Adenosine A_2A Receptor Up-Regulation Pre-Dates Deficits of Synaptic Plasticity and of Memory in Mice Exposed to Aβ_1-42 to Model Early Alzheimer's Disease.

ABSTRACT: The intracerebroventricular (icv) injection of amyloid peptides (Aβ) models Alzheimer's disease (AD) in mice, as typified by the onset within 15 days of deficits of memory and of hippocampal long-term potentiation (LTP) that are prevented by the blockade of adenosine A_2A receptors (A_2AR). Since A_2AR overfunction is sufficient to trigger memory deficits, we tested if A_2AR were upregulated in hippocampal synapses before the onset of memory deficits to support the hypothesis that A_2AR overfunction could be a trigger of AD. Six to eight days after Aβ-icv injection, mice displayed no alterations of hippocampal dependent memory; however, they presented an increased excitability of hippocampal synapses, a slight increase in LTP magnitude in S

SUBMITTER: Lopes CR 

PROVIDER: S-EPMC10452250 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature