Intrinsic hypoexcitability of thalamic nucleus reuniens inputs to hippocampal CA1 in the 5xFAD mouse model of amyloidosis

Excitatory flow from nRT to CA1 is reduced in the setting of amyloidosis due to reduced intrinsic low threshold burst and spike firing within the nRT. In contrast, the relative stability of nRT→CA1 synapse itself suggests that this pathway may serve as a salvage mechanism to excite distal CA1 dendrites in the setting of compromised EC→CA1 excitation.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70855_106177
Primary Topic
Neuroscience and Neuropharmacology Research
Type
article
Field-Weighted Citation Impact
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article

Intrinsic hypoexcitability of thalamic nucleus reuniens inputs to hippocampal CA1 in the 5xFAD mouse model of amyloidosis

Arjun V. Masurkar, Isabel Reyes, Chengju Tian, Mohankumar Thangavel
Alzheimer s & Dementia
Neuroscience and Neuropharmacology Research
article

Intrinsic hypoexcitability of thalamic nucleus reuniens inputs to hippocampal CA1 in the 5xFAD mouse model of amyloidosis

Arjun V. Masurkar, Isabel Reyes, Chengju Tian, Mohankumar Thangavel
article en

Abstract

Excitatory flow from nRT to CA1 is reduced in the setting of amyloidosis due to reduced intrinsic low threshold burst and spike firing within the nRT. In contrast, the relative stability of nRT→CA1 synapse itself suggests that this pathway may serve as a salvage mechanism to excite distal CA1 dendrites in the setting of compromised EC→CA1 excitation.

Alzheimer s & DementiaVol. 21(S1)
New York University (US)
Gender equality
Openalex Percentile: Top 37%
Neuroscience and Neuropharmacology Research
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