:Ion Transport Signal Pathways Mediated by Neurotransmitter(Biogenic Amines) of Litopenaeus vannamei Under Low Salinity Challenge论文

:Ion Transport Signal Pathways Mediated by Neurotransmitter(Biogenic Amines) of Litopenaeus vannamei Under Low Salinity Challenge论文

本文主要研究内容

作者(2019)在《Ion Transport Signal Pathways Mediated by Neurotransmitter(Biogenic Amines) of Litopenaeus vannamei Under Low Salinity Challenge》一文中研究指出:The Pacific white shrimp, Litopenaeus vannamei, is widely farmed in China. Salinity is a major environmental factor that affects its growth and distribution. Crustacean hyperglycemic hormone is verified to participate in ion transport in response to the salinity challenge mediated by endocrine neurotransmitters(biogenic amines, BAs). In the present study, the contents of BAs and expressions of their receptors were detected in gills of Litopenaeus vannamei exposed to low salinity. The intracellular signaling molecules such as cyclic adenosine monophosphate(cAMP), protein kinase A(PKA), 14-3-3 protein, FXYD2 protein and cAMP response element-binding protein(CREB) were detected. The effects of low salinity on the expressions of Na~+-K~+-ATPase, Na~+/K~+/2 Cl-co-transporter and Cl-transporter and activity of Na~+-K~+-ATPase were also analyzed. The results showed that dopamine and epinephrine concentrations and their receptor expressions were significantly affected by low salinity. The changes of c AMP and PKA were obvious and the expressions of 14-3-3 and FXYD2 peaked at early stages. However, the expression of CREB was only significantly up-regulated on day 9. The activity and expression of Na~+-K~+-ATPase(α subunit) reached a peak on day 1. The expressions of Na~+/K~+/2 Cl-co-transporter and Cl-transporter up-regulated obviously. It suggests that BAs can activate the cAMP-PKA pathway, which further acts on the 14-3-3 and FXYD2 proteins, and ultimately improve the activity of Na~+-K~+-ATPase. Furthermore, after BAs stimulate the cAMP-PKA pathway, PKA phosphorylates the transcription factor CREB and regulates the expressions of ion transport enzymes/transporters. The results in this study are helpful for understanding the response mechanism of endocrine neurotransmitters on osmoregulation in crustaceans.

Abstract

The Pacific white shrimp, Litopenaeus vannamei, is widely farmed in China. Salinity is a major environmental factor that affects its growth and distribution. Crustacean hyperglycemic hormone is verified to participate in ion transport in response to the salinity challenge mediated by endocrine neurotransmitters(biogenic amines, BAs). In the present study, the contents of BAs and expressions of their receptors were detected in gills of Litopenaeus vannamei exposed to low salinity. The intracellular signaling molecules such as cyclic adenosine monophosphate(cAMP), protein kinase A(PKA), 14-3-3 protein, FXYD2 protein and cAMP response element-binding protein(CREB) were detected. The effects of low salinity on the expressions of Na~+-K~+-ATPase, Na~+/K~+/2 Cl-co-transporter and Cl-transporter and activity of Na~+-K~+-ATPase were also analyzed. The results showed that dopamine and epinephrine concentrations and their receptor expressions were significantly affected by low salinity. The changes of c AMP and PKA were obvious and the expressions of 14-3-3 and FXYD2 peaked at early stages. However, the expression of CREB was only significantly up-regulated on day 9. The activity and expression of Na~+-K~+-ATPase(α subunit) reached a peak on day 1. The expressions of Na~+/K~+/2 Cl-co-transporter and Cl-transporter up-regulated obviously. It suggests that BAs can activate the cAMP-PKA pathway, which further acts on the 14-3-3 and FXYD2 proteins, and ultimately improve the activity of Na~+-K~+-ATPase. Furthermore, after BAs stimulate the cAMP-PKA pathway, PKA phosphorylates the transcription factor CREB and regulates the expressions of ion transport enzymes/transporters. The results in this study are helpful for understanding the response mechanism of endocrine neurotransmitters on osmoregulation in crustaceans.

论文参考文献

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