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Dopamine stimulates somatostatin release from perifused hypothalamic cells
The American Journal of Physiology
|June 1, 1983
Summary
This study demonstrates that immunoreactive somatostatin (IR-SRIF) release from rat hypothalamic cells is stimulated by potassium depolarization and dopamine. This release is calcium-dependent, offering insights into neuroendocrine regulation.
Area of Science:
- Neuroendocrinology
- Cell Physiology
Background:
- Hypothalamic somatostatin plays a crucial role in regulating endocrine functions.
- Understanding the mechanisms of somatostatin release is vital for neuroendocrine research.
Purpose of the Study:
- To investigate the release of immunoreactive somatostatin (IR-SRIF) from dispersed rat hypothalamic cells.
- To identify factors that stimulate IR-SRIF release, including depolarization and dopamine.
Main Methods:
- Dispersed rat hypothalamic cells were cultured and perifused using a Biogel P2 matrix.
- Somatostatin release was measured following stimulation with potassium chloride, ouabain, and dopamine.
- Calcium dependency and the effect of dopamine antagonists were assessed.
Main Results:
- Potassium depolarization (56 mM) and ouabain significantly stimulated IR-SRIF release.
- Dopamine stimulated IR-SRIF release at concentrations as low as 10(-11) M.
- Stimulation by depolarization was calcium-dependent and blocked by EDTA; metoclopramide abolished dopamine's effect.
Conclusions:
- A simple perifusion system effectively studies IR-SRIF release from rat hypothalamic cells.
- IR-SRIF release is stimulated by membrane depolarization in a calcium-dependent manner.
- Dopamine at physiological concentrations also stimulates IR-SRIF release.