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Investigating GABA and its function in platelets as compared to neurons.

机译:与神经元相比,研究GABA及其在血小板中的功能。

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We have recently suggested that platelets could be used as a model for neuronal receptors. In this paper we have investigated gamma-aminobutyric acid (GABA) metabolism and GABA receptors in platelets and in cultured neurons to see whether platelets' GABA mimics neuronal GABA receptor activities. We used the ELISA technique for detecting the GABA concentration in platelet rich plasma and cultured neurons. The functional effects of GABA and its receptor ligands on platelets were determined using an aggregometer. We found that the GABA concentration is 30% lower in platelets than in neurons and in both preparations GABA was metabolized by GABA transaminase (GABA-T). GABA potentiated calcium dependent platelet aggregation with a higher value in washed platelets suspension (WPS) then in platelet rich plasma (PRP). This effect was inhibited by benzodiazepines, calcium channel blockers and the selective phosphoinositide 3-kinase antagonist Wortmannin. GABA neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. We concluded that platelets could be further developed to be used as a peripheral model to study neuronal GABAergic function and its abnormality in diseases such as epilepsy and schizophrenia. Furthermore our results indicated that PI3-kinase is involved in calcium dependent GABA induced platelet aggregation as this synergistic effect is inhibited by Wortmannin in dose dependent manner.
机译:我们最近建议血小板可以用作神经元受体的模型。在本文中,我们研究了血小板和培养的神经元中的γ-氨基丁酸(GABA)代谢和GABA受体,以了解血小板的GABA是否模仿神经元GABA受体的活性。我们使用ELISA技术检测富含血小板的血浆和培养的神经元中GABA的浓度。使用凝集计测定GABA及其受体配体对血小板的功能作用。我们发现血小板中的GABA浓度比神经元低30%,在两种制剂中,GABA均由GABA转氨酶(GABA-T)代谢。 GABA增强的钙依赖性血小板聚集在洗涤后的血小板悬浮液(WPS)中比在富含血小板的血浆(PRP)中具有更高的值。苯二氮卓类,钙通道阻滞剂和选择性磷酸肌醇3-激酶拮抗剂Wortmannin抑制了这种作用。 GABA神经传递涉及正常脑功能的大多数方面,并可在许多神经病理学状况中受到干扰。我们得出的结论是,可以进一步开发血小板作为外周模型,以研究神经元GABA能功能及其在癫痫和精神分裂症等疾病中的异常情况。此外,我们的结果表明PI3激酶参与了钙依赖性GABA诱导的血小板聚集,因为这种协同作用被Wortmannin抑制,呈剂量依赖性。

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