Department of Anatomical Sciences and Cognitive Neuroscience, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Student Research Committee, Neuroscience Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Exp Brain Res. 2022 Oct;240(10):2581-2594. doi: 10.1007/s00221-022-06435-2. Epub 2022 Aug 17.
Research characterizing the neuronal substrate of anxiety has implicated different brain areas, including the medial septal nucleus (m-SEPT). Previous reports indicated a role of dopamine and nitric oxide (NO) in anxiety-related behaviors. In this study, the extracellular single-unit recording was performed from the m-SEPT in adult male albino Wistar rats. Baseline activity was recorded for 5 min, and the post-injection recording was performed for another 5 min after the microinjection of each drug. The results showed that (1) both D1- and D2-like receptor agonists (SKF-38393 and quinpirole) enhanced the firing rate of m-SEPT neurons; (2) both D1- and D2-like antagonists (SCH-23390 and sulpiride) attenuated the firing rate of m-SEPT neurons; (3) L-arginine (NO precursor) increased the firing rate of m-SEPT neurons, but a non-specific NOS inhibitor, L-NAME, elicited no significant alterations; (4) the non-specific NOS inhibitor reversed the enhanced firing rate produced by SKF-38393 and quinpirole; (5) neither of the dopaminergic antagonists changed the enhanced activity resulted from the application of the NO precursor. These results contribute to our understanding of the complex neurotransmitter interactions in the m-SEPT and showed that both dopaminergic and NO neurotransmission are involved in the modulation of the firing rate of neurons in the m-SEPT.
研究表明,不同的脑区与焦虑的神经基础有关,包括中隔核(m-SEPT)。先前的报告表明,多巴胺和一氧化氮(NO)在焦虑相关行为中起作用。在这项研究中,从成年雄性白化 Wistar 大鼠的 m-SEPT 进行了细胞外单细胞记录。记录了 5 分钟的基线活动,然后在每种药物注射后再进行 5 分钟的记录。结果表明:(1)D1 样和 D2 样受体激动剂(SKF-38393 和喹吡罗)均增强了 m-SEPT 神经元的放电率;(2)D1 样和 D2 样拮抗剂(SCH-23390 和舒必利)均减弱了 m-SEPT 神经元的放电率;(3)L-精氨酸(NO 前体)增加了 m-SEPT 神经元的放电率,但非特异性 NOS 抑制剂 L-NAME 没有引起明显的变化;(4)非特异性 NOS 抑制剂逆转了 SKF-38393 和喹吡罗引起的放电率增强;(5)两种多巴胺拮抗剂均未改变应用 NO 前体产生的增强活性。这些结果有助于我们理解 m-SEPT 中复杂的神经递质相互作用,并表明多巴胺能和 NO 能神经传递都参与了 m-SEPT 中神经元放电率的调节。