Dataset Information

The time window of reconsolidation: A replication.

ABSTRACT: Reconsolidation is a process by which a consolidated memory that has been destabilized by reactivation is updated, strengthened, or weakened by the restabilization of the trace. A critical assumption of the reconsolidation theory is that reconsolidation is a time-dependent process. Hupbach, Gomez, Hardt, and Nadel (2007, Learning & Memory, 14, 47-53) conducted a set of experiments demonstrating that memory updating is only found when the reconsolidation process has time to complete. This finding strengthens reconsolidation theory and poses a challenge to other accounts of memory updating (e.g., context and interference accounts). Because this finding is so critical to the reconsolidation theory, we attempted to directly replicate these experiments, which showed memory updating in a 3-day paradigm (when reconsolidation has time to complete), but not in a 2-day paradigm (when reconsolidation does not have time to complete). We replicated these results, thereby bolstering the reconsolidation theory of memory updating.

SUBMITTER: Parks CM

PROVIDER: S-EPMC9012516 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

The time window of reconsolidation: A replication.

Parks Colleen M CM Mohawk Kevin D KD Werner Laura L S LLS Kiley Christopher C

Psychonomic bulletin & review 20220415 5

Reconsolidation is a process by which a consolidated memory that has been destabilized by reactivation is updated, strengthened, or weakened by the restabilization of the trace. A critical assumption of the reconsolidation theory is that reconsolidation is a time-dependent process. Hupbach, Gomez, Hardt, and Nadel (2007, Learning & Memory, 14, 47-53) conducted a set of experiments demonstrating that memory updating is only found when the reconsolidation process has time to complete. This finding ...[more]

PMID: 35428932

Similar Datasets

Project description:Nair2016 - Integration of calcium and dopamine signals by D1R-expressing medium-sized spiny neurons This model is described in the article: Role of DARPP-32 and ARPP-21 in the Emergence of Temporal Constraints on Striatal Calcium and Dopamine Integration. Nair AG, Bhalla US, Hellgren Kotaleski J. PLoS Comput. Biol. 2016 Sep; 12(9): e1005080 Abstract: In reward learning, the integration of NMDA-dependent calcium and dopamine by striatal projection neurons leads to potentiation of corticostriatal synapses through CaMKII/PP1 signaling. In order to elicit the CaMKII/PP1-dependent response, the calcium and dopamine inputs should arrive in temporal proximity and must follow a specific (dopamine after calcium) order. However, little is known about the cellular mechanism which enforces these temporal constraints on the signal integration. In this computational study, we propose that these temporal requirements emerge as a result of the coordinated signaling via two striatal phosphoproteins, DARPP-32 and ARPP-21. Specifically, DARPP-32-mediated signaling could implement an input-interval dependent gating function, via transient PP1 inhibition, thus enforcing the requirement for temporal proximity. Furthermore, ARPP-21 signaling could impose the additional input-order requirement of calcium and dopamine, due to its Ca2+/calmodulin sequestering property when dopamine arrives first. This highlights the possible role of phosphoproteins in the temporal aspects of striatal signal transduction. This model is hosted on BioModels Database and identified by: MODEL1603270000. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:BackgroundRetinal ganglion cell (RGC) degeneration and death cause vision loss in patients with glaucoma. Regulated cell death, once initiated, is generally considered to be an irreversible process. Recently, we showed that, by timely removing the cell death stimulus, stressed neuronal PC12 cells can recover from phosphatidylserine (PS) exposure, nuclear shrinkage, DNA damage, mitochondrial fragmentation, mitochondrial membrane potential loss, and retraction of neurites, all hallmarks of an activated cell death program. Whether the cell death process can be reversed in neurons of the central nervous system, like RGCs, is still unknown. Here, we studied reversibility of the activated cell death program in primary rat RGCs (prRGCs).MethodsprRGCs were exposed to ethanol (5%, vol/vol) to induce cell death. At different stages of the cell death process, ethanol was removed by washing and injured prRGCs were further cultured in fresh medium to see whether they recovered. The dynamics of single cells were monitored by high-resolution live-cell spinning disk microscopy. PS exposure, mitochondrial structure, membrane potential, and intracellular Ca2+ were revealed by annexin A5-FITC, Mito-tracker, TMRM, and Fluo 8-AM staining, respectively. The distribution of cytochrome c was investigated by immunofluorescence. The ultrastructure of mitochondria was studied by electron microscopy.ResultsAnalysis of temporal relationships between mitochondrial changes and PS exposure showed that fragmentation of the mitochondrial network and loss of mitochondrial membrane potential occurred before PS exposure. Mitochondrial changes proceeded caspase-independently, while PS exposure was caspase dependent. Interestingly, prRGCs recovered quickly from these mitochondrial changes but not from PS exposure at the plasma membrane. Correlative light and electron microscopy showed that stress-induced decrease in mitochondrial area, length and cristae number was reversible. Intracellular Ca2+ was elevated during this stage of reversible mitochondrial injury, but there was no sign of mitochondrial cytochrome c release.ConclusionsOur study demonstrates that RGCs with impaired mitochondrial structure and function can fully recover if there is no mitochondrial cytochrome c release yet, and no PS is exposed at the plasma membrane. This finding indicates that there is a time window for rescuing dying or injured RGCs, by simply removing the cell death stimulus. Video Abstract.

Dataset Information

The time window of reconsolidation: A replication.

Publications

The time window of reconsolidation: A replication.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets