ArticleNaunyn-Schmiedeberg's archives of pharmacology1995
Inhibition of nicotinic acetylcholine receptor channels in bovine adrenal chromaffin cells by Y3-type neuropeptide Y receptors via the adenylate cyclase/protein kinase A system.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 35 citations in OpenAlex.
- Interaction of P2 purinergic receptors with cellular macromolecules.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- Deletion of the neuropeptide Y (NPY) Y1 receptor gene reveals a regulatory role of NPY on catecholamine synthesis and secretion.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Regulation of neuronal ion channels via P2Y receptors.Purinergic signalling · 2004Article
- Neuropeptide Y modulates ATP-induced increases in internal calcium via the adenylate cyclase/protein kinase A system in a human neuroblastoma cell line.The Biochemical journal · 1997Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of neuropeptide Y [NPY(1-36)] and related peptides on the voltage-dependent currents and the nicotinic acetylcholine receptor (nAChR) currents (IACh) of bovine adrenal chromaffin cells was investigated using the whole-cell patch clamp technique. Catecholamine release from single chromaffin cells was measured by means of fast cyclic voltammetry. The potency order of these peptides in inhibiting IACh evoked by nicotine was NPY(1-36), NPY (16-36) > peptide YY(PYY) > [Leu31, Pro34]NPY. NPY(16-36) produced a similar degree of inhibition, irrespective of whether nicotine or an equipotent concentration of acetylcholine was used to evoke IACh. NPY(16-36) failed to alter voltage-dependent inward or outward currents. Intracellular cAMP, and extracellular dibutyryl-cAMP, produced a slowly developing increase in IACh. Intracellular cAMP, extracellular 8-Br-cAMP or dibutyryl-cAMP, and an inhibitor of cyclic nucleotide phosphodiesterases 3-isobutyl-1-methyl-xanthine (IBMX), decreased the inhibitory effect of NPY(16-36) on IACh. Although the intracellular application of the cAMP-dependent protein kinase A inhibitor [PKI(14-24)amide] alone did not alter IACh, it potentiated the effect of NPY(16-36) in interaction experiments. While the NPY(16-36)-induced inhibition of IACh was reversed on washout of the peptide, the slightly shorter C-terminal fragment NPY(18-36) caused a long-lasting depression of both IACh and catecholamine secretion evoked by nicotine. This depression was smaller in the presence of extracellular 8-Br-cAMP than in its absence. NPY(18-36) did not alter the secretory activity induced by a high concentration of potassium. It appears that, by activating Y3-receptors, NPY inhibits nAChR-current and the resulting secretion of catecholamines from bovine chromaffin cells. This process may involve a G protein-mediated decrease in intracellular cAMP with a subsequent decrease in the degree of phosphorylation of the nAChR-channel.
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