4.4 Article

Ionoregulatory and endocrine responses to disturbed salt and water balance in Mozambique tilapia exposed to confinement and handling stress

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpa.2009.10.033

关键词

GH/IGF-I axis; Ion transporter; Na+/K+-ATPase; Osmoregulation; Prolactin; Stress; Tilapia

资金

  1. National Science Foundation [IOB05-17769]
  2. National Research Initiative Competitive [2008-35206-18785]
  3. USDA Cooperative State Research, Education, and Extension Service
  4. Office Of Internatl Science &Engineering [852518] Funding Source: National Science Foundation
  5. Office Of The Director [852518] Funding Source: National Science Foundation

向作者/读者索取更多资源

This study assessed the endocrine and ionoregulatory responses by tilapia (Oreochromis mossambicus) to disturbances of hydromineral balance during confinement and handling. In fresh water (FW), confinement and handling for 0.5, 1, 2 and 6 h produced elevations in plasma cortisol and glucose; a reduction in plasma osmolality was observed at 6 h. Elevations in plasma prolactins (PRL177 and PRL188) accompanied this fall in osmolality while no effect upon growth hormone (GH) was evident; an increase in insulin-like growth-factor I (IGF-I) occurred at 0.5 h. In seawater (SW), confinement and handling increased plasma osmolality and glucose between 0.5 and 6 h; no effect on plasma cortisol was seen due to variable control levels. Concurrently, both PRLs were reduced in stressed fish with only transient changes in the GH/IGF-I axis. Next, the branchial expression of Na+/K+/2Cl(-) cotransporter (NKCC) and Na+/Cl- cotransporter (NCC) was characterized following confinement and handling for 6 h. In SW, NKCC mRNA levels increased in stressed fish concurrently with elevated plasma osmolality and diminished gill Na+, K+-ATPase activity; NCC was unchanged in stressed fish irrespective of salinity. Taken together, PRL and NKCC participate in restoring osmotic balance during acute stress while the GH/IGF-I axis displays only modest responses. (C) 2009 Elsevier Inc. All rights reserved.

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