NMDA receptor activity bidirectionally controls active decay of long‐term spatial memory in the dorsal hippocampus

Migues, Paola V.; Wong, Jacinda; Lyu, Jeongho; Hardt, Oliver

doi:10.1002/hipo.23096

Cited by 13 publications

(8 citation statements)

References 31 publications

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“…In the hippocampus, different modes of neuron oscillations occur depending on the active state. They can be divided into five categories according to different frequencies: delta oscillation (1-4Hz), theta oscillation (4-8 Hz), alpha oscillation (8)(9)(10)(11)(12)(13), beta oscillation (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), and gamma oscillation (30-80 Hz). These rhythmic oscillations of the hippocampus are closely related to the behavior and physiological state of the hippocampus, are produced by specific mechanisms, and are related to the distribution characteristics of neurons, and participate in different brain functions independently or synergistically.…”

Section: Discussionmentioning

confidence: 99%

“…Since ketamine inhibits the neuronal activity by interfering the NMDA receptor, [2] [13] we were wondering whether interfering the NMDA receptor mediated the inhibitory effect of ketamine on hippocampal oscillation. Therefore, we added the (2R)-amino-5phosphonopentanoate (APV, 50 μM), an NMDA receptor antagonist, [14] with ketamine for bath application. We found that all the frequency bands were not affected by the ketamine with the concentration we chose (Fig.7A, B Fig.7B).…”

Section: Nmda Receptor May Be Not Essential For Ketamine Inhibiting Tmentioning

confidence: 99%

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Effects of Propofol and Ketamine on The Neural Oscillations in CA1 of Rat Intact Hippocampus

Zhang

Chen

et al. 2020

Preprint

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In this study, in vitro intact hippocampal preparation model was utilized to observe the effects of propofol and ketamine on the neural oscillations in CA1 of rat hippocampus. The intact hippocampi were dissected from the brain tissues of rats aged 14-16 days postnatal. Local field potential (LFP) recordings were performed with propofol and ketamine bath application at different concentrations. The power spectrum intensity of LFP in all the frequency bands, including delta (1-4 Hz), theta (4-8 Hz), alpha (8-13 Hz), beta (13-30 Hz) and gamma (30-80 Hz), were inhibited in a concentrationdependent manner by both general anesthetics. In order to further investigate the underlying mechanisms, the major binding site of propofol and ketamine were blocked respectively by picrotoxin and (2R)-amino-5-phosphonopentanoate when bath applying the general anesthetics. It revealed that the inhibitory effect of propofol on hippocampal oscillations might be via γ-aminobutyric acid A receptor, while the inhibitory effect of ketamine might be unconcerned with N-methyl-D-aspartic acid receptor.

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Section: Discussionmentioning

confidence: 99%

Section: Nmda Receptor May Be Not Essential For Ketamine Inhibiting Tmentioning

confidence: 99%

Effects of Propofol and Ketamine on The Neural Oscillations in CA1 of Rat Intact Hippocampus

Zhang

Chen

et al. 2020

Preprint

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“…In their work, rats were trained in an object location task and were locally infused with different NMDAR‐blockers in the hippocampus during the retention window (up to a few days after learning). Blocking GluN2B‐NMDARs (with the antagonist Ro25‐6981) decreased forgetting as compared to controls (Migues, Wong, Lyu, & Hardt, 2019). These behavioral studies support the idea that GluN2B‐NMDARs might play a direct role in promoting forgetting.…”

Section: Proposed Molecular Mechanisms Underlying Forgettingmentioning

confidence: 98%

Molecular mechanisms of forgetting

Moreno

2020

Eur J of Neuroscience

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While every culture has attributed different meanings to forgetting throughout history (Eliade, 1963), it was not until the late nineteenth century that it started to attract the attention of the scientific community (e.g., Ebbinghaus, 1885). It still remains one of the least studied phenomena within the field of learning and memory. However, during the last years, an increasing number of publications have addressed the study of forgetting from different perspectives-ranging from genetic manipulations of fruit flies to in vivo electrophysiological studies in rodents. A number of these publications have proposed an actively modulated forgetting network with dedicated machinery as the primary molecular mechanism for forgetting. This review considers the molecules allegedly involved in forgetting and memory decay and integrates them into a common framework. Despite there being excellent reviews on the topic of forgetting (Bauer

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“…The aim of the current experiments was to determine whether reducing sensory stimulation after encoding would also enhance hippocampus-dependent memory in rats. To do this, we used a spontaneous object exploration task that assesses memory for object locations (Ennaceur and Delacour 1988;Hardt et al 2010;Migues et al 2016Migues et al , 2019. Using this approach, we replicated in rats the basic effect that quiet wakefulness promotes memory retention as previously observed in humans.…”

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confidence: 92%

The Black Box effect: sensory stimulation after learning interferes with the retention of long-term object location memory in rats

et al. 2021

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Reducing sensory experiences during the period that immediately follows learning improves long-term memory retention in healthy humans, and even preserves memory in patients with amnesia. To date, it is entirely unclear why this is the case, and identifying the neurobiological mechanisms underpinning this effect requires suitable animal models, which are currently lacking. Here, we describe a straightforward experimental procedure in rats that future studies can use to directly address this issue. Using this method, we replicated the central findings on quiet wakefulness obtained in humans: We show that rats that spent 1 h alone in a familiar dark and quiet chamber (the Black Box) after exploring two objects in an open field expressed long-term memory for the object locations 6 h later, while rats that instead directly went back into their home cage with their cage mates did not. We discovered that both visual stimulation and being together with conspecifics contributed to the memory loss in the home cage, as exposing rats either to light or to a cage mate in the Black Box was sufficient to disrupt memory for object locations. Our results suggest that in both rats and humans, everyday sensory experiences that normally follow learning in natural settings can interfere with processes that promote long-term memory retention, thereby causing forgetting in form of retroactive interference. The processes involved in this effect are not sleep-dependent because we prevented sleep in periods of reduced sensory experience. Our findings, which also have implications for research practices, describe a potentially useful method to study the neurobiological mechanisms that might explain why normal sensory processing after learning impairs memory both in healthy humans and in patients suffering from amnesia.

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NMDA receptor activity bidirectionally controls active decay of long‐term spatial memory in the dorsal hippocampus

Cited by 13 publications

References 31 publications

Effects of Propofol and Ketamine on The Neural Oscillations in CA1 of Rat Intact Hippocampus

Effects of Propofol and Ketamine on The Neural Oscillations in CA1 of Rat Intact Hippocampus

Molecular mechanisms of forgetting

The Black Box effect: sensory stimulation after learning interferes with the retention of long-term object location memory in rats

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