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

Abstract

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.