Rapid activation of presynaptic nicotinic acetylcholine receptors by nerve-released transmitter.
Rapid activation of presynaptic nicotinic acetylcholine receptors by nerve-released transmitter.
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神经释放的递质快速激活突触前烟碱乙酰胆碱受体。
DOI：
10.1111/j.1460-9568.2003.03064.x
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Sargent,PeterB
中科院分区：
文献类型：
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作者：
Rogers,Marc;Sargent,PeterB
尼古丁增强神经递质释放的能力涉及突触前烟碱乙酰胆碱受体（nAChR）在突触调节中的作用，但已知突触前nAChR被神经释放的递质激活的例子很少。我们通过使用葡聚糖偶联指示剂染料对突触前钙瞬变进行成像，来寻找鸡睫状神经节的萼神经末梢中突触前nAChR的内源性激活。在2-50 Hz频率范围内，单个神经末梢记录到的Ca ~（2+）信号幅度具有频率依赖性。 非特异性nAChR拮抗剂d-筒箭毒碱（d-TC; 100 µm）和α7特异性拮抗剂甲基卡乌头碱（20-50 nm）可显著降低（约10-15%）刺激节前神经诱发的钙瞬变，但10 µ m二氢-β-赤藓定不受影响，它应抑制几种非α7 nAChR。 反馈迅速，不需要刺激依赖性的发射器建立，asd-TC和MLA降低了2-Hz序列中第一个钙瞬变的幅度。胆碱是α7 nAChR的激动剂，但不是该系统中唯一的激动剂，因为乙硫磷对乙酰胆碱酯酶的抑制作用未能减少钙瞬变。这些结果表明，神经释放的乙酰胆碱（ACh）反馈到突触前α7 nAChR上，以增强终末内的钙信号。这种反馈可能有助于维持胆碱能突触的高传输速率。
Nicotine's ability to enhance neurotransmitter release has implicated presynaptic nicotinic acetylcholine receptors (nAChRs) in synaptic modulation, but there are few examples where presynaptic nAChRs are known to be activated by nerve‐released transmitter. We searched for endogenous activation of presynaptic nAChRs in the calyceal nerve terminals of the chick ciliary ganglion by imaging presynaptic calcium transients using dextran‐coupled indicator dyes. The amplitude of Ca2+signals recorded in individual nerve terminals was frequency dependent over 2–50 Hz. Calcium transients evoked by stimulation of the preganglionic nerve were significantly reduced (≈10–15%) by the nonspecific nAChR antagonistd‐tubocurarine (d‐TC; 100 µm) and the α7‐specific antagonist methyllycaconitine (20–50 nm) but were not affected by 10 µmdihydro‐β‐erythroidine, which should inhibit several non‐α7 nAChRs. Feedback was rapid and did not require a stimulation‐dependent build‐up of transmitter, asd‐TC and MLA reduced the amplitude of the first calcium transient in a 2‐Hz train. Choline is an agonist at α7 nAChRs but is not the sole agonist in this system, as inhibition of acetylcholinesterase by echothiophate failed to reduce calcium transients. These results show that nerve‐released acetylcholine (ACh) feeds back onto presynaptic α7 nAChRs to enhance calcium signals within the terminal. This feedback may help maintain the high rate of transmission at this cholinergic synapse.