ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023
Progressive Excitability Changes in the Medial Entorhinal Cortex in the 3xTg Mouse Model of Alzheimer's Disease Pathology.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 17 citations in OpenAlex.
- Multimodal MRI combined with RNA sequencing reveals pathological signatures in the 9-month-old 3×Tg-AD mouse brain.Neural regeneration research · 2026Article
- Medial entorhinal-hippocampal desynchronization parallels the emergence of memory impairment in a mouse model of Alzheimer's disease pathology.Cell reports · 2026Article
- Coordinating Cognition: The Entorhinal Cortex in Mnemonic, Temporal and Spatial Representation.Cells · 2026Review
- A novel PGK1 activator improves Alzheimer's disease by regulating glycolysis.Alzheimer's research & therapy · 2026Article
- Aberrant medial entorhinal cortex dynamics link tau pathology to spatial memory impairment.bioRxiv : the preprint server for biology · 2026Article
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Exercise and neural circuit stability in early Alzheimer's disease: evidence across memory, executive, cholinergic, and circadian systems.Frontiers in aging neuroscience · 2026Review
- Inhibition of the GSK3β/Nav1.6 complex suppresses early-stage Alzheimer's hyperexcitability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Sex and region-specific disruption of autophagy and mitophagy in Alzheimer's disease: linking cellular dysfunction to cognitive decline.Cell death discovery · 2025Article
- Selective vulnerability of stellate cells to gut dysbiosis: neuroanatomical changes in the medial entorhinal cortex.Frontiers in neuroanatomy · 2025Article
- Ryanodex Reduces Persistent Hippocampal Effects of Single Mild Traumatic Brain Injury in Rats.Neurotrauma reports · 2025Article
- Article
- Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.Nature communications · 2024Article
- Projection neurons from medial entorhinal cortex to basolateral amygdala are critical for the retrieval of morphine withdrawal memory.iScience · 2024Article
- Impairment of entorhinal cortex network activity in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Serial reversal learning in an olfactory discrimination task in 3xTg-AD mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2023Article
- Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.Research square · 2023Article
- Chronotate: An open-source tool for manual timestamping and quantification of animal behavior.Neuroscience letters · 2023Article
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12 authors at 4 institutions in 1 country.
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Abstract
Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by memory loss and progressive cognitive impairments. In mouse models of AD pathology, studies have found neuronal and synaptic deficits in hippocampus, but less is known about changes in medial entorhinal cortex (MEC), which is the primary spatial input to the hippocampus and an early site of AD pathology. Here, we measured neuronal intrinsic excitability and synaptic activity in MEC layer II (MECII) stellate cells, MECII pyramidal cells, and MEC layer III (MECIII) excitatory neurons at 3 and 10 months of age in the 3xTg mouse model of AD pathology, using male and female mice. At 3 months of age, before the onset of memory impairments, we found early hyperexcitability in intrinsic properties of MECII stellate and pyramidal cells, but this was balanced by a relative reduction in synaptic excitation (E) compared with inhibition (I; E/I ratio), suggesting intact homeostatic mechanisms regulating MECII activity. Conversely, MECIII neurons had reduced intrinsic excitability at this early time point with no change in synaptic E/I ratio. By 10 months of age, after the onset of memory deficits, neuronal excitability of MECII pyramidal cells and MECIII excitatory neurons was largely normalized in 3xTg mice. However, MECII stellate cells remained hyperexcitable, and this was further exacerbated by an increased synaptic E/I ratio. This observed combination of increased intrinsic and synaptic hyperexcitability suggests a breakdown in homeostatic mechanisms specifically in MECII stellate cells at this postsymptomatic time point, which may contribute to the emergence of memory deficits in AD.
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