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Key goals of studies in the field of molecular cellular cognition (MCC) include the derivation of explanations of cognitive processes that integrate molecular, cellular, and behavioral mechanisms, and finding mechanism and treatments for cognitive disorders. Although closely connected with behavioral genetics, MCC emphasizes the integration of molecular and cellular explanations of behavior, instead of focusing on the connections between genes and behavior. MCC is a field of neuroscience.
Unlike cognitive neuroscience, which historically has focused on the connection between human brain systems and behavior, the field of MCC has used model organisms such as mice to study how molecular (ie. receptor, kinase activation), intra-cellular (i.e. dendritic processes), and inter-cellular processes (i.e. synaptic plasticity; network representations such as place fields) modulate cognitive function.
Methods employed in MCC include transgenic organisms (i.e. mice), in vitro and in vivo electrophysiology, and behavioral analysis. Modeling is becoming an essential component of the field because of the complexity of the multilevel data generated
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Scientific roots
The field of MCC has its roots in the pioneering studies of the role of NMDA receptor in long-term potentiation and spatial learning. The studies that crystallized the field used knock out mice to look at the role of the alpha calcium calmodulin kinase II and fyn kinase in hippocampal long-term potentiation and spatial learning.
Foundation of the science
Molecular cellular cognition became an organized field with the formation of the Molecular Cellular Cognition Society, an organization with no membership fees and meetings that emphasize the participation of junior scientists. Its first meeting took place in Orlando, Florida on November first, 2002. As of November, 2006 the society had organized 9 meetings in North America, Europe and Asia, and included more than 1200 members.
References
- Morris RG, Anderson E, Lynch GS, Baudry M (1986). "Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5". Nature 319 (6056): 774–6. doi:. PMID 2869411.
- Silva AJ, Paylor R, Wehner JM, Tonegawa S (1992). "Impaired spatial learning in alpha-calcium-calmodulin kinase II mutant mice". Science (journal) 257 (5067): 206–11. PMID 1321493.
- Silva AJ, Stevens CF, Tonegawa S, Wang Y (1992). "Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice". Science (journal) 257 (5067): 201–6. PMID 1378648.
- Grant SG, O'Dell TJ, Karl KA, Stein PL, Soriano P, Kandel ER (1992). "Impaired long-term potentiation, spatial learning, and hippocampal development in fyn mutant mice". Science (journal) 258 (5090): 1903–10. PMID 1361685.
- Silva AJ (2003). "Molecular and cellular cognitive studies of the role of synaptic plasticity in memory". J. Neurobiol. 54 (1): 224–37. doi:. PMID 12486706.
External links
See also
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