Sodium salicylate enhances neural excitation via reducing GABAergic transmission in the dentate gyrus area of rat hippocampus in vivo

Hippocampus ◽  
2021 ◽  
Author(s):  
Hui‐Ping Tang ◽  
Hua‐Rui Gong ◽  
Xu‐Lai Zhang ◽  
Yi‐Na Huang ◽  
Chuan‐Yun Wu ◽  
...  
2000 ◽  
Vol 83 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Hai L. Wang ◽  
Li Y. Tsai ◽  
Eminy H. Y. Lee

Corticotropin-releasing factor (CRF) was shown to produce a long-lasting potentiation of synaptic efficacy in dentate gyrus neurons of the rat hippocampus in vivo. This potentiation was shown to share some similarities with tetanization-induced long-term potentiation (LTP). In the present study, we further examined the mechanism underlying CRF-induced long-lasting potentiation in rat hippocampus in vivo. Results indicated that the RNA synthesis inhibitor actinomycin-D, at a concentration that did not change basal synaptic transmission alone (5 μg), significantly decreased CRF-induced potentiation. Similarly, the protein synthesis inhibitor emetine, at a concentration that did not affect hippocampal synaptic transmission alone (5 μg), also markedly inhibited CRF-induced potentiation. These results suggest that like the late phase of LTP, CRF-induced long-lasting potentiation also critically depend on protein synthesis. Further, prior maximum excitation of dentate gyrus neurons with tetanization occluded further potentiation of these neurons produced by CRF and vise versa. Moreover, quantitative reverse transcription-polymerase chain reaction analysis revealed that CRF mRNA level in the dentate gyrus was significantly increased 1 h after LTP recording. Together with our previous findings that CRF antagonist dose-dependently diminishes tetanization-induced LTP, these results suggest that both CRF-induced long-lasting potentiation and tetanization-induced LTP require protein synthesis and that CRF neurons are possibly involved in the neural circuits underlying LTP.


2020 ◽  
Vol 16 (1) ◽  
pp. 200-204
Author(s):  
Li Yang ◽  
De Wu ◽  
Baotian Wang ◽  
Xiaosong Bu ◽  
Jing Zhu ◽  
...  

Neuroscience ◽  
2000 ◽  
Vol 100 (2) ◽  
pp. 221-227 ◽  
Author(s):  
M.G Stewart ◽  
E Harrison ◽  
D.A Rusakov ◽  
G Richter-Levin ◽  
M Maroun

1972 ◽  
Vol 126 (2) ◽  
pp. 347-350 ◽  
Author(s):  
A. A.-B. Badawy

1. Salicylate, in concentrations of 0.25mm and above, enhances the basal activity of tyrosine–2-oxoglutarate aminotransferase in homogenates of rat liver incubated in the absence of added pyridoxal 5′-phosphate (endogenous activity). The effect is decreased by increasing the concentration of the cofactor. 2. The intraperitoneal administration of sodium salicylate enhances the activity of rat liver tyrosine aminotransferase; the major effect during the first hour being on the enzyme in the absence of added pyridoxal phosphate. Actinomycin D prevents the induction of the enzyme by cortisol and tryptophan. Induction by pyridoxine or salicylate is 50% inhibited by actinomycin D. The effects of the injections of various combinations of cortisol, pyridoxine and salicylate were also studied in the absence or presence of actinomycin D. 3. It is suggested that salicylate induces rat liver tyrosine aminotransferase by displacing its protein-bound cofactor and that a cofactor-type induction of the hepatic enzyme occurs in pyridoxine-treated rats.


1990 ◽  
Vol 26 (2) ◽  
pp. 159-167 ◽  
Author(s):  
J. M. Solis ◽  
A. S. Herranz ◽  
O. Herreras ◽  
N. Menéndez ◽  
R. Martin del Rio

Sign in / Sign up

Export Citation Format

Share Document