Consolidated memories can return to a labile state if they are reactivated by unpredictable reminders. To persist, active memories must be re-stabilized through a process known as reconsolidation. Although there is consistent behavioral evidence about this process in humans, the retrieval process of reconsolidated memories remains poorly understood. In this context, one fundamental question is whether the same or different neurophysiological mechanisms are involved in retrieval of consolidated and reconsolidated memories. Because it has been demonstrated that the exposure to the reconsolidation process may restructure and strengthen memories, we hypothesized distinct neurophysiological patterns during retrieval of reconsolidated memories. In addition, we hypothesized that interfering with the reconsolidation process using a new learning can prevent these neurophysiological changes. To test it, consolidated, reconsolidated and declarative memories whose reconsolidation process was interfered (i.e., picture-word pairs) were evaluated in humans in an old/new associative recall task while the brain activity and the pupillary response were recorded using electroencephalography and eyetracking. Our results showed that retrieval of reconsolidated memories elicits specific patterns of brain activation, characterized by an earlier peak latency and a smaller magnitude of the left parietal ERP old/new effect compared to memories that were only consolidated or whose reconsolidation process was interfered by a new learning. Moreover, our results demonstrated that only retrieval of reconsolidated memories is associated with a late reversed mid-frontal effect in a 600-690 time window. Complementarily, memories that were reactivated showed an earlier peak latency of the pupil old/new effect compared to non-reactivated memories. These findings support the idea that reconsolidation has an important impact in how memories are retrieved in the future, showing that retrieval of reconsolidated memories is partially supported by specific brain mechanisms.
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http://dx.doi.org/10.1016/j.nlm.2020.107279 | DOI Listing |
Prog Neuropsychopharmacol Biol Psychiatry
January 2025
Department of Pharmacology, Federal University of Parana, Curitiba, Parana, Brazil. Electronic address:
Fear generalization, a lack of discrimination between safe and unsafe cues, is a hallmark of posttraumatic stress disorder. The phosphodiesterase 5 (PDE5) regulates the cyclic guanosine monophosphate (cGMP) pathway, which has been proposed to be involved in fear memory generalization. However, whether PDE5 activity underlies fear memory generalization remains unexplored.
View Article and Find Full Text PDFClin Neuroradiol
January 2025
Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran.
Background: Hypertension (HTN) is a prevalent cardiovascular condition associated with cognitive impairments, including memory deficits and attention lapses. Understanding the neural mechanisms underlying HTN-related cognitive dysfunction is crucial for optimizing treatment strategies.
Method: A systematic review was conducted to explore the impact of antihypertensive medications on cognition, focusing on memory, attention, and emotion processing using functional magnetic resonance imaging (fMRI).
Vision Res
January 2025
School of Psychological and Cognitive Sciences, and Beijing Key Laboratory of Behavior and Mental Health, Peking University, Beijing, China. Electronic address:
Visual perceptual learning often requires a substantial number of trials to observe significant learning effects. Previously Amar-Halpert et al. (2017) have shown that brief reactivation (5 trials/day) is sufficient to improve the performance of the texture discrimination task (TDT), yielding comparable improvements to those achieved through full practice (252 trials/day).
View Article and Find Full Text PDFNeuropsychopharmacology
January 2025
Department of Psychiatry, Oxford University, Warneford Hospital, Oxford, UK.
There is an ongoing need to identify novel pharmacological agents for the effective treatment of depression. One emerging candidate, which has demonstrated rapid-acting antidepressant effects in treatment-resistant groups, is nitrous oxide (NO)-a gas commonly used for sedation and pain management in clinical settings and with a range of pharmacological effects, including antagonism of NMDA glutamate receptors. A growing body of evidence suggests that subanaesthetic doses of NO (50%) can interfere with the reconsolidation of maladaptive memories in healthy participants and across a range of disorders.
View Article and Find Full Text PDFMed Gas Res
June 2025
McLean Hospital, Harvard Medical School, Belmont, MA, USA.
Xenon gas is considered to be a safe anesthetic and imaging agent. Research on its other potentially beneficial effects suggests that xenon may have broad efficacy for treating health disorders. A number of reviews on xenon applications have been published, but none have focused on substance use disorders.
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