scholarly journals Effects of Immobilization Stress on Serotonin Release in Rat Brain as Determined by in vivo Microdialysis

1992 ◽  
Vol 46 (1) ◽  
pp. 319-328
Author(s):  
Yuji Amano
1994 ◽  
Vol 64 ◽  
pp. 234
Author(s):  
Kiyofumi Itoh ◽  
Hiroyuki Konya ◽  
Hiroshi Masuda ◽  
Eizo Kakishita ◽  
Naoko Hayashi ◽  
...  

1996 ◽  
Vol 39 ◽  
pp. 232-232
Author(s):  
Wako Nakajima ◽  
Akira Ishida ◽  
Hirokazu Arai ◽  
Yasushi Takahashi ◽  
Tadahiko Ito ◽  
...  

Author(s):  
B. Scatton ◽  
L. Rouquier ◽  
G. Bonvento ◽  
A. Serrano ◽  
P. Blier
Keyword(s):  

1999 ◽  
Vol 79 ◽  
pp. 255
Author(s):  
Masago Ishikawa ◽  
Kazuo Isomae ◽  
Megumi Ohta ◽  
Yoichiro Ogawa ◽  
Hiroshi Hasegawa ◽  
...  

2019 ◽  
Vol 22 (10) ◽  
pp. 665-674 ◽  
Author(s):  
Yukio Ago ◽  
Wataru Tanabe ◽  
Momoko Higuchi ◽  
Shinji Tsukada ◽  
Tatsunori Tanaka ◽  
...  

Abstract Background Although recent studies provide insight into the molecular mechanisms of the effects of ketamine, the antidepressant mechanism of ketamine enantiomers and their metabolites is not fully understood. In view of the involvement of mechanisms other than the N-methyl-D-aspartate receptor in ketamine’s action, we investigated the effects of (R)-ketamine, (S)-ketamine, (R)-norketamine [(R)-NK], (S)-NK, (2R,6R)-hydroxynorketamine [(2R,6R)-HNK], and (2S,6S)-HNK on monoaminergic neurotransmission in the prefrontal cortex of mice. Methods The extracellular monoamine levels in the prefrontal cortex were measured by in vivo microdialysis. Results (R)-Ketamine and (S)-ketamine acutely increased serotonin release in a dose-dependent manner, and the effect of (R)-ketamine was greater than that of (S)-ketamine. In contrast, (S)-ketamine caused a robust increase in dopamine release compared with (R)-ketamine. Both ketamine enantiomers increased noradrenaline release, but these effects did not differ. (2R,6R)-HNK caused a slight but significant increase in serotonin and noradrenaline but not dopamine release. (S)-NK increased dopamine and noradrenaline but not serotonin release. Differential effects between (R)-ketamine and (S)-ketamine were also observed in a lipopolysaccharide-induced model of depression. An α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor antagonist, 2,3-dioxo-6-nitro-1,2,3,4- tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX), attenuated (S)-ketamine-induced, but not (R)-ketamine-induced serotonin release, whereas NBQX blocked dopamine release induced by both enantiomers. Local application of (R)-ketamine into the prefrontal cortex caused a greater increase in prefrontal serotonin release than that of (S)-ketamine. Conclusions (R)-Ketamine strongly activates the prefrontal serotonergic system through an AMPA receptor-independent mechanism. (S)-Ketamine-induced serotonin and dopamine release was AMPA receptor-dependent. These findings provide a neurochemical basis for the underlying pharmacological differences between ketamine enantiomers and their metabolites.


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