Abstract:
:Memory reactivation has been shown to open a time window for memory modulation. The majority of the methodological or pharmacological approaches target disruption of reconsolidation to weaken aversive memories. However, methods to improve appetitive memory persistence through reconsolidation or to reverse drug-induced reconsolidation impairment are limited. To improve memory persistence, previous studies show that a novel event, introduced around the time of memory encoding, enables the persistence of an otherwise decayed memory. This is mainly through a memory consolidation process. The current study first investigated if a novel event introduced during memory reactivation improves memory persistence through reconsolidation. Using a rodent appetitive spatial paradigm, similar to the human everyday experience of recalling where an item is located, a novel event around memory reactivation facilitated the persistence of spatial memory. This facilitation did not occur when the novel event was omitted and the protein synthesis-dependent reconsolidation was not affected by zif268 anti-sense in the dorsal hippocampus. Furthermore, beta-adrenergic antagonists, propranolol, impaired reconsolidation of appetitive spatial memory and contextual fear conditioning. A novel event after memory reactivation could reverse this impairment due to propranolol. Together, this study provides methods and confirmation for improving memory persistence during memory reactivation and reconsolidation.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Wang SHdoi
10.1016/j.neuropharm.2018.08.015subject
Has Abstractpub_date
2018-10-01 00:00:00pages
42-54eissn
0028-3908issn
1873-7064pii
S0028-3908(18)30521-5journal_volume
141pub_type
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