Tachykinin Agonists Modulate Cholinergic Neurotransmission at Guinea-Pig Intracardiac Ganglia
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- Zhang Lili
- Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University
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- Hancock John C.
- Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University
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- Hoover Donald B.
- Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University
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Effects of substance P (SP) and selective tachykinin agonists on neurotransmission at guinea-pig intracardiac ganglia were studied in vitro. Voltage responses of neurons to superfused tachykinins and nerve stimulation were measured using intracellular microelectrodes. Predominant effects of SP (1 μM) were to cause slow depolarization and enable synaptic transmission at low intensities of nerve stimulation. Augmented response to nerve stimulation occurred with 29 of 40 intracardiac neurons (approx. 73%). SP inhibited synaptic transmission at 23% of intracardiac neurons but also caused slow depolarization. Activation of NK3 receptors with 100 nM [MePhe7]neurokinin B caused slow depolarization, enhanced the response of many intracardiac neurons to low intensity nerve stimulation or local application of acetylcholine, and triggered action potentials independent of other stimuli in 6 of 42 neurons. The NK1 agonist [Sar9,Met(O2)11]SP had similar actions but was less effective and did not trigger action potentials independently. Neither selective agonist inhibited cholinergic neurotransmission. We conclude that SP can function as a positive or negative neuromodulator at intracardiac ganglion cells, which could be either efferent neurons or interneurons. Potentiation occurs primarily through NK3 receptors and may enable neuronal responses with less preganglionic nerve activity. Inhibition of neurotransmission by SP is most likely explained by the known blocking action of this peptide at ganglionic nicotine receptors.<br>
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 99 (3), 228-238, 2005
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205175804160
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- NII論文ID
- 10025731143
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7709971
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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