Effects of inhibitory and excitatory amino acid neurotransmitters on isolated cerebral parenchymal arterioles

1989 ◽  
Vol 482 (2) ◽  
pp. 393-396 ◽  
Author(s):  
Masakazu Takayasu ◽  
Ralph G. Dacey
1994 ◽  
Vol 1 (1) ◽  
pp. 21-25
Author(s):  
Akio Tateishi ◽  
Tsuyoshi Maekawa ◽  
Yasuhiro Kuroda ◽  
Yasuhiro Morimoto ◽  
Yoshiyuki Soejima ◽  
...  

Endocrine ◽  
2005 ◽  
Vol 28 (3) ◽  
pp. 281-286 ◽  
Author(s):  
Anne-Simone Parent ◽  
Valérie Matagne ◽  
Jean-Pierre Bourguignon

2016 ◽  
Vol 11 ◽  
pp. S55-S60
Author(s):  
Mingxian Shi ◽  
Rui Chen ◽  
Cen Guo ◽  
Li Gao

In order to study the influence of amino acid neurotransmitters secreted by the nerve cells after ketamine treatment, the nerve cells were cultured in vitro to exclude the interference of other factors in vivo and treated with three different doses of ketamine (1, 3 and 5 µg/mL). Then, the concentration of neuronal amino acid neurotransmitters was examined at 0, 15, 30, 45, 60, 90, 120 min after treatment. The trends of each amino acid concentration after ketamine treatment were nearly the same among the different treatment doses. After 15 min of adapting time, ketamine decreased the excitatory amino acid glutamic acid and aspartic acid concentration, and increased the concentration of the inhibitory amino acid glycine. Their concentrations showed a tendency to return approximately to the original level after 120 min. 


1993 ◽  
Vol 71 (5-6) ◽  
pp. 348-351 ◽  
Author(s):  
Francisco Mora ◽  
Alberto Porras

The effects of systemic injections of amphetamine sulfate on the release of aspartic acid, glutamic acid, and glutamine were studied using a push–pull perfusion system in the conscious rat. Amphetamine produced a dose-related increase of the extracellular levels of aspartic acid and glutamic acid. The mean time effect of amphetamine was 40 min, followed by a recovery to baseline levels. The mean percentage increase in amino acids released by the highest dose of amphetamine (5 mg/kg) was as follows: Asp, 334.6%; Glu, 224.5%; and Gln, 317.6%. All these effects were blocked by the dopamine D1–D2 receptor blocker haloperidol. It is suggested that dopamine, released by amphetamine, induces the release of amino acid neurotransmitters in the neostriatum. In addition, it is proposed that dopamine could mediate the neurotoxic effects produced by amphetamines through their secondary action on the release of excitatory amino acids.Key words: amphetamine, dopamine, excitatory amino acids, neostriatum, conscious rat.


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