de Souza Mayara Machado, Silote Gabriela Pandini, Herbst Leticia Santos, Funck Vinicius Rafael, Joca Samia Regiane Lourenço, Beijamini Vanessa
Department of Pharmaceutical Sciences, Health Science Centre, Federal University of Espirito Santo, Vitoria, ES, 29043-900, Brazil.
Department of Physics and Chemistry, School of Pharmaceutical Sciences, University of São Paulo, Ribeirão Preto, SP, Brazil; Biochemistry and Pharmacology Postgraduate Program, Health Science Center, Federal University of Espirito Santo, Vitoria, ES, 29043-900, Brazil.
Neurosci Lett. 2018 Aug 10;681:26-30. doi: 10.1016/j.neulet.2018.05.029. Epub 2018 May 19.
Galanin is a neuropeptide distributed in human and rat brain regions that are involved with emotional regulation, such as the dorsal raphe nucleus (DRN). Galanin effects in the DRN are mediated by GAL and GAL receptors Intracerebral infusion of a GAL (AR-M1896) or a GAL (M617) agonist induced either antidepressant or depressive-like effect, respectively, in rats exposed to the forced swimming test (FST). However, it is not clear if GAL and/or GAL receptors present in the DRN would be involved in such effects. Therefore, we investigated the effects induced by intra-DRN infusion of galanin (0.3 nmol), AR-M1896 (1 nmol, GAL agonist), or M617 (GAL agonist) in rats exposed to the FST. Galanin and AR-M1896 intra-DRN administration induced antidepressant-like effect in the FST. However, M617 did not induce any change in the FST. Neither M617 nor AR-M1896 changed the locomotor activity of rats in the open field test. Intra-DRN pre-treatment with M871 (1 nmol), a selective GAL antagonist, counteracted the antidepressant-like effect induced by galanin. These results suggest that galanin signaling through GAL receptors in the DRN produces triggers antidepressant-like effect.
甘丙肽是一种神经肽，分布于参与情绪调节的人类和大鼠脑区，如中缝背核（DRN）。甘丙肽在中缝背核中的作用由甘丙肽及其受体介导。在强迫游泳试验（FST）的大鼠中，脑室内注入甘丙肽（AR-M1896）或甘丙肽（M617）激动剂分别诱导出抗抑郁或抑郁样效应。然而，尚不清楚中缝背核中存在的甘丙肽和/或其受体是否参与此类效应。因此，我们研究了在FST大鼠中，向中缝背核内注入甘丙肽（0.3 nmol）、AR-M1896（1 nmol，甘丙肽激动剂）或M617（甘丙肽激动剂）所诱导的效应。向中缝背核内注射甘丙肽和AR-M1896在FST中诱导出抗抑郁样效应。然而，M617在FST中未诱导任何变化。在旷场试验中，M617和AR-M1896均未改变大鼠的运动活性。用选择性甘丙肽拮抗剂M871（1 nmol）进行中缝背核内预处理，可抵消甘丙肽诱导的抗抑郁样效应。这些结果表明，甘丙肽通过中缝背核中的甘丙肽受体发出信号，产生触发抗抑郁样效应。
