Estudo dos efeitos da exposição única à cocaína sobre o acoplamento oscilatório em circuitos hipocampo-corticais, arquitetura do sono e memória em ratos.

• Ano de defesa: 2020
• Autor(a) principal: Alan Patrick Silva Gusmão
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais
• Palavras-chave em Português: Neurociência; Cocaína; Sono; Córtex pré-frontal; Hipocampo; Eletrofisiologia; Memória; Córtex Pré-Frontal
• Link de acesso: https://hdl.handle.net/1843/34004

Cocaine, a drug with high potential for abuse, can produce persistent changes in networks responsible for reward and memory processing, such as medial prefrontal cortex (mPFC), ventral tegmental area, hippocampus, nucleus accumbens, among others, which can lead to addiction. The effects induced by cocaine during sleep can be fundamental to understand how memory traces related to the use of this substance are established in a lasting way in associative cortical networks. Our study tested whether a single exposure to cocaine is able to persistently affect oscillatory patterns and coordination between CA1 and mPFC during sleep. In addition, we tested whether such electrophysiological changes are: (1) dose-dependent and (2) associated with impaired memory consolidation. Adult Wistar male rats were chronically implanted with electrodes in the mPFC and CA1 subfield of the hippocampus for extracellular records of local field potentials. One week later, the animals were habituated to the recording chamber and, on the following day, to the first recording session (day 1). On day 2, immediately after the training session in the task of object-location memory task (OLM), animals received a systemic injection of 0.9% saline (SAL), cocaine 2.5 mg/kg (COCA-2.5) or cocaine 15 mg/kg (COCA-15), and underwent to a recording session. On the third day, the animals were submitted to the OLM test and electrophysiological records. Both the COCA-2.5 and COCA-15 groups showed increased latency for sleep onset. During the awake state, we observed an increase in coherence between CA1 and mPFC in the theta frequency band (7-9 Hz) when comparing the COCA-15 and SAL groups. Surprisingly, the theta-phase - fast gamma amplitude (100-140 Hz) coupling in CA1 decreased during the first three hours after COCA-15. After this initial effect, we observed an increase in delta power (1-4 Hz) in both CA1 and mPFC during slow-wave sleep in both groups treated with COCA (2,5 and 15) compared to the SAL group. This rebound effect was associated with an increase in the incidence of hippocampal ripple events (140-220 Hz) only in the COCA-15 group. Treatment with COCA-2.5 was able to induce an increase in delta power only in mPFC, but not in CA1, suggesting that these regions are differentially modulated by hyperdopaminergic state. Despite the diversity of reported effects, all parameters evaluated in this study returned to baseline conditions 24 h after treatment. Finally, we did not see any significant effects induced by COCA on memory consolidation in OLM task. In conclusion, our study demonstrated that cocaine is able to affect oscillatory patterns and the coordination of hippocampal-cortical networks in a dose-dependent and transitory manner without affecting the formation of object location memories.