| dc.creator |
Naziroglu, M. |
|
| dc.creator |
Ozgul, C. |
|
| dc.date |
2012-05-15T00:00:00Z |
|
| dc.date.accessioned |
2021-12-03T11:38:55Z |
|
| dc.date.available |
2021-12-03T11:38:55Z |
|
| dc.identifier |
9af6f4e2-14ba-4acb-af3e-49e95d596aca |
|
| dc.identifier |
10.1016/j.physbeh.2012.01.014 |
|
| dc.identifier |
https://avesis.sdu.edu.tr/publication/details/9af6f4e2-14ba-4acb-af3e-49e95d596aca/oai |
|
| dc.identifier.uri |
http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/93561 |
|
| dc.description |
N-acetylcysteine (NAC) is a thiol-containing (sulphydryl donor) antioxidant, which contributes to regeneration of glutathione (GSH) and also acts through a direct reaction with free radicals. Thiol depletion has been implicated in the neurobiology of sensory neurons and pain. We reported recently an activator role of intracellular GSH depletion on calcium influx through transient receptor potential melastatin-like 2 (TRPM2) channels in rat dorsal root ganglion (DRG). NAC may have a protective role on calcium influx through regulation of TRPM2 channels in the neurons. Therefore, we tested the effects of NAC on TRPM2 channel currents in cytosolic GSH depleted DRG in rats. |
|
| dc.language |
eng |
|
| dc.rights |
info:eu-repo/semantics/closedAccess |
|
| dc.title |
TRPM2 channel protective properties of N-acetylcysteine on cytosolic glutathione depletion dependent oxidative stress and Ca2+ influx in rat dorsal root ganglion |
|
| dc.type |
info:eu-repo/semantics/article |
|