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Long-term potentiation prevents ketamine-induced aberrant neurophysiological dynamics in the hippocampus-prefrontal cortex pathway in vivo.
Lopes-Aguiar, Cleiton; Ruggiero, Rafael N; Rossignoli, Matheus T; Esteves, Ingrid de Miranda; Peixoto-Santos, José Eduardo; Romcy-Pereira, Rodrigo N; Leite, João P.
Afiliação
  • Lopes-Aguiar C; Núcleo de Neurociências, Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, 31270-901, Brazil.
  • Ruggiero RN; Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, 14049-900, Brazil. rafaruggiero@usp.br.
  • Rossignoli MT; Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, 14049-900, Brazil.
  • Esteves IM; Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, 14049-900, Brazil.
  • Peixoto-Santos JE; Department of Neurology and Neurosurgery, UNIFESP, São Paulo, SP, 04039-032, Brazil.
  • Romcy-Pereira RN; Brain Institute, Federal University of Rio Grande do Norte, Natal, RN, 59056-450, Brazil.
  • Leite JP; Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, 14049-900, Brazil.
Sci Rep ; 10(1): 7167, 2020 04 28.
Article em En | MEDLINE | ID: mdl-32346044
N-methyl-D-aspartate receptor (NMDAr) antagonists such as ketamine (KET) produce psychotic-like behavior in both humans and animal models. NMDAr hypofunction affects normal oscillatory dynamics and synaptic plasticity in key brain regions related to schizophrenia, particularly in the hippocampus and the prefrontal cortex. It has been shown that prior long-term potentiation (LTP) occluded the increase of synaptic efficacy in the hippocampus-prefrontal cortex pathway induced by MK-801, a non-competitive NMDAr antagonist. However, it is not clear whether LTP could also modulate aberrant oscillations and short-term plasticity disruptions induced by NMDAr antagonists. Thus, we tested whether LTP could mitigate the electrophysiological changes promoted by KET. We recorded HPC-PFC local field potentials and evoked responses in urethane anesthetized rats, before and after KET administration, preceded or not by LTP induction. Our results show that KET promotes an aberrant delta-high-gamma cross-frequency coupling in the PFC and an enhancement in HPC-PFC evoked responses. LTP induction prior to KET attenuates changes in synaptic efficiency and prevents the increase in cortical gamma amplitude comodulation. These findings are consistent with evidence that increased efficiency of glutamatergic receptors attenuates cognitive impairment in animal models of psychosis. Therefore, high-frequency stimulation in HPC may be a useful tool to better understand how to prevent NMDAr hypofunction effects on synaptic plasticity and oscillatory coordination in cortico-limbic circuits.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Córtex Pré-Frontal / Potenciação de Longa Duração / Disfunção Cognitiva / Hipocampo / Ketamina Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Sci Rep Ano de publicação: 2020 Tipo de documento: Article País de afiliação: Brasil País de publicação: Reino Unido
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Córtex Pré-Frontal / Potenciação de Longa Duração / Disfunção Cognitiva / Hipocampo / Ketamina Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Sci Rep Ano de publicação: 2020 Tipo de documento: Article País de afiliação: Brasil País de publicação: Reino Unido