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Calcium/Calmodulin-dependent Protein Kinase II is a Ubiquitous Molecule in Human Long-term Memory Synaptic Plasticity: A Systematic Review.

Ataei N, Sabzghabaee AM, Movahedian A - Int J Prev Med (2015)

Bottom Line: Calcium linked calmodulin can activate CaMKII.After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity.Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

View Article: PubMed Central - PubMed

Affiliation: Student Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.

ABSTRACT

Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms include changes in structure and proteins of brain's neurons. In this article, we systematically reviewed the studies that indicate calcium/calmodulin kinase II (CaMKII) is a ubiquitous molecule among different enzymes involved in human long-term memory and the main downstream signaling pathway of long-term memory.

Methods: All of the observational, case-control and review studies were considered and evaluated by the search engines PubMed, Cochrane Central Register of Controlled Trials and ScienceDirect Scopus between 1990 and February 2015. We did not carry out meta-analysis.

Results: At the first search, it was fined 1015 articles which included "synaptic plasticity" OR "neuronal plasticity" OR "synaptic density" AND memory AND "molecular mechanism" AND "calcium/calmodulin-dependent protein kinase II" OR CaMKII as the keywords. A total of 335 articles were duplicates in the databases and eliminated. A total of 680 title articles were evaluated. Finally, 40 articles were selected as reference.

Conclusions: The studies have shown the most important intracellular signal of long-term memory is calcium-dependent signals. Calcium linked calmodulin can activate CaMKII. After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity. Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

No MeSH data available.


Study-flow diagram showing the number of studies screened, excluded and included in the review.
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Figure 1: Study-flow diagram showing the number of studies screened, excluded and included in the review.

Mentions: A total of articles were found including “synaptic plasticity” OR “neuronal plasticity” OR “synaptic density” AND memory AND “molecular mechanism” as the keywords, a total of 788 article in PubMed, 144 in ScienceDirect Scopus and 83 in Cochrane Central Register of Controlled Trials [Table 1]. A total 335 articles were duplicated in the databases and were eliminated. A total of 680 title articles were evaluated and 600 articles that were not related, were excluded, then the abstracts of 80 articles were reviewed and 35 articles that had no original data and sufficient information and did not relate were excluded, then 45 articles were reviewed and the articles that did not have any original data and sufficient information, which did not evaluate synaptic plasticity, and did not have interest in the outcome and did not apply key questions also were excluded. Finally, 34 articles were selected as reference that 3 of them were about physiology and biochemistry of long-term memory, 8 articles about the role of synaptic plasticity in the memory formation and learning and 23 about molecular mechanism and effective downstream signals in long-term memory formation [Figure 1 and Table 2].


Calcium/Calmodulin-dependent Protein Kinase II is a Ubiquitous Molecule in Human Long-term Memory Synaptic Plasticity: A Systematic Review.

Ataei N, Sabzghabaee AM, Movahedian A - Int J Prev Med (2015)

Study-flow diagram showing the number of studies screened, excluded and included in the review.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4587077&req=5

Figure 1: Study-flow diagram showing the number of studies screened, excluded and included in the review.
Mentions: A total of articles were found including “synaptic plasticity” OR “neuronal plasticity” OR “synaptic density” AND memory AND “molecular mechanism” as the keywords, a total of 788 article in PubMed, 144 in ScienceDirect Scopus and 83 in Cochrane Central Register of Controlled Trials [Table 1]. A total 335 articles were duplicated in the databases and were eliminated. A total of 680 title articles were evaluated and 600 articles that were not related, were excluded, then the abstracts of 80 articles were reviewed and 35 articles that had no original data and sufficient information and did not relate were excluded, then 45 articles were reviewed and the articles that did not have any original data and sufficient information, which did not evaluate synaptic plasticity, and did not have interest in the outcome and did not apply key questions also were excluded. Finally, 34 articles were selected as reference that 3 of them were about physiology and biochemistry of long-term memory, 8 articles about the role of synaptic plasticity in the memory formation and learning and 23 about molecular mechanism and effective downstream signals in long-term memory formation [Figure 1 and Table 2].

Bottom Line: Calcium linked calmodulin can activate CaMKII.After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity.Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

View Article: PubMed Central - PubMed

Affiliation: Student Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.

ABSTRACT

Background: Long-term memory is based on synaptic plasticity, a series of biochemical mechanisms include changes in structure and proteins of brain's neurons. In this article, we systematically reviewed the studies that indicate calcium/calmodulin kinase II (CaMKII) is a ubiquitous molecule among different enzymes involved in human long-term memory and the main downstream signaling pathway of long-term memory.

Methods: All of the observational, case-control and review studies were considered and evaluated by the search engines PubMed, Cochrane Central Register of Controlled Trials and ScienceDirect Scopus between 1990 and February 2015. We did not carry out meta-analysis.

Results: At the first search, it was fined 1015 articles which included "synaptic plasticity" OR "neuronal plasticity" OR "synaptic density" AND memory AND "molecular mechanism" AND "calcium/calmodulin-dependent protein kinase II" OR CaMKII as the keywords. A total of 335 articles were duplicates in the databases and eliminated. A total of 680 title articles were evaluated. Finally, 40 articles were selected as reference.

Conclusions: The studies have shown the most important intracellular signal of long-term memory is calcium-dependent signals. Calcium linked calmodulin can activate CaMKII. After receiving information for learning and memory, CaMKII is activated by Glutamate, the most important neurotransmitter for memory-related plasticity. Glutamate activates CaMKII and it plays some important roles in synaptic plasticity modification and long-term memory.

No MeSH data available.