Article

The molecular and cellular biology of enhanced cognition

Department of Neurobiology, Brain Research Institute, University of California, Los Angeles, California 90095, USA.
Nature Reviews Neuroscience (Impact Factor: 31.43). 03/2009; 10(2):126-40. DOI: 10.1038/nrn2572
Source: PubMed

ABSTRACT

Most molecular and cellular studies of cognitive function have focused on either normal or pathological states, but recent research with transgenic mice has started to address the mechanisms of enhanced cognition. These results point to key synaptic and nuclear signalling events that can be manipulated to facilitate the induction or increase the stability of synaptic plasticity, and therefore enhance the acquisition or retention of information. Here, we review these surprising findings and explore their implications to both mechanisms of learning and memory and to ongoing efforts to develop treatments for cognitive disorders. These findings represent the beginning of a fundamental new approach in the study of enhanced cognition.

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Available from: Yong-Seok Lee, Jun 11, 2014
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    • "The iGluRs are the ligand-gated ion channels regulating cation influx for excitatory synapses and they are subdivided into N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate (KA) receptors [39, 40]. In general, the iGuRs mediate synaptic plasticity leading to a long-term potentiation (LTP) [41, 42]. In embryonic brain and neurogenic zone of adult brain, the iGluRs are highly expressed and involved in regulation of neural development and neurogenesis [43– 49]. "
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    • "Therefore, investigations on mechanisms leading to cognitive enhancement will have both basic and translational interest. Genetic studies on animal models have already offered a catalog of molecular alterations that result in enhanced cognition (Lee and Silva, 2009). Notably, most of these genetic changes can be related more or less directly with the process of synaptic plasticity, particularly long-term potentiation (LTP) and long-term depression (LTD). "
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