Laboratório de Neurociências and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil.
Behav Brain Res. 2012 Aug 1;233(2):526-35. doi: 10.1016/j.bbr.2012.05.039. Epub 2012 May 31.
The present study was aimed at investigating the behavioral and molecular effects of tianeptine. To this aim, Wistar rats were treated with tianeptine (5, 10 and 15 mg/kg) or imipramine (30 mg/kg) acutely and chronically. The results showed that both treatments reduced the immobility time. The BDNF levels were increased in the prefrontal cortex with tianeptine and decreased in the nucleus accumbens after acute treatment; in chronic treatment, BDNF levels were increased in the prefrontal and hippocampus with tianeptine. Acute treatment decreased the citrate synthase activity in the prefrontal cortex with tianeptine, and increased it in the amygdala with imipramine; chronic treatment increased the citrate synthase in the hippocampus with tianeptine. The creatine kinase was increased in the prefrontal cortex with tianeptine and in the amygdala with imipramine after acute treatment; chronic treatment increased the creatine kinase activity in the hippocampus with imipramine and tianeptine. The complex I activity was decreased in the prefrontal cortex with imipramine and increased in the hippocampus with tianeptine. The other complexes were increased with imipramine and tianeptine at all doses, but were related to the treatment given and the brain area studied. Chronic treatment increased the malate dehydrogenase activity in the amygdala with tianeptine. Acute treatment decreased the succinate activity in the prefrontal cortex, hippocampus and amygdala with tianeptine; chronic treatment increased the succinate activity in the hippocampus with tianeptine at all doses. In conclusion, tianeptine exerted antidepressant-like behavior which can be attributed to its effects on pathways related to depression, such as BDNF and metabolism energy.
本研究旨在探讨噻奈普汀的行为和分子效应。为此，Wistar 大鼠急性和慢性给予噻奈普汀（5、10 和 15mg/kg）或丙咪嗪（30mg/kg）治疗。结果显示，两种治疗均减少了不动时间。BDNF 水平在前额叶皮质中升高，而在急性治疗后在伏隔核中降低；在慢性治疗中，BDNF 水平在前额叶和海马中升高。急性治疗降低了噻奈普汀治疗的前额叶皮质中的柠檬酸合酶活性，而丙咪嗪增加了杏仁核中的柠檬酸合酶活性；慢性治疗增加了噻奈普汀治疗的海马中的柠檬酸合酶。急性治疗中，噻奈普汀增加了前额叶皮质中的肌酸激酶，丙咪嗪增加了杏仁核中的肌酸激酶；慢性治疗增加了海马中的肌酸激酶，丙咪嗪和噻奈普汀均可增加。急性治疗中，丙咪嗪降低了前额叶皮质中的复合物 I 活性，而噻奈普汀增加了海马中的复合物 I 活性。其他复合物在所有剂量下均随丙咪嗪和噻奈普汀而增加，但与给予的治疗和研究的脑区有关。慢性治疗增加了噻奈普汀治疗的杏仁核中的苹果酸脱氢酶活性。急性治疗降低了噻奈普汀治疗的前额叶皮质、海马和杏仁核中的琥珀酸活性；慢性治疗增加了噻奈普汀在所有剂量下的海马中的琥珀酸活性。总之，噻奈普汀具有抗抑郁样行为，这可归因于其对与抑郁相关的途径的影响，如 BDNF 和代谢能量。
