Roles of calcium/calmodulin-dependent kinase II in long-term memory formation in crickets.
Roles of calcium/calmodulin-dependent kinase II in long-term memory formation in crickets.
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DOI：
10.1371/journal.pone.0107442
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Matsumoto Y
中科院分区：
文献类型：
--
作者：
Mizunami M;Nemoto Y;Terao K;Hamanaka Y;Matsumoto Y
Ca2+/calmodulin (CaM)-dependent protein kinase II （CaMKII）是脊椎动物许多学习和记忆系统中的关键分子，但CaMKII在无脊椎动物中的作用尚未被详细描述。我们已经提出，NO/cGMP信号、环核苷酸门控通道、Ca2+/CaM和cAMP信号的连续激活参与了蟋蟀嗅觉调节的长期记忆（LTM）的形成。在这里，我们发现CaMKII参与了LTM的形成，并提出了其在生化级联中的作用位点。经过3次条件反射，将气味与奖励联系起来的蟋蟀表现出持续数天的记忆，其特征是蛋白质合成依赖性LTM。相比之下，接受1次条件反射的动物表现出仅持续数小时的记忆（中期记忆，MTM）。在3次试验前注射CaMKII抑制剂会损害1天的记忆保留，但不会损害1小时的记忆保留，这表明CaMKII参与LTM的形成，但不参与MTM的形成。在1次试验前注射cGMP类似物、钙离子亲和物或cAMP类似物的动物表现出1天的滞留，同时注射CaMKII抑制剂会破坏cGMP类似物或钙离子亲和物对LTM的诱导，但不会破坏cAMP类似物对LTM的诱导，这表明在LTM形成的生化级联中，CaMKII是cGMP生产和Ca2+内流的下游，cAMP生产的上游。在1次试验前注射腺苷酸环化酶（AC）激活剂的动物表现出1天的保留期。有趣的是，CaMKII抑制剂破坏了AC激活剂对LTM的诱导，尽管AC被认为是CaMKII的下游靶点。结果表明，CaMKII与AC相互作用，促进LTM形成的cAMP的产生。我们认为CaMKII是Ca2+信号和cAMP信号相互作用的关键分子，LTM的形成是CaMKII在学习和记忆中的新作用。
Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is a key molecule in many systems of learning and memory in vertebrates, but roles of CaMKII in invertebrates have not been characterized in detail. We have suggested that serial activation of NO/cGMP signaling, cyclic nucleotide-gated channel, Ca2+/CaM and cAMP signaling participates in long-term memory (LTM) formation in olfactory conditioning in crickets, and here we show participation of CaMKII in LTM formation and propose its site of action in the biochemical cascades. Crickets subjected to 3-trial conditioning to associate an odor with reward exhibited memory that lasts for a few days, which is characterized as protein synthesis-dependent LTM. In contrast, animals subjected to 1-trial conditioning exhibited memory that lasts for only several hours (mid-term memory, MTM). Injection of a CaMKII inhibitor prior to 3-trial conditioning impaired 1-day memory retention but not 1-hour memory retention, suggesting that CaMKII participates in LTM formation but not in MTM formation. Animals injected with a cGMP analogue, calcium ionophore or cAMP analogue prior to 1-trial conditioning exhibited 1-day retention, and co-injection of a CaMKII inhibitor impaired induction of LTM by the cGMP analogue or that by the calcium ionophore but not that by the cAMP analogue, suggesting that CaMKII is downstream of cGMP production and Ca2+ influx and upstream of cAMP production in biochemical cascades for LTM formation. Animals injected with an adenylyl cyclase (AC) activator prior to 1-trial conditioning exhibited 1-day retention. Interestingly, a CaMKII inhibitor impaired LTM induction by the AC activator, although AC is expected to be a downstream target of CaMKII. The results suggest that CaMKII interacts with AC to facilitate cAMP production for LTM formation. We propose that CaMKII serves as a key molecule for interplay between Ca2+ signaling and cAMP signaling for LTM formation, a new role of CaMKII in learning and memory.
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影响因子：
34.7
作者：
Lisman, John;Yasuda, Ryohei;Raghavachari, Sridhar
通讯作者：
Raghavachari, Sridhar
DOI：
10.1523/jneurosci.1882-10.2010
发表时间：
2010-12-08
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Akalal DB;Yu D;Davis RL
通讯作者：
Davis RL
影响因子：
3.5
作者：
Malik BR;Gillespie JM;Hodge JJ
通讯作者：
Hodge JJ
影响因子：
2.9
作者：
CHAVEZNORIEGA, LE;STEVENS, CF
通讯作者：
STEVENS, CF
影响因子：
0.9
作者：
Matsumoto, Y;Noji, S;Mizunami, M
通讯作者：
Mizunami, M