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Cited by 17Neuroscience and Neuropharmacology ResearchEpilepsy research and treatmentMemory and Neural Mechanisms

Interplay of epilepsy and long-term potentiation: implications for memory

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Marin-Castañeda, Luis A., Pacheco Aispuro, Gerónimo, Gonzalez-Garibay, Guillermo, Martínez Zamora, Carlos Alejandro, Romo-Parra, Hector, Rubio-Osornio, Moisés, Rubio, Carmen·2025·Frontiers in Neuroscience
DOI 10.3389/fnins.2024.1451740PMC PMC11760605
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Abstract

The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy. This state is conceptualized as a dysregulation between LTP and LTD (Long-term depression), leading to pathologically enhanced synaptic efficacy. Additionally, the role of neuroinflammation in both LTP and epilepsy is examined, highlighting how inflammatory mediators can influence synaptic plasticity. The dual role of neuroinflammatory pathways, enhancing or inhibiting LTP, is a focal area of ongoing research. The significance of various signaling pathways, including the MAPK, mTOR, and WNT/β-catenin pathways, in the modulation of synaptic plasticity and their relevance in both LTP and epilepsy. These pathways are instrumental in memory formation, consolidation, and epileptogenesis, illustrating a complex interaction between cellular mechanisms in the nervous system. Lastly, the role of calcium signaling in the relationship between LTP and epilepsy is scrutinized. Aberrant calcium signaling in epilepsy leads to an enhanced, yet pathologically altered, LTP. This dysregulation disrupts normal neural pathways, potentially leading to cognitive dysfunction, particularly in memory encoding and retrieval. The review emphasizes the need for targeted interventions in epilepsy that address cognitive functions alongside seizure control.

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  • Spatial transcriptomics (Visium) has shown that in vivo conversion of astrocytes into neurons can reverse AD-associated signaling patterns, such as the increase in neuregulin signaling between neurons.

    “These models inform strategies like the in vivo conversion of astrocytes into neurons; spatial transcriptomics (Visium) has shown that this conversion can reverse AD-associated signaling patterns, such as the increase in neuregulin signaling between neurons [90,96].”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [96]

    The Neuroinflammatory pathway section discusses astrocyte signaling in long-term potentiation and epilepsy, but not astrocyte-to-neuron conversion in Alzheimer’s disease. Searches for Visium, neuregulin, and conversion or reprogramming found no passage addressing the claimed reversal of signaling patterns. (LLM, conf=0.78)

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Cited by

Sorted by citations

  • Molecular Physiology of the Neuronal Synapse

    Ramírez-Expósito, M. J., Cueto-Ureña, C., & Martínez-Martos, J. M. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48010088 · Cited by 6 · see citing works

    “These models inform strategies like the in vivo conversion of astrocytes into neurons; spatial transcriptomics (Visium) has shown that this conversion can reverse AD-associated signaling patterns, such as the increase in neuregulin signaling between neurons [90,96].”

Authors
Marin-Castañeda, L. A., Pacheco Aispuro, G., Gonzalez-Garibay, G., Martínez Zamora, C. A., Romo-Parra, H., Rubio-Osornio, M., & Rubio, C.
Affiliations
Instituto Nacional de Neurología y Neurocirugía (MX)
Corresponding author
Rubio, Carmen
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2025-01-10
Volume
18
Pages
1451740-1451740
ISSN
1662-453X (ISSN-L)
DOI
10.3389/fnins.2024.1451740
PMC
PMC11760605
OpenAlex
W4406253003
Cited by
17
References
2
Citations by year
2026: 10 · 2025: 7
FWCI
2.05
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
epilepsy, long-term potentiation, synaptic plasticity, long-term depression, hippocampus, memory, neuroinflammation, MAPK signaling, mTOR signaling, Wnt/β-catenin signaling, calcium signaling, epileptogenesis, cognitive impairment, hyperexcitability

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