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Pulse Stimulation with Odors or IBMX/Forskolin Potentiates Responses in Isolated Olfactory Neurons

机译:气味刺激或IBMX / Forskolin的脉冲刺激增强了孤立嗅觉神经元的反应。

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摘要

Many odor responses are mediated by the adenosine 3′,5′-cyclic monophosphate (cAMP) pathway in which the cAMP-gated current is amplified by Ca2+-dependent Cl current. In olfactory neurons, prolonged exposure to odors decreases the odor response and is an adaptive effect. Several studies suggest that odor adaptation is linked to elevated intracellular Ca2+. In the present study, using the perforated configuration of the patch clamp technique, we found that repetitive odor stimulation elicits a potentiation of the subsequent responses in olfactory neurons. This potentiation is mimicked by stimulating the cAMP pathway and does not appear to be related to phosphorylation of ion channels since protein kinase inhibitors could not block it. Our data suggest that local increases in [Ca2+]i via activation of the cAMP pathway mediate the pulse-elicited potentiation. In the first odor application, entry of Ca2+ through cyclic nucleotide–gated channels appears to be buffered. Repetitive stimulation allows local increases in [Ca2+]i, recruiting more Ca2+-dependent Cl channels with each subsequent odor pulse.
机译:腺苷3',5'-环一磷酸(cAMP)途径介导了许多气味反应,其中cAMP门控电流通过依赖Ca 2 + 的Cl -当前。在嗅觉神经元中,长时间暴露于气味会降低气味反应,是一种适应性作用。多项研究表明,气味适应与细胞内Ca 2 + 升高有关。在本研究中,使用膜片钳技术的穿孔结构,我们发现重复的气味刺激会引起嗅觉神经元中后续反应的增强。这种增强作用可通过刺激cAMP途径来模拟,并且似乎与离子通道的磷酸化无关,因为蛋白激酶抑制剂无法阻断它。我们的数据表明,通过激活cAMP途径,[Ca 2 + ] i的局部增加介导了脉冲诱发的增强作用。在第一个气味应用中,Ca 2 + 通过环状核苷酸门控通道的进入似乎被缓冲了。重复刺激可以使[Ca 2 + ] i局部增加,并在随后的每个气味脉冲中募集更多的Ca 2 + 依赖性Cl -通道。

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