Abstract
There has been nearly a century of interest in the idea that information is stored in the brain as changes in the efficacy of synaptic connections between neurons that are activated during learning. The discovery and detailed report of the phenomenon generally known as long-term potentiation opened a new chapter in the study of synaptic plasticity in the vertebrate brain, and this form of synaptic plasticity has now become the dominant model in the search for the cellular and molecular bases of learning and memory. Accumulating evidence suggests that the rapid activation of the genetic machinery is a key mechanism underlying the enduring modification of neural networks required for the laying down of memory. Here we briefly review these mechanisms and illustrate with a few examples of animal models of neurological disorders how new knowledge about these mechanisms can provide valuable insights into identifying the mechanisms that go awry when memory is deficient, and how, in turn, characterisation of the dysfunctional mechanisms offers prospects to design and evaluate molecular and biobehavioural strategies for therapeutic prevention and rescue.
Keywords: hippocampus, ageing, memory formation, duchenne muscular dystrophy, environmental enrichment, animal models
Current Molecular Medicine
Title: Gene Control of Synaptic Plasticity and Memory Formation: Implications for Diseases and Therapeutic Strategies
Volume: 2 Issue: 7
Author(s): Cyrille Vaillend, Claire Rampon, Sabrina Davis and Serge Laroche
Affiliation:
Keywords: hippocampus, ageing, memory formation, duchenne muscular dystrophy, environmental enrichment, animal models
Abstract: There has been nearly a century of interest in the idea that information is stored in the brain as changes in the efficacy of synaptic connections between neurons that are activated during learning. The discovery and detailed report of the phenomenon generally known as long-term potentiation opened a new chapter in the study of synaptic plasticity in the vertebrate brain, and this form of synaptic plasticity has now become the dominant model in the search for the cellular and molecular bases of learning and memory. Accumulating evidence suggests that the rapid activation of the genetic machinery is a key mechanism underlying the enduring modification of neural networks required for the laying down of memory. Here we briefly review these mechanisms and illustrate with a few examples of animal models of neurological disorders how new knowledge about these mechanisms can provide valuable insights into identifying the mechanisms that go awry when memory is deficient, and how, in turn, characterisation of the dysfunctional mechanisms offers prospects to design and evaluate molecular and biobehavioural strategies for therapeutic prevention and rescue.
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Cite this article as:
Vaillend Cyrille, Rampon Claire, Davis Sabrina and Laroche Serge, Gene Control of Synaptic Plasticity and Memory Formation: Implications for Diseases and Therapeutic Strategies, Current Molecular Medicine 2002; 2 (7) . https://dx.doi.org/10.2174/1566524023361952
DOI https://dx.doi.org/10.2174/1566524023361952 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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