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Molecular cellular cognition (MCC) is that branch of neuroscience that deals with the study of cognitive processes with approaches that integrate molecular, cellular and behavioral mechanisms. Key goals of MCC studies include the derivation of molecular and cellular explanations of cognitive processes, as well as finding mechanisms and treatments for cognitive disorders.
Although closely connected with behavioral genetics, MCC emphasizes the integration of molecular and cellular explanations of behaviour, instead of focusing on the connections between genes and behavior.
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, phosphatase regulation), 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 (but are not limited to) transgenic organisms (i.e. mice), viral vectors, pharmacology, in vitro and in vivo electrophysiology, optogenetics, in vivo imaging, and behavioral analysis. Modeling is becoming an essential component of the field because of the complexity of the multilevel data generated.
Scientific roots[edit | edit source]
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. The field has expanded to include a large array of molecules including CREB.
Foundation of the science[edit | edit source]
MCC 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 August, 2009 the society had organized 16 meetings in North America, Europe and Asia, and included more than 1600 members.
References[edit | edit source]
- 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.
- 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.
- 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.
- 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.
- Silva AJ (2003). Molecular and cellular cognitive studies of the role of synaptic plasticity in memory. J. Neurobiol. 54 (1): 224–37.
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See also[edit | edit source]
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