To date, there is insufficient evidence to explain the role of adenosinergic receptors in the reconsolidation of long-term spatial memory. In this work, the role of the adenosinergic receptor family (A1, A2A, A2B, and A3) in this process has been elucidated. It was demonstrated that when infused bilaterally into the hippocampal CA1 region immediately after an early nonreinforced test session performed 24 h posttraining in the Morris water maze task, adenosine can cause anterograde amnesia for recent and late long-term spatial memory. This effect on spatial memory reconsolidation was blocked by A1 or A3 receptor antagonists and mimicked by A1 plus A3 receptor agonists, showing that this effect occurs through A1 and A3 receptors simultaneously. The A3 receptor alone participates only in the reconsolidation of late long-term spatial memory. When the memory to be reconsolidated was delayed (reactivation 5 d posttraining), the amnesic effect of adenosine became transient and did not occur in a test performed 5 d after the reactivation of the mnemonic trace. Finally, it has been shown that the amnesic effect of adenosine on spatial memory reconsolidation depends on the occurrence of protein degradation and that the amnesic effect of inhibition of protein synthesis on spatial memory reconsolidation is dependent on the activation of A3 receptors.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10561635 | PMC |
http://dx.doi.org/10.1101/lm.053785.123 | DOI Listing |
Neuromolecular Med
December 2024
Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, 410012, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The neuropathology of AD appears in the hippocampus. The purpose of this work was to reveal key differentially expressed genes (DEGs) in the hippocampus of AD patients and healthy individuals.
View Article and Find Full Text PDFAging Dis
December 2024
Central Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China.
Vascular cognitive impairment and dementia (VCID), resulting from chronic cerebral hypoperfusion, represent the second most prevalent form of dementia globally. Aerobic exercise is widely acknowledged as an effective intervention for various cognitive disorders. This study utilized a bilateral common carotid artery stenosis (BCAS) model to investigate whether aerobic exercise promotes cognitive recovery through the Annexin-A1 (ANXA1)/mitogen-activated protein kinase (MAPK) axis in BCAS mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Sapienza University of Rome, Rome, Rome, Italy.
Background: Biological sex influences Alzheimer's disease (AD) development, particularly concerning brain insulin resistance (bIR) and early energy metabolism defects. Biliverdin reductase-A (BVR-A) plays a crucial role in insulin signaling, and its downregulation leads to bIR. However, the sex-related differences in AD neuropathology and underlying mechanisms remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Background: Alzheimer's disease (AD) is the most common tauopathy and characterized by the progressive accumulation of Aß and tau. Tau is expressed in two major isoforms containing either 3 or 4 c-terminal repeats labeled as 3R and 4R tau. While these two isoforms occur in roughly equimolar ratios in AD, most research focus and mouse models of tau center only the 4Rtau protein and not 3Rtau.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
Background: Soluble Aβ oligomers (AβOs) induce synapse dysfunction, leading to cognitive impairment and memory deficits in Alzheimer's disease (AD). Our laboratory and several research groups characterized neurexin family members' physiological roles, pivotal synaptic adhesion molecules for development, plasticity, and maintenance. Beyond their normal functions, we found neurexins binding to AβOs causes AβO-induced neurexin dysregulation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!