Glutamate regulates neurite outgrowth of cultured descending brain neurons from larval lamprey

Ryan, Sarah Kathleen; Shotts, Lindsay R.; Hong, Su Hyung; Nehra, Deepika; Groat, Carl R.; Armstrong, Jon R.; McClellan, Andrew D.

doi:10.1002/neu.20335

Cited by 3 publications

(3 citation statements)

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“…Glutamate is utilized as a neurotransmitter by most organisms and is the major excitatory neurotransmitter of the vertebrate brain. It also plays an important role in brain development by modulating neuronal migration (Komuro and Rakic, 1993; Gudz et al, 2006; Manent et al, 2006), outgrowth of neuronal processes (Rajan and Cline, 1998; Wilson et al, 2000; Ryan et al, 2006), and synapse elimination (Rabacchi et al, 1992; Hashimoto et al, 2001). In addition, glutamate released from nerve terminals helps to refine the synaptic connections that link neurons into circuits (Verderio et al, 1995; van Kesteren and Spencer, 2003).…”

Section: Introductionmentioning

confidence: 99%

Vesicular glutamate transporters VGLUT1 and VGLUT2 in the developing mouse barrel cortex

Liguz-Lecznar

Skangiel-Kramska

2007

Intl J of Devlp Neuroscience

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Three vesicular glutamate transporters have been identified in mammals. Two of them, VGLUT1 and VGLUT2, define the glutamatergic phenotype and their distribution in the brain is almost complementary. In the present study we examined the distribution and expression levels of these two VGLUTs during postnatal development of the mouse barrel cortex. We also investigated changes in the localization of VGLUT1 and VGLUT2 within particular compartments of the barrel field (barrels/septa) during its development. We found differences in the time course of developmental expression, with VGLUT1 peaking around P14, while VGLUT2 increased gradually until adulthood. Over the examined period (P3 - adult) both transporters had stronger expression in the barrel interiors, and in this compartment VGLUT2 dominated, whereas in the inter-barrel septa VGLUT1 dominated over VGLUT2. Furthermore, we found that some nerve terminals in the barrel cortex coexpressed both transporters until adulthood. Colocalization was observed within the barrels, but not within the septa.

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Section: Introductionmentioning

confidence: 99%

Vesicular glutamate transporters VGLUT1 and VGLUT2 in the developing mouse barrel cortex

Liguz-Lecznar

Skangiel-Kramska

2007

Intl J of Devlp Neuroscience

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“…In the hippocampus, evidence has been provided for NO to act as the elusive retrograde messenger in synaptic plasticity, namely long-term potentiation (Bohme et al, 1991;O'Dell et al, 1991;Schuman and Madison, 1991;Garthwaite, 2001, 2003;Hopper and Garthwaite, 2006). There is a convincing literature that neurotransmitters can affect neurite outgrowth (McCobb et al, 1988;Lipton and Kater, 1989;Spencer et al, 2000;van Kesteren and Spencer, 2003;Fricker et al, 2005;Homma et al, 2006;Ryan et al, 2007), and a sender/receiver paradigm similar to the one used in our study was employed with Lymnaea neurons to demonstrate that dopamine can affect growth cone motility. In this study, dopamine released from the right pedal dorsal 1 (RPeD1) neuron was shown to regulate growth cone behavior of target and nontarget neurons differentially (Spencer et al, 2000).…”

Section: No Released From a Physiological Source Affects Growth Cone mentioning

confidence: 75%

Nitric oxide release from a single cell affects filopodial motility on growth cones of neighboring neurons

Tornieri

Rehder

2007

Developmental Neurobiology

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Nitric oxide (NO), a gaseous messenger, has been reported to be involved in a variety of functions in the nervous system, ranging from neuronal pathfinding to learning and memory. We have shown previously that the application of NO via NO donors to growth cones of identified Helisoma buccal neurons B5 in vitro induces an increase in filopodial length, a decrease in filopodial number, and a slowing in neurite advance. It is unclear, however, whether NO released from a physiological source would affect growth cone dynamics. Here we used cell bodies of identified neurons known to express the NO synthesizing enzyme nitric oxide synthase (NOS) as a source of constitutive NO production and tested their effect on growth cones of other cells in a sender-receiver paradigm. We showed that B5 cell bodies induced a rapid increase in filopodial length in NO-responsive growth cones, and that this effect was blocked by the NOS inhibitor 7-NI, suggesting that the effect was mediated by NO. Inhibition of soluble guanylyl cyclase (sGC) with ODQ blocked filopodial elongation induced by B5 somata, confirming that NO acted via sGC. We also demonstrate that the effect of NO was reversible and that a cell releasing NO can affect growth cones over a distance of at least 100 microm. Our results suggest that NO released from a physiological source can affect the motility of nearby growth cones and thus should be considered a signaling molecule with the potential to affect the outcome of neuronal pathfinding in vivo.

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“…A normal value of Cd is essential in pain management because this trace element has been shown to influence dopaminergic, glutamate, acid-sensing ion channels (ASICs), and gamma-aminobutyric acid systems. Cd may be a potent neurotoxin even at reduced doses, while Cd deficit can rise oxidative stress and promote mitochondrial abnormalities [24,25,27], both being mechanisms vastly implicated in pain modulation [29][30][31]. Moreover, Cd may inhibit voltage-gated calcium channels and evoked release of neurotransmitters from the nerves, two other potential mechanisms that can stimulate pain transmission [32].…”

Section: Cadmium Chloridementioning

confidence: 99%

Intracerebroventricular Coadministration of Protoxin-II and Trace Elements in Rats Enhances the Analgesic Effect of the 1.7 Voltage-Gate Sodium Channel Blocker

Stanciu

Luca

Marza

et al. 2019

BioMed Research International

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Pain continues to be a global unmet medical need, and the current recommendations for its management require a constant exploration of new drugs that target multiple pain mechanisms, with an improved safety profile and increased treatment adherence. Currently, the enriched distribution and localization within nociceptors of the selective channel blockers and the critical role played by sodium channels in neuronal excitability nominate isoforms as specific targets to generate innovative compounds. In the present report, we verified the hypothesis that coadministration of Protoxin-II, a selective sodium channel inhibitor, and trace elements has direct and improved antinociceptive effects. Groups of seven Wistar rats were treated intracerebroventricularly with a combination of MgCl 2 , CdCl 2 , and ZnCl 2 and Protoxin-II, respectively, and with Protoxin-II alone (positive) or saline (negative) for controls. Evaluations were performed by nociception assay. Coadministration of these drugs caused an increase in the maximum possible effect of up to 40% as compared with the control groups. Our findings indicate that selective channel blockers continue to be an important nociception target and that the use of trace elements may provide simple but effective means of control over sodium channel blockers' risks, potentially lowering the necessary analgesic doses, thus improving the efficacy and safety profile.

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Glutamate regulates neurite outgrowth of cultured descending brain neurons from larval lamprey

Cited by 3 publications

References 68 publications

Vesicular glutamate transporters VGLUT1 and VGLUT2 in the developing mouse barrel cortex

Vesicular glutamate transporters VGLUT1 and VGLUT2 in the developing mouse barrel cortex

Nitric oxide release from a single cell affects filopodial motility on growth cones of neighboring neurons

Intracerebroventricular Coadministration of Protoxin-II and Trace Elements in Rats Enhances the Analgesic Effect of the 1.7 Voltage-Gate Sodium Channel Blocker

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