Abstract
The γ-aminobutyric acid (GABA) signal transmission system (GSTS) contributes to larval swimming through the regulation of ciliary beating. However, whether this system also contributes to the primary podia (PP)-generated motility of juveniles remained unclear. The present study aimed to elucidate the involvement of the GSTS in the motility of metamorphic juveniles (juveniles) (1) by immunohistochemically elucidating the location of molecular constituents of the PP, and (2) by inhibiting the activity of GΑΒΑ decarboxylase (GAD) with 3-mercaptopropionic acid (3-MPA). During metamorphosis, the echinus rudiment protrudes its PP out of the body surface in 8-arm plutei. The PP expresses immunopositive signal (-IS) of GAD, GABA, GABAA receptor and tropomyosin, and is constituted with the GABA-IS negative distal tip and the GABA/GAD-IS gaiter region. The latter radiates distal projections to the disc that contains a GAD-IS cellular network. The juvenile body cavity houses a GABA/βIII-tubulin-IS Penta-radial ring (PrR) that extends branches into each PP and several bridges to the GAD/GABA-IS Penta-radial plate (PrP) on the oral side but does not reach to the gaiter region. 3-MPA reversibly inhibits the juvenile motility and GABA-IS expression in the PrR/PrP complex. This indicates that the complex is the major contributor to the GABAergic motility in juveniles.
Highlights
The swimming activity of sea urchin plutei is carried out by the body surface ciliary beating and is regulated by various neurotransmitters, including GABA1, serotonin[2,3,4], and dopamine[5,6]
Consistent with our previous report[7], primary podia (PP) were detected in the larva as Syt-IS small protrusions in echinus rudiment (EcR) (Fig. 2A, pp)
In slightly older plutei than that mentioned above, the EcR bulged slightly toward the left side of the larval body surface, and TM-IS and GABAA Receptor (GABAAR)-IS were faintly detected in all five PP (Fig. 2D,D1,D2)
Summary
The swimming activity of sea urchin plutei is carried out by the body surface ciliary beating and is regulated by various neurotransmitters, including GABA1, serotonin[2,3,4], and dopamine[5,6]. GABAergic NS involvement in the motile activity throughout sea urchin development appears to be consistently taken over from the ciliary beating in the larval stage[1,13,14] to creeping movement by the TF of the adult sea urchins. The circumoral synaptotagmin (Syt)-expressing Penta-radial nerve ring appears to control the tube feet movements[15]. The present study aimed to elucidate the following by means of immunohistochemistry of a GABA-immunopositive signal (-IS), glutamate decarboxylase (GAD)-IS, GABAA Receptor (GABAAR)-IS, and tropomyosin (TM)-IS constituents, and through 3-D reconstruction, and pharmaceutical bioassay analysis. They are (1) to elucidate the detailed developmental process of the GABAergic
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