On the participation of adenosinergic receptors in the reconsolidation of spatial long-term memory in male rats

  1. Weber Cláudio da Silva1,2
  1. 1Laboratório de Neuropsicofarmacologia, Departamento de Farmácia, Universidade Estadual do Centro-Oeste, Guarapuava, Paraná 85040-167, Brasil
  2. 2Programa de Pós-Graduação em Ciências Biológicas: Fisiologia, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul 90035-003, Brasil
  3. 3Laboratório de Neurociências e Comportamento, Departamento de Farmácia, Universidade Estadual do Centro-Oeste, Guarapuava, Paraná 85040-167, Brasil
  1. Corresponding author: wwwclaudion{at}gmail.com

Abstract

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.

Footnotes

  • Received April 22, 2023.
  • Accepted August 9, 2023.

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