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Nitric oxide in the control of luminescence from lantern shark (Etmopterus spinax)
Claes, J.M.; Krönström, J.; Holmgren, S.; Mallefet, J. (2010). Nitric oxide in the control of luminescence from lantern shark (Etmopterus spinax). J. Exp. Biol. 213(17): 3005-3011.
In: Journal of Experimental Biology. Cambridge University Press: London. ISSN 0022-0949; e-ISSN 1477-9145, more
Peer reviewed article  

Available in  Authors 
    VLIZ: Open Repository 296038 [ OMA ]

Author keywords
    acetylated tubulin; bioluminescence; Chondrichthyes; melatonin; nitricoxide synthase; prolactin

Authors  Top 
  • Claes, J.M., more
  • Krönström, J.
  • Holmgren, S.
  • Mallefet, J., more

    Photophores (photogenic organs) of the lantern shark Etmopterus spinax are under hormonal control, with prolactin (PRL) and melatonin (MT) triggering the light emission. Differential sensitivity to these hormones in adult individuals suggests, however, that the luminescence of this shark is controlled by an additional mechanism. In this study, different techniques were used to investigate a potential modulator of E. spinax luminescence – nitric oxide (NO). NO synthase (NOS)-like immunoreactivity (IR) was found in the photocytes (photogenic cells) of the photophores. In addition, acetylated tubulin IR also supported the presence of nerves running through the photogenic tissue and innervating different structural elements of the photophores: photocytes, pigmented cells from the iris-like structure and lens cells. Pharmacological experiments confirmed a modulatory action of NO on the hormonally induced luminescence: NO donors sodium nitroprusside (SNP) and hydroxylamine decreased the time to reach the maximum amplitude (TLmax) of MT-induced luminescence while these substances decreased the maximum amplitude of PRL-induced luminescence (and also the TLmax in the case of SNP). The small impact of the NOS inhibitor l-NAME on hormonally induced luminescence suggests that NO is only produced on demand. The cGMP analogue 8BrcGMP mimicked the effects of NO donors suggesting that the effects of NO are mediated by cGMP.

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