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The substrates of memory: defects, treatments, and enhancement Lynch G; Rex CS; Chen LY; Gall CMEur J Pharmacol 2008[May]; 585 (1): 2-13Recent work has added strong support to the long-standing hypothesis that the stabilization of both long-term potentiation and memory requires rapid reorganization of the spine actin cytoskeleton. This development has led to new insights into the origins of cognitive disorders, and raised the possibility that a diverse array of memory problems, including those associated with diabetes, reflect disturbances to various components of the same mechanism. In accord with this argument, impairments to long-term potentiation in mouse models of Huntington's disease and in middle-aged rats have both been linked to problems with modulatory factors that control actin polymerization in spine heads. Complementary to the common mechanism hypothesis is the idea of a single treatment for addressing seemingly unrelated memory diseases. First tests of the point were positive: Brain-Derived Neurotrophic Factor (BDNF), a potent activator of actin signaling cascades in adult spines, rescued potentiation in Huntington's disease mutant mice, middle-aged rats, and a mouse model of Fragile-X syndrome. A similar reversal of impairments to long-term potentiation was obtained in middle-aged rats by up-regulating BDNF production with brief exposures to ampakines, a class of drugs that positively modulate AMPA-type glutamate receptors. Work now in progress will test if chronic elevation of BDNF enhances memory in normal animals.|*Long-Term Potentiation[MESH]|*Memory Disorders/drug therapy/physiopathology[MESH]|Actins/physiology[MESH]|Aging/physiology[MESH]|Animals[MESH]|Brain-Derived Neurotrophic Factor/physiology[MESH]|Brain/physiopathology[MESH]|Cytoskeleton/physiology[MESH]|Dendritic Spines/physiology[MESH]|Fragile X Syndrome/physiopathology[MESH]|Humans[MESH]|Huntington Disease/physiopathology[MESH]|Learning/physiology[MESH]|Memory/drug effects/*physiology[MESH]|Nootropic Agents/pharmacology/therapeutic use[MESH]|Synapses/physiology[MESH] |
