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Botulinum neurotoxin type A modulates vesicular release of glutamate from satellite glial cells.

da Silva LB, Poulsen JN, Arendt-Nielsen L, Gazerani P - J. Cell. Mol. Med. (2015)

Bottom Line: Ionomycin significantly increased glutamate release from cultured SGCs 30 min. following the treatment (P < 0.001).BoNTA (100 pM) significantly decreased glutamate release (P < 0.01).In addition, interaction of BoNTA with non-neuronal cells at the level of TG suggests a potential analgesic mechanism of action of BoNTA.

View Article: PubMed Central - PubMed

Affiliation: Center for Sensory - Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg East, Denmark.

No MeSH data available.


Related in: MedlinePlus

Time-dependent modulation of glutamate release by ionomycin. Glutamate concentration (μM) in culture medium after 4, 8, 12 and 30 min. of 5 μM ionomycin incubation. **P < 0.01 indicates the significant difference of glutamate release when ionomycin is compared with control at 30 min.; #P < 0.05 indicates that glutamate release at 30 min is different compared with other stimulation time-points. Results are shown as mean ± SEM.
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fig05: Time-dependent modulation of glutamate release by ionomycin. Glutamate concentration (μM) in culture medium after 4, 8, 12 and 30 min. of 5 μM ionomycin incubation. **P < 0.01 indicates the significant difference of glutamate release when ionomycin is compared with control at 30 min.; #P < 0.05 indicates that glutamate release at 30 min is different compared with other stimulation time-points. Results are shown as mean ± SEM.

Mentions: The time-dependent stimulatory effect of ionomycin on glutamate release was investigated in the cultured SGCs. Samples were obtained at 4, 8, 12 and 30 min. after treatment with ionomycin and control. Ionomycin increased glutamate levels at 30 min., when compared to control (P < 0.01). No significant difference was detected between control and the first three time-points (4, 8 and 12 min.) after ionomycin treatment (Fig.5).


Botulinum neurotoxin type A modulates vesicular release of glutamate from satellite glial cells.

da Silva LB, Poulsen JN, Arendt-Nielsen L, Gazerani P - J. Cell. Mol. Med. (2015)

Time-dependent modulation of glutamate release by ionomycin. Glutamate concentration (μM) in culture medium after 4, 8, 12 and 30 min. of 5 μM ionomycin incubation. **P < 0.01 indicates the significant difference of glutamate release when ionomycin is compared with control at 30 min.; #P < 0.05 indicates that glutamate release at 30 min is different compared with other stimulation time-points. Results are shown as mean ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549040&req=5

fig05: Time-dependent modulation of glutamate release by ionomycin. Glutamate concentration (μM) in culture medium after 4, 8, 12 and 30 min. of 5 μM ionomycin incubation. **P < 0.01 indicates the significant difference of glutamate release when ionomycin is compared with control at 30 min.; #P < 0.05 indicates that glutamate release at 30 min is different compared with other stimulation time-points. Results are shown as mean ± SEM.
Mentions: The time-dependent stimulatory effect of ionomycin on glutamate release was investigated in the cultured SGCs. Samples were obtained at 4, 8, 12 and 30 min. after treatment with ionomycin and control. Ionomycin increased glutamate levels at 30 min., when compared to control (P < 0.01). No significant difference was detected between control and the first three time-points (4, 8 and 12 min.) after ionomycin treatment (Fig.5).

Bottom Line: Ionomycin significantly increased glutamate release from cultured SGCs 30 min. following the treatment (P < 0.001).BoNTA (100 pM) significantly decreased glutamate release (P < 0.01).In addition, interaction of BoNTA with non-neuronal cells at the level of TG suggests a potential analgesic mechanism of action of BoNTA.

View Article: PubMed Central - PubMed

Affiliation: Center for Sensory - Motor Interaction (SMI), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg East, Denmark.

No MeSH data available.


Related in: MedlinePlus