Inhibitory effect of interleukin-6 on NMDA-stimulated neuronal firing activity and possible mechanism involved in the effect.
- Author:
Xian-Feng ZHAN
1
;
Bing LI
;
Bei WU
;
Yu-Ping PENG
;
Yi-Hua QIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cerebellum; drug effects; metabolism; In Vitro Techniques; Interleukin-6; pharmacology; N-Methylaspartate; pharmacology; Nerve Growth Factors; metabolism; Neurons; drug effects; metabolism; physiology; Phosphorylation; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; metabolism
- From: Chinese Journal of Applied Physiology 2010;26(3):365-369
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect and the possible mechanism of IL-6 on NMDA-excited neuronal discharges of rats in vitro.
METHODSThe cerebellar slices were prepared and spontaneous discharges of single cerebellar interposed nuclear (IN) neurons were recorded by extracellular recordings. The cerebellar slices were perfused with artificial cerebral spinal fluid (ACSF) containing N-methyl-D-aspartate (NMDA), IL-6, JAK inhibitor AG490. The changes in firing activities of the neurons treated with the drugs were recorded. The levels of phosphorylation at serine 897 site of NMDA receptor subunit 1 (NR1) in the neurons treated with various drugs mentioned above were detected by Western blot.
RESULTSThe discharge rates of the neurons that were treated with IL-6 together with NMDA were significantly lower than those of the neurons treated with NMDA alone. AG490 partially blocked the inhibitory effect of IL-6 on the NMDA-stimulated neuronal firing activity. The treatment of the neurons with IL6 and NMDA led to a concentration-dependent suppression of the phospho-NR1 expression relative to those neurons treated with NMDA alone. AG490 blocked the effect of the IL-6-induced depression of phospho-NR1 expression.
CONCLUSIONIL-6 inhibits NMDA-stimulated neuronal firing activity, and simultaneously down-regulates the phosphorylation of NR1 at serine 897 site.
