Muscarinic Receptor Stimulation Does Not Inhibit Voltage-dependent Ca2+ Channels in Rat Adrenal Medullary Chromaffin Cells.

IF 1.6 4区 生物学 Q4 CELL BIOLOGY
Keita Harada, Masumi Inoue
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Abstract

Adrenal medullary chromaffin (AMC) and sympathetic ganglion cells are derived from the neural crest and show a similar developmental path. Thus, these two cell types have many common properties in membrane excitability and signaling. However, AMC cells function as endocrine cells while sympathetic ganglion cells are neurons. In rat sympathetic ganglion cells, muscarinic M1 and M4 receptors mediate excitation and inhibition via suppression of M-type K+ channels and suppression of voltage-dependent Ca2+ channels, respectively. On the other hand, M1 receptor stimulation in rat AMC cells also produces excitation by suppressing TWIK-related acid sensitive K+ (TASK) channels. However, whether M4 receptors are coupled with voltage-dependent Ca2+ channel suppression is unclear. We explore this issue electrophysiologically and biochemically. Electrical stimulation of nerve fibers in rat adrenal glands trans-synaptically increased the Ca2+ signal in AMC cells. This electrically evoked increased Ca2+ signal was not altered during muscarine-induced increase in Ca2+ signal, whereas it decreased significantly during a GABA-induced increase, due to a shunt effect of increased Cl- conductance. The whole-cell current recordings revealed that voltage-dependent Ca2+ currents in AMC cells were suppressed by adenosine triphosphate, but not by muscarinic agonists. The fractionation analysis and immunocytochemistry indicated that CaV1.2 Ca2+ channels and M4 receptors are located in the raft and non-raft membrane domains, respectively. We concluded that muscarinic stimulation in rat AMC cells does not produce voltage-dependent Ca2+ channel inhibition. This lack of muscarinic inhibition is at least partly due to physical separation of voltage-dependent Ca2+ channels and M4 receptors in the plasma membrane.

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毒蕈碱受体刺激不会抑制大鼠肾上腺髓质染色质细胞中电压依赖性Ca2+通道。
肾上腺髓质染色质(AMC)和交感神经节细胞来源于神经嵴,并表现出相似的发育途径。因此,这两种细胞类型在膜兴奋性和信号传导方面有许多共同的特性。AMC细胞作为内分泌细胞,交感神经节细胞作为神经元。在大鼠交感神经节细胞中,毒蕈碱M1和M4受体分别通过抑制m型K+通道和抑制电压依赖性Ca2+通道介导兴奋和抑制。另一方面,M1受体刺激大鼠AMC细胞也通过抑制twik相关的酸敏感K+ (TASK)通道产生兴奋。然而,M4受体是否与电压依赖性Ca2+通道抑制偶联尚不清楚。我们从电生理和生物化学的角度探讨了这个问题。大鼠肾上腺神经纤维的电刺激经突触增加了AMC细胞中的Ca2+信号。在肌碱诱导的Ca2+信号增加过程中,这种电诱发的Ca2+信号增加没有改变,而在gaba诱导的Ca2+信号增加过程中,由于Cl-电导增加的分流效应,Ca2+信号明显减少。全细胞电流记录显示,三磷酸腺苷抑制了AMC细胞中电压依赖性的Ca2+电流,但没有被毒蕈碱激动剂抑制。分离分析和免疫细胞化学表明,CaV1.2 Ca2+通道和M4受体分别位于筏膜结构域和非筏膜结构域。我们得出结论,毒蕈碱刺激大鼠AMC细胞不产生电压依赖性Ca2+通道抑制。这种毒蕈碱抑制的缺乏至少部分是由于质膜中电压依赖性Ca2+通道和M4受体的物理分离。
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来源期刊
Acta Histochemica Et Cytochemica
Acta Histochemica Et Cytochemica 生物-细胞生物学
CiteScore
3.50
自引率
8.30%
发文量
17
审稿时长
>12 weeks
期刊介绍: Acta Histochemica et Cytochemica is the official online journal of the Japan Society of Histochemistry and Cytochemistry. It is intended primarily for rapid publication of concise, original articles in the fields of histochemistry and cytochemistry. Manuscripts oriented towards methodological subjects that contain significant technical advances in these fields are also welcome. Manuscripts in English are accepted from investigators in any country, whether or not they are members of the Japan Society of Histochemistry and Cytochemistry. Manuscripts should be original work that has not been previously published and is not being considered for publication elsewhere, with the exception of abstracts. Manuscripts with essentially the same content as a paper that has been published or accepted, or is under consideration for publication, will not be considered. All submitted papers will be peer-reviewed by at least two referees selected by an appropriate Associate Editor. Acceptance is based on scientific significance, originality, and clarity. When required, a revised manuscript should be submitted within 3 months, otherwise it will be considered to be a new submission. The Editor-in-Chief will make all final decisions regarding acceptance.
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