Kim Jae Heon, Ahn Young Soo, Song Yun Seob
Department of Urology, Soonchunhyang University College of Medicine, Seoul, Korea.
Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.
Int Neurourol J. 2021 Nov;25(Suppl 2):S114-119. doi: 10.5213/inj.2142350.175. Epub 2021 Nov 30.
Raised cerebral titers of acetylcholine have notable links with storage symptomatology related to lower urinary tract symptoms. The hippocampus contributes to the normal control of continence in the majority of instances (circuit 3). Owing to synaptic connections with other nerve cells, acetylcholine affects the micturition pathway via the liberation of additional cerebral neurotransmitters. Despite the fact that cerebral serotonin is a key inhibitor of reflex bladder muscle contractions, the influence of acetylcholine on its liberation is poorly delineated. The current research was conducted in order to explore the role of acetylcholine in serotonin liberation from sections of rat hippocampus in order to improve the comprehension of the relationship between cholinergic and serotonergic neurons.
Hippocampal sections from 6 mature male Sprague-Dawley rats were equilibrated over a 30-minute period in standard incubation medium so as to facilitate [3H]5-hydroxytryptamine (5-HT) uptake. The cerebral neurotransmitter, acetylcholine, was applied to the sections. Aliquots of drained medium solution were utilized in order to quantify the radioactivity associated with [3H]5-HT liberation; any alterations in this parameter were noted.
When judged against the controls, [3H]5-HT liberation from the hippocampal sections remained unaltered following the administration of acetylcholine, implying that this agent has no inhibitory action on this process.
Serotonin liberation from murine hippocampal sections is unaffected by acetylcholine. It is postulated that the bladder micturition reflex responds to acetylcholine through its immediate cholinergic activity rather than by its influence on serotonin release. These pathways are a promising target for the design of de novo therapeutic agents.
脑内乙酰胆碱水平升高与下尿路症状相关的储存症状学有显著联系。在大多数情况下，海马体有助于正常控制尿失禁（回路3）。由于与其他神经细胞的突触连接，乙酰胆碱通过释放额外的脑神经递质影响排尿途径。尽管脑内血清素是膀胱肌肉反射性收缩的关键抑制剂，但乙酰胆碱对其释放的影响尚不清楚。进行本研究以探讨乙酰胆碱在大鼠海马体切片中血清素释放中的作用，以增进对胆碱能神经元和血清素能神经元之间关系的理解。
从6只成年雄性Sprague-Dawley大鼠获取海马体切片，在标准孵育培养基中平衡30分钟，以促进[3H]5-羟色胺（5-HT）摄取。将脑神经递质乙酰胆碱应用于切片。利用沥干的培养基溶液等分试样来量化与[3H]5-HT释放相关的放射性；记录该参数的任何变化。
与对照组相比，给予乙酰胆碱后，海马体切片中[3H]5-HT的释放未发生改变，这表明该药物对这一过程没有抑制作用。
乙酰胆碱不影响小鼠海马体切片中血清素的释放。据推测，膀胱排尿反射对乙酰胆碱的反应是通过其直接的胆碱能活性，而不是通过其对血清素释放的影响。这些途径是设计新型治疗药物的有希望的靶点。
