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首页> 外文期刊>The European Journal of Neuroscience >Activation of muscarinic receptors induces protein synthesis-dependent long-lasting depression in the perirhinal cortex.
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Activation of muscarinic receptors induces protein synthesis-dependent long-lasting depression in the perirhinal cortex.

机译：毒蕈碱受体的激活在周围神经皮层中诱导依赖蛋白质合成的长期抑制。

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摘要

There is strong evidence that decrements in neuronal activation in perirhinal cortex when a novel stimulus is repeated provide a neural substrate of visual recognition memory. There is also strong evidence that muscarinic acetylcholine (ACh) receptors are involved in learning and memory. However, the mechanisms underlying neuronal decrements in the perirhinal cortex and the basis of ACh involvement in learning and memory are not understood. In an in vitro preparation of rat perirhinal cortex we now demonstrate that activation of ACh receptors by carbachol (CCh) produces long-lasting depression (LLD) of synaptic transmission that is dependent on muscarinic M1 receptor activation. Crucially, the induction of this form of LLD requires neither N-methyl-D-aspartate receptor activation nor synaptic stimulation. CCh-induced LLD was not blocked by the protein kinase C inhibitors staurosporine or BIM, or by the protein phosphatase inhibitor okadaic acid. However, each of cyclopiazonic acid (an agent that depletes intracellular calcium stores) and anisomycin (an inhibitor of protein synthesis) significantly reduced the magnitude of CCh-induced LLD. These mechanisms triggered by muscarinic receptor activation could play a role in the induction and/or expression of certain forms of activity-dependent long-term depression in perirhinal cortex. An understanding of CCh-induced LLD may thus provide clues to the mechanisms underlying lasting neuronal decrements that occur in the perirhinal cortex and hence for neural substrates of visual recognition memory.
机译：有强有力的证据表明，当重复进行新的刺激时，周围神经皮层神经元激活的减少会为视觉识别记忆提供神经基础。也有强有力的证据表明毒蕈碱型乙酰胆碱（ACh）受体参与了学习和记忆。但是，尚不清楚周围神经皮层神经元递减的机制以及ACh参与学习和记忆的基础。现在，在体外制备大鼠周围神经皮层的过程中，我们证明了卡巴胆碱（CCh）对ACh受体的激活会产生依赖于毒蕈碱M1受体激活的突触传递的持久抑制（LLD）。至关重要的是，这种形式的LLD的诱导既不需要N-甲基-D-天冬氨酸受体活化也不需要突触刺激。 CCh诱导的LLD不受蛋白激酶C抑制剂星形孢菌素或BIM或蛋白磷酸酶抑制剂冈田酸的阻断。但是，环吡嗪酸（一种消耗细胞内钙的药物）和茴香霉素（一种蛋白质合成抑制剂）均显着降低了CCh诱导的LLD的数量。毒蕈碱性受体激活触发的这些机制可能在诱导和/或表达某些形式的依赖活性的长期抑制性周围皮层皮质中发挥作用。因此，对CCh诱导的LLD的了解可能为在神经周围皮层中发生的持续神经元递减的机制提供线索，从而为视觉识别记忆的神经基质提供了线索。

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