Memory destabilization during reconsolidation: a consequence of homeostatic plasticity?

被引:0
|
作者
Amorim, Felippe E. [1 ]
Chapot, Renata L. [1 ]
Moulin, Thiago C. [2 ]
Lee, Jonathan L. C. [3 ]
Amaral, Olavo B. [1 ]
机构
[1] Univ Fed Rio de Janeiro, Inst Med Biochem Leopoldo de Meis, BR-21941902 Rio De Janeiro, Brazil
[2] Uppsala Univ, Dept Neurosci, Funct Pharmacol Unit, S-75124 Uppsala, Sweden
[3] Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England
关键词
LONG-TERM DEPRESSION; UBIQUITIN-PROTEASOME SYSTEM; PROTEIN-SYNTHESIS; FEAR MEMORY; SYNAPTIC PLASTICITY; NMDA RECEPTORS; MOLECULAR-MECHANISMS; INHIBITORY SYNAPSES; DORSAL HIPPOCAMPUS; IDENTIFIED SYNAPSE;
D O I
10.1101/lm.053418.121
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Remembering is not a static process: When retrieved, a memory can be destabilized and become prone to modifications. This phenomenon has been demonstrated in a number of brain regions, but the neuronal mechanisms that rule memory destabilization and its boundary conditions remain elusive. Using two distinct computational models that combine Hebbian plasticity and synaptic downscaling, we show that homeostatic plasticity can function as a destabilization mechanism, accounting for behavioral results of protein synthesis inhibition upon reactivation with different re-exposure times. Furthermore, by performing systematic reviews, we identify a series of overlapping molecular mechanisms between memory destabilization and synaptic downscaling, although direct experimental links between both phenomena remain scarce. In light of these results, we propose a theoretical framework where memory destabilization can emerge as an epiphenomenon of homeostatic adaptations prompted by memory retrieval.
引用
收藏
页码:371 / 389
页数:19
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