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The tilapia prolactin cell: A model for stimulus-secretion coupling.

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Tilapia prolactin (PRL) cells release hormone in response to osmotic pressure changes, modulated by calcium (Ca++) and cAMP. Somatostatin (SRIF) inhibits this release, suggesting complex intracellular signaling pathways regulate PRL secretion.

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Area of Science:

  • Endocrinology
  • Cell Signaling
  • Fish Physiology

Background:

  • Tilapia prolactin (PRL) cells exhibit rapid responses to osmotic pressure (OP) changes.
  • Hormone release is modulated by intracellular calcium (Ca++) and cyclic adenosine monophosphate (cAMP).
  • Somatostatin (SRIF) is a known inhibitor of PRL release.

Purpose of the Study:

  • To investigate the roles of Ca++ and cAMP in tilapia PRL cell function.
  • To determine the effects of osmotic pressure and SRIF on Ca++ and cAMP signaling.
  • To elucidate the interplay between OP, SRIF, Ca++, and cAMP in regulating PRL secretion.

Main Methods:

  • Incubation of tilapia PRL cells under varying osmotic pressures and with/without SRIF.
  • Measurement of PRL release.
  • Quantification of intracellular Ca++ levels using 45Ca++.
  • Assessment of cAMP levels using IBMX and forskolin stimulation.

Main Results:

  • Reduced OP stimulated PRL release, which was inhibited by SRIF.
  • Increased intracellular Ca++ augmented PRL release, while Ca++ depletion blocked it.
  • SRIF suppressed OP-induced Ca++ influx and forskolin-stimulated cAMP accumulation.
  • Sustained low OP enhanced cAMP accumulation, suggesting a role in prolonged PRL release.
  • Ca++ is essential for PRL release, even with activated cAMP pathways.

Conclusions:

  • Both Ca++ influx and cAMP signaling are critical for tilapia PRL release.
  • SRIF inhibits PRL release by suppressing Ca++ influx and potentially adenylate cyclase activity.
  • OP-induced PRL release may involve indirect stimulation of cAMP turnover via cytosolic Ca++.
  • These findings highlight the complex, integrated signaling mechanisms regulating fish PRL secretion.