期刊
EUROPEAN JOURNAL OF NEUROSCIENCE
卷 55, 期 1, 页码 78-90出版社
WILEY
DOI: 10.1111/ejn.15568
关键词
CA1; dopaminergic system; neuromodulation; novel object recognition
资金
- Unipampa/Brazil
- CNPq/Brazil
- CAPES/Brazil
- Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
- Federal University of Pampa
- Federal University of Rio Grande do Sul
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior
This study demonstrated that exposure to novelty and activation of D1Rs can promote memory persistence in rats, with this effect depending on the activation of the PKA pathway.
Strategies for improving memory are increasingly studied, and exposure to a novel experience can be an efficient neuromodulator. Novelty effects on memory depend on D1-family dopamine receptors (D1Rs) activation. Here, we evaluated the novelty effect on memory persistence of Wistar rats and investigated the contribution of D1Rs and their signalling pathways by protein kinase A (PKA) and C (PKC). Animals with infusion cannulae inserted into the CA1 hippocampus area were trained on the novel object recognition (NOR) task, which involved exploring two different objects. After training, some rats received intrahippocampal infusions of vehicle or D1Rs agonist; others explored a novel environment for 5 min and were infused with a variety of drugs targeting D1Rs and their signalling pathways. We demonstrated that pharmacological stimulation of D1Rs or novelty exposure promoted NOR memory persistence for 14 days and that the novelty effect depended on D1Rs activation. To determine if the D1 and D5 receptor subtypes were necessary for the impact of novelty exposure on memory, we blocked or stimulated PKA or PKC-protein kinases activated mainly by D1 and D5, respectively. Only PKA inhibition impaired the effect of novelty on memory persistence. After novelty and D1Rs blocking, PKA but not PKC stimulation maintained the memory persistence effect. Thus, we concluded that novelty promoted memory persistence by a mechanism-dependent on activating hippocampal D1Rs and PKA pathway.
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