Joseph-Bravo P, Charli J L, Palacios J M, Kordon C
Endocrinology. 1979 Mar;104(3):801-6. doi: 10.1210/endo-104-3-801.
The in vitro release of TRH from hypothalamic fragments or purified nerve endings (synaptosomes) has been evaluated after incubation for 10 min in the presence of various concentrations of K+ or neurotransmitters. Release of the hormone from fragments but not from synaptosomes was enhanced in the presence of 56 mM K+ in a Ca++ -dependent manner. Neurotransmitter effects were thus tested on the fragments. Addition of histamine (10 (-7)-10(-5) M) induced a significant increase over the basal release of TRH. A comparable effect was obtained with dimaprit (10(-5) M), a highly specific agonist of histamine H2 receptors; conversely, the response to histamine was blocked by the addition of a H2 (metiamide; 10(-6) M) but not of a H1 (mepyramine; 10(-6) M) antagonist to the incubation medium. Dopamine (10(-7) M) slightly inhibited the release of TRH, but antagonists of dopamine receptors (10(-7)-10(-6) M fluphenazine or 10(-6) M alpha-flupentixol) exhibited an inhibitory effect by themselves, so that specific receptors involved in mediating dopamine actions could not be further characterized. In contrast, noradrenalin, serotonin gamma-aminobutyric acid and acetylcholine (tested at concentration of 10(-7) M) did not alter the basal release of the tripeptide.
在存在不同浓度的钾离子(K⁺)或神经递质的情况下,将下丘脑片段或纯化的神经末梢(突触体)孵育10分钟后,对促甲状腺激素释放激素(TRH)的体外释放进行了评估。在56 mM K⁺存在下,片段中激素的释放(而非突触体中的释放)以钙离子(Ca²⁺)依赖的方式增强。因此,对片段进行了神经递质作用的测试。添加组胺(10⁻⁷ - 10⁻⁵ M)导致TRH基础释放量显著增加。组胺H2受体的高度特异性激动剂二甲双胍(10⁻⁵ M)也获得了类似的效果;相反,向孵育培养基中添加H2拮抗剂(甲硫咪特;10⁻⁶ M)可阻断对组胺的反应,而添加H1拮抗剂(甲氧苄二胺;10⁻⁶ M)则无此作用。多巴胺(10⁻⁷ M)对TRH的释放略有抑制作用,但多巴胺受体拮抗剂(10⁻⁷ - 10⁻⁶ M氟奋乃静或10⁻⁶ M α-氟哌噻吨)自身就表现出抑制作用,因此无法进一步确定介导多巴胺作用的特定受体。相比之下,去甲肾上腺素、5-羟色胺、γ-氨基丁酸和乙酰胆碱(浓度为10⁻⁷ M时进行测试)并未改变三肽的基础释放量。