Susceptibility to Aβo and TBOA of LTD and Extrasynaptic NMDAR-Dependent Tonic Current in the Aged Rat Hippocampus.
Aging
Amino Acid Transport System X-AG
/ metabolism
Amyloid beta-Peptides
/ metabolism
Animals
Excitatory Postsynaptic Potentials
/ physiology
Hippocampus
/ metabolism
Long-Term Potentiation
/ physiology
Neuronal Plasticity
/ physiology
Rats, Sprague-Dawley
Receptors, Metabotropic Glutamate
/ metabolism
Receptors, N-Methyl-D-Aspartate
/ metabolism
Aging
Alzheimer
Extracellular glutamate
NMDA receptors
Synaptic plasticity
Tonic current
Journal
Neurochemical research
ISSN: 1573-6903
Titre abrégé: Neurochem Res
Pays: United States
ID NLM: 7613461
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
30
04
2018
accepted:
02
11
2018
revised:
26
10
2018
pubmed:
15
11
2018
medline:
8
5
2019
entrez:
15
11
2018
Statut:
ppublish
Résumé
Aging, as the major risk factor of Alzheimer's disease (AD), may increase susceptibility to neurodegenerative diseases through many gradual molecular and biochemical changes. Extracellular glutamate homeostasis and extrasynaptic glutamate N-methyl-D-aspartate receptors (NMDAR) are among early synaptic targets of oligomeric amyloid β (Aβo), one of the AD related synaptotoxic protein species. In this study, we asked for the effects of Aβo on long-term depression (LTD), a form of synaptic plasticity dependent on extrasynaptic NMDAR activation, and on a tonic current (TC) resulting from the activation of extrasynaptic NMDAR by ambient glutamate in hippocampal slices from young (3-6-month-old) and aged (24-28-month-old) Sprague-Dawley rats. Aβo significantly enhanced the magnitude of LTD and the amplitude of TC in aged slices compared to young ones. TBOA, a glutamate transporter inhibitor, also significantly increased LTD magnitude and TC amplitude in slices from aged rats, suggesting either an age-related weakness of the glutamate clearance system and/or a facilitated extrasynaptic NMDAR activation. From our present data, we hypothesize that senescence-related impairment of the extrasynaptic environment may be a vector of vulnerability of the aged hippocampus to neurodegenerative promotors such as Aβo.
Identifiants
pubmed: 30426348
doi: 10.1007/s11064-018-2677-6
pii: 10.1007/s11064-018-2677-6
doi:
Substances chimiques
Amino Acid Transport System X-AG
0
Amyloid beta-Peptides
0
Receptors, Metabotropic Glutamate
0
Receptors, N-Methyl-D-Aspartate
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
692-702Références
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