Substance P plays a critical role in synaptic transmission in striatal neurons
Substance P is one of the major neuropeptides released by striatal neurons; however, its function in the striatum remains unclear. In this study, we found substance P triggers spontaneous neurotransmitter release and rapid synaptic vesicle exocytosis in cultured striatal neurons, as substance P knoc...
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Published in | Biochemical and biophysical research communications Vol. 511; no. 2; pp. 369 - 373 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
02.04.2019
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Subjects | |
Online Access | Get full text |
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Summary: | Substance P is one of the major neuropeptides released by striatal neurons; however, its function in the striatum remains unclear. In this study, we found substance P triggers spontaneous neurotransmitter release and rapid synaptic vesicle exocytosis in cultured striatal neurons, as substance P knockdown in these neurons impaired spontaneous neurotransmitter release and calcium-dependent rapid synaptic neurotransmission. Furthermore, treatment with exogenous substance P completely rescued the synaptic dysfunction phenotype in striatal neurons lacking this neuropeptide. On the other hand, substance P knockdown had no effect on the size of the readily releasable pool of synaptic vesicles, but decreased the probability of presynaptic release of synaptic vesicles in cultured striatal neurons. Treatment with CP96345, a NK1 receptor antagonist, also resulted in synaptic defects in cultured striatal neurons. In summary, we propose substance P is critical for synaptic transmission in striatal neurons.
•Substance P knockdown in striatal neurons impairs spontaneous release.•Diminished rapid synaptic transmission in striatal neurons lacking substance P.•Substance P is critical for the regulation of the probability of presynaptic release in striatal neurons.•NK1 receptors is important for the modulation of synaptic transmission by substance P. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2019.02.055 |