Modulation of the Substance P Release From Cultured Rat Primary Afferent Neurons by Zinc Ions

Tang, He-Bin; Miyano, Kanako; Nakata, Yoshihiro

doi:10.1254/jphs.09033sc

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…Additionally, a recent study indicated that Kyn released from the fat body induces the formation of zinc storage granules in Malpighian tubules, where 3-HK and the xanthurenic acid act as endogenous zinc chelators. 43 Considering that zinc is a known modulator of SP release, 44 , 45 humoral Kyn may also regulate Tk release through zinc homeostasis during disc repair.…”

Section: Discussionmentioning

confidence: 99%

Involvement of neuronal tachykinin-like receptor at 86C in Drosophila disc repair via regulation of kynurenine metabolism

Kashio,

Masuda,

Miura

2023

iScience

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Section: Discussionmentioning

confidence: 99%

Involvement of neuronal tachykinin-like receptor at 86C in Drosophila disc repair via regulation of kynurenine metabolism

Kashio,

Masuda,

Miura

2023

iScience

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“…MMPs, particularly MMP‐9 [18,19], MMP‐2 [19], and MMP‐5 [20], have been strongly implicated in the pathogenesis of neuropathic pain. Zinc is also known to modulate the secretion of the pain‐associated neuropeptide substance P in afferent rat neurons [21], with high zinc concentrations strongly inhibiting the release of substance P. It is possible that gallium has a similar effect.…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment of Refractory Postherpetic Neuralgia with Topical Gallium Maltolate: Case Report

Bernstein

2012

Pain Med

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Gallium has significant anti-inflammatory activity, inhibiting the activation and proliferation of pro-inflammatory T cells. Because gallium is chemically similar to zinc, it can interfere with the activity of matrix metalloproteinases (zinc-bearing proteases), which have been implicated in the etiology of neuropathic pain, and it may suppress the secretion of substance P. Gallium may also inhibit viral replication and the inflammatory activity of viral proteins. This case provides rationale to study topical gallium maltolate in patients with refractory peripheral neuropathic pain.

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“…Evidence from a variety of studies suggests that zinc modulation of calcium channels affects calcium influx and transmitter release. A study in rat dorsal root ganglion neurons found that low concentrations (10–100 nM) of zinc evoked an extracellular calcium influx through L-, N- and T-type voltage-gated calcium channels, thus, increasing the release of substance P; higher concentrations (1–100 μM) of zinc attenuated or completely masked these responses (Tang et al, 2009 ). In the hippocampus and amygdala, high-frequency stimulation with the membrane-impermeable zinc chelator CaEDTA present enhanced exocytosis (Minami et al, 2006 ; Takeda et al, 2007 , 2010 ).…”

Section: Zinc Modulation Of Voltage-gated Ion Channels With a Focus Omentioning

confidence: 99%

Zinc as a Neuromodulator in the Central Nervous System with a Focus on the Olfactory Bulb

Blakemore

Trombley

2017

Front. Cell. Neurosci.

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The olfactory bulb (OB) is central to the sense of smell, as it is the site of the first synaptic relay involved in the processing of odor information. Odor sensations are first transduced by olfactory sensory neurons (OSNs) before being transmitted, by way of the OB, to higher olfactory centers that mediate olfactory discrimination and perception. Zinc is a common trace element, and it is highly concentrated in the synaptic vesicles of subsets of glutamatergic neurons in some brain regions including the hippocampus and OB. In addition, zinc is contained in the synaptic vesicles of some glycinergic and GABAergic neurons. Thus, zinc released from synaptic vesicles is available to modulate synaptic transmission mediated by excitatory (e.g., N-methyl-D aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)) and inhibitory (e.g., gamma-aminobutyric acid (GABA), glycine) amino acid receptors. Furthermore, extracellular zinc can alter the excitability of neurons through effects on a variety of voltage-gated ion channels. Consistent with the notion that zinc acts as a regulator of neuronal activity, we and others have shown zinc modulation (inhibition and/or potentiation) of amino acid receptors and voltage-gated ion channels expressed by OB neurons. This review summarizes the locations and release of vesicular zinc in the central nervous system (CNS), including in the OB. It also summarizes the effects of zinc on various amino acid receptors and ion channels involved in regulating synaptic transmission and neuronal excitability, with a special emphasis on the actions of zinc as a neuromodulator in the OB. An understanding of how neuroactive substances such as zinc modulate receptors and ion channels expressed by OB neurons will increase our understanding of the roles that synaptic circuits in the OB play in odor information processing and transmission.

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Modulation of the Substance P Release From Cultured Rat Primary Afferent Neurons by Zinc Ions

Cited by 7 publications

References 15 publications

Involvement of neuronal tachykinin-like receptor at 86C in Drosophila disc repair via regulation of kynurenine metabolism

Involvement of neuronal tachykinin-like receptor at 86C in Drosophila disc repair via regulation of kynurenine metabolism

Successful Treatment of Refractory Postherpetic Neuralgia with Topical Gallium Maltolate: Case Report

Zinc as a Neuromodulator in the Central Nervous System with a Focus on the Olfactory Bulb

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