Efeitos do canabigerol na memória contextual aversiva

Detalhes bibliográficos
Ano de defesa: 2024
Autor(a) principal: Julia Peres Andreotti
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Minas Gerais
Brasil
ICB - DEPARTAMENTO DE FARMACOLOGIA
Programa de Pós-Graduação em Neurociências
UFMG
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://hdl.handle.net/1843/77384
Resumo: Fear is a physiological response to noxious stimuli, and the formation of memories related to such aversive events protects us from future threats. Disruption of mechanisms involved in this process results in dysfunctional and maladaptive behaviors. There is a high demand for the development of new drugs that can act on the neural basis of this phenomenon. Substances from the herb Cannabis sativa, such as cannabidiol (CBD), have been extensively investigated. However, the effects of other phytocannabinoids, have remained under-investigated. Cannabigerol (CBG) is a phytocannabinoid that, similarly to CBD, does not induce psychotomimetic effects and targets multiple receptors, including those involved in fear-related pathways. The aim of this study was to teste the hypothesis that CBG inhibits the acquisition, consolidation and expression of contextual fear memories. Male and female C57BL/6J mice were submitted to contextual fear conditioning (CFC), and CBG (3, 10 or 30 mg/kg) was administered at different timepoints to assess its effect in each memory process. Our results demonstrate that CBG does not impair the acquisition, consolidation or expression of contextual fear memories. Because CFC relies on nociceptive stimuli (shocks), we also evaluated the effects of CBG on the tail-flick test. There was a major effect seen 30 min after injection only in females. CBG at 3 mg/kg increased the latency for withdrawal response, while the 30 mg/kg dose decreased it. Finally, the rota-rod test was performed to assess motor coordination, and no changes caused by CBG were observed. In summary, we did not observe any effects of CBG on CFC under this protocol and at the doses administered. Future experiments could investigate the role of this substance in different protocols, memory phases or aversive memory models.