Brain K L
University Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK.
Exp Physiol. 2009 Jan;94(1):25-30. doi: 10.1113/expphysiol.2008.043679. Epub 2008 Sep 19.
Determining whether ATP and noradrenaline are released from the same vesicle at mature autonomic neuroeffector junctions is challenging because of the difficulty of simultaneously detecting the packeted release of these neurotransmitters. Contraction, overflow and electrophysiology experiments all show that both ATP and noradrenaline are released following field stimulation (although the ratio might vary) from autonomic nerves in tissues including the vas deferens, rat tail artery and mesenteric artery. The occurrence of purinergic neuroeffector Ca(2+) transients (NCTs) has been used to detect the packeted release of the neurotransmitter ATP acting on postjunctional P2X receptors to cause Ca(2+) influx. Neuroeffector Ca(2+) transients can also be used to detect the local effects of noradrenaline through its alpha(2)-adrenoceptor-mediated prejunctional autoinhibitory effects on nerve terminal Ca(2+) concentration and the probability of exocytosis (measured by counting NCTs). Evidence is presented that exocytosis from sympathetic varicosities does not occur in a manner independent of the history of that varicosity, but rather that the release of a packet of ATP transiently suppresses (or predicts the transient suppression of) subsequent release. This could arise by autoinhibition (by the prejunctional action of noradrenaline or purines) or due to a transient shortage of vesicles readily available for release. In summary, two high-resolution approaches are proposed to measure the intermittent release of packets of neurotransmitter: (1) local transient suppression of nerve terminal Ca(2+) transients; and (2) the local and transient inhibition of NCTs to infer local autoinhibition, hence transmitter release. Such approaches may allow the packeted corelease of ATP and noradrenaline to be investigated without the need to measure both neurotransmitters directly.
在成熟的自主神经效应器接头处,确定三磷酸腺苷(ATP)和去甲肾上腺素是否从同一囊泡释放具有挑战性,因为同时检测这些神经递质的成簇释放存在困难。收缩、溢出和电生理学实验均表明,在包括输精管、大鼠尾动脉和肠系膜动脉在内的组织中,自主神经受到场刺激后,ATP和去甲肾上腺素都会释放(尽管比例可能有所不同)。嘌呤能神经效应器钙(Ca2+)瞬变(NCTs)的出现已被用于检测作用于节后P2X受体以引起Ca2+内流的神经递质ATP的成簇释放。神经效应器Ca2+瞬变也可用于检测去甲肾上腺素的局部效应,其通过α2 -肾上腺素能受体介导的对神经末梢Ca2+浓度和胞吐概率的节前自身抑制作用(通过计数NCTs来测量)。有证据表明,交感曲张体的胞吐作用并非以与该曲张体历史无关的方式发生,而是一包ATP的释放会短暂抑制(或预测随后释放的短暂抑制)。这可能是通过自身抑制(通过去甲肾上腺素或嘌呤的节前作用)或由于可用于释放的囊泡暂时短缺所致。总之,提出了两种高分辨率方法来测量神经递质包的间歇性释放:(1)局部短暂抑制神经末梢Ca2+瞬变;(2)局部和短暂抑制NCTs以推断局部自身抑制,从而推断递质释放。此类方法可能无需直接测量两种神经递质就能研究ATP和去甲肾上腺素的成簇共同释放。