，甲基苯丙胺暴露损害了LTM的表达，但这似乎是一个上下文依赖性的影响。然而，蜗牛暴露于3.3 μ mol l（-1）甲基在训练过程中有一个速度下降的灭绝的操作性条件记忆。然后，我们测试了蜗牛消除记忆的能力下降是由于增强的LTM还是记忆的消退受损。蜗牛operantly条件在水中，并暴露于甲基后16小时，他们的最后一次试验，但4-5小时前灭绝。甲基苯丙胺使灭绝率增加而不是减少。因此，只有当蜗牛在训练过程中暴露于甲硫氨酸时，甲硫氨酸才会损害灭绝。最后，我们测试了Meth对形成LTM的能力的影响，使用一个单一的训练程序，这是次优的LTM形成。对照蜗牛没有表现出LTM，正如预期的那样，但预先暴露的蜗牛到3.3 μ mol l（-1）甲基24小时之前的单次培训课程产生LTM 24小时后，表明甲基预暴露引发的LTM形成蜗牛。综上所述，我们的研究表明，LTM被Meth加强，这样灭绝训练就不那么有效了。Armenaea提供了一个简单而有用的模型系统来剖析Meth如何启动更强记忆形成的细胞和/或分子机制。
Amphetamines have been used as cognitive enhancers to promote learning and memory. Amphetamines are also drugs of abuse that may promote the initiation of strong memories that ultimately lead to addiction. To understand how methamphetamine (Meth) may be augmenting learning and memory, we chose a relatively simple system, the pond snail, Lymnaea stagnalis. We studied the effects of Meth exposure on the long-term memory (LTM), extinction and reinstatement of operantly conditioned aerial respiratory behavior in Lymnaea. We first determined doses of Meth that would acutely alter respiratory behavior. Next, we measured the impact of training snails in Meth solution or water (control group) using a training procedure that produces LTM (>6 h) in control conditions. Meth exposure impaired the expression of LTM 21 h after two training sessions, but this appeared to be a context-dependent effect only. However, snails exposed to 3.3 mu mol l(-1) Meth during training had a decreased rate of extinction of the operantly conditioned memory. We then tested whether this decreased ability of snails to extinguish memory was due to enhanced LTM or impaired extinction of that memory. Snails were operantly conditioned in water and exposed to Meth 16 h after their last trial but 4-5 h prior to extinction. Meth produced an increase rather than a decrease in extinction rate. Thus, Meth impaired extinction only when snails were exposed to Meth during training. Last, we tested the effect of Meth on the ability to form LTM using a single training procedure that is suboptimal for LTM formation. Control snails did not demonstrate LTM, as expected, but pre-exposure of snails to 3.3 mu mol l(-1) Meth 24 h prior to the single training session produced LTM 24 h later, indicating that Meth pre-exposure primed snails for LTM formation. Taken together, our studies suggest that LTM is strengthened by Meth such that extinction training is less effective. Lymnaea provides a simple and useful model system to dissect the cellular and/or molecular mechanisms of how Meth may initiate the formation of stronger memories.