scholarly journals Mechanism of Delayed Convulsion in Fish: The Actions of Norepinephrine in Spinal Cord

Fishes ◽  
2021 ◽  
Vol 6 (2) ◽  
pp. 12
Author(s):  
Cheng-Linn Lee ◽  
Yuri Kominami ◽  
Hideki Ushio

Cranial spiking (CS) is among the most popular slaughtering methods for delaying the rigor mortis progress of fish muscles. However, it may cause a convulsion (subsequently referred to as delayed convulsion), which undermines the meat quality and taste. This study aimed to elucidate the mechanism underlying the delayed convulsion and examine its influence on ATP consumption. Ten carps, nine tilapias, ten rainbow trouts, two ayus, three greenling, thirty-five red seabreams, two striped jack and two stone flounders underwent CS around the medulla oblongata area, which induced different delayed convulsion profiles specific to each species. To investigate the norepinephrine (NE) actions related to delayed convulsion, 27 red seabreams, a representative fish species that exhibits delayed convulsion, were treated with a monoamine-depleting agent, reserpine, or with a monoamine oxidase inhibitor, pargyline, two hours before CS. Spinal cord destruction (SCD) was employed to completely prevent spinal cord functions of the fish in another group. Compared with the control group (CS only), the reserpine, pargyline, and SCD groups showed significantly inhibited delayed convulsion and ATP consumption. This suggests that delayed convulsion is the main ATP-consuming response. Our findings suggest that delayed clonic convulsion in red seabreams is associated with the rapid decrease in spinal cord NE levels, which triggered the rebound motor neuron hyperactivity.

1989 ◽  
Vol 4 (3) ◽  
pp. 175-181
Author(s):  
J.F. Lipinski ◽  
R.C. Alexander

SummaryThe authors have reviewed 13 published studies on methionine administration, usually in combination with a monoamine oxidase inhibitor (MAOI), to chronically psychotic patients, using modern (DSM-III) diagnostic criteria. Four of these studies contained sufficient descriptive data to allow reappraisal of the effects. The results of the review suggest that a proportion of the patients experienced the induction of a manic episode/antidepressant effects rather than the reported worsening of schizophrenia while treated with a methionine-MAOI combination. It is suggested that these observations are consistent with recent findings that S-adenosyl-L-methionine (SAMe) has antidepressant and mania-inducing effects.


1995 ◽  
Vol 22 (s1) ◽  
pp. S86-S87 ◽  
Author(s):  
N. Hamaue ◽  
T. Endo ◽  
M. Hirafuji ◽  
N. Yamazaki ◽  
H. Togashi ◽  
...  

2010 ◽  
Vol 3 (4) ◽  
pp. 213-215
Author(s):  
Junji Takeshita ◽  
Deborah Goebert ◽  
John Huh ◽  
Brett Lu ◽  
Diane Thompson ◽  
...  

2000 ◽  
Vol 52 (4) ◽  
pp. 451-459 ◽  
Author(s):  
B. D. SLOLEY ◽  
L. J. URICHUK ◽  
P. MORLEY ◽  
J. DURKIN ◽  
J. J. SHAN ◽  
...  

Author(s):  
Amedeo S. Marrazzi ◽  
E. Ross Hart ◽  
Jose M. Rodriguez ◽  
Melvyn I. Gluckman ◽  
Zola P. Horovitz ◽  
...  

1997 ◽  
Vol 3 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Eleni Palazidou

The development of the first effective antidepressants in the late 1950s marked a turning point in the treatment of depressive illness. In 1957 the monoamine oxidase inhibitor (MAOI) iproniazid was discovered by chance, while searching for new antituberculous drugs. One year later the tricyclic antidepressant (TCA) imipramine was introduced, having been developed originally as an antipsychotic. A number of other drugs were subsequently added to these two groups of antidepressants, which dominated the field for the next three decades.


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