Endogenous regulation of rat brain mast cell serotonin release.

K Marathias, M Lambracht-Hall, J Savala, T C Theoharides
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引用次数: 26

Abstract

Mast cells are involved in allergic reactions where they release numerous vasoactive and other mediators in response to IgE and antigen. They are also activated by neuropeptides and are found in close contact with neurons. Mast cell heterogeneity has now been documented for mucosal mast cells and connective tissue mast cells. Rat brain mast cells were studied in a perfusion system and were shown to release serotonin in response to the mast cell secretagogue compound 48/80 (C48/80). High-potassium neuronal depolarization also released serotonin, but this was calcium dependent, not associated with beta-hexosaminidase, and was unaffected by prior treatment with C48/80. Neuronal depolarization, however, was associated with somatostatin secretion and substantially reduced subsequent C48/80 stimulation, an effect abolished by neonatal treatment of the animals with capsaicin. Perfusion with somatostatin and substance P also induced brain mast cell serotonin release. C48/80 stimulation of combined thalamic and hypothalamic slices after neuronal depolarization substantially reduced the C48/80 effect, suggesting the possible presence of endogenous inhibitors released from the hypothalamus. Finally, the alpha 2-receptor agonist clonidine had a slight stimulatory effect. These results indicate that brain mast cell serotonin release may be regulated by endogenous neurotransmitters and/or neuromodulators.

内源性调节大鼠脑肥大细胞血清素释放。
肥大细胞参与过敏反应,它们释放许多血管活性和其他介质,以响应IgE和抗原。它们也被神经肽激活,并与神经元密切接触。肥大细胞异质性已被证实为粘膜肥大细胞和结缔组织肥大细胞。在灌注系统中对大鼠脑肥大细胞进行了研究,发现肥大细胞分泌素化合物48/80 (C48/80)会释放血清素。高钾神经元去极化也释放血清素,但这是钙依赖的,与β -己糖氨酸酶无关,并且不受先前使用C48/80治疗的影响。然而,神经元去极化与生长抑素分泌有关,并大大减少了随后的C48/80刺激,这一效应被新生期用辣椒素治疗的动物所消除。灌注生长抑素和P物质也能诱导脑肥大细胞血清素释放。神经元去极化后对丘脑和下丘脑联合切片进行C48/80刺激可显著降低C48/80效应,提示可能存在下丘脑释放的内源性抑制剂。最后,α 2受体激动剂可乐定有轻微的刺激作用。这些结果表明,脑肥大细胞血清素的释放可能受内源性神经递质和/或神经调节剂的调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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