AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 1 387-R392, Copyright © 1997 by American Physiological Society
Acid stress induces a D1-like dopamine receptor in pituitary MSH cells of Oreochromis mossambicus
A. E. Lamers, P. J. Ter Brugge, G. Flik and S. E. Wendelaar Bonga
Department of Animal Physiology, Faculty of Science, University of Nijmegen, The Netherlands.
A 7-day exposure of tilapia (Oreochromis mossambicus) to water with a pH of
4.5 activates their pituitary melanophore-stimulating hormone (MSH) cells
to preferentially release diacetyl alpha-MSH as an important corticotrope
(13). We here focus on the control of alpha-MSH release by dopamine in
tilapia exposed to water with low pH ("low-pH tilapia"). The MSH cells of
low-pH tilapia showed a decreased sensitivity to inhibitory concentrations
(10(-7)-10(-5) M) of dopamine compared with controls. Low concentrations
(10(-14)-10(-8) M) of dopamine stimulated the release of alpha-MSH in
low-pH tilapia but not in controls. Strong pharmacological evidence for a
stimulatory dopamine receptor (D1-like) was obtained: the D1-agonists
SKF-38393 and
6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazep
ine hydrobromide (6-chloro APB) had a stimulatory effect on the release of
alpha-MSH in low-pH tilapia MSH cells but not in controls. The selective
D2-agonists quinpirole and 2-hydroxy apomorphin inhibited the release of
alpha-MSH in controls as well as in low-pH tilapia, and there was no
difference in the sensitivity of the cells to these agonists. We conclude
that only MSH cells of low-pH exposed tilapia exhibit a D1-like receptor
activity. A comparable D2-like receptor activity, as demonstrated by
specific D2-receptor agonists, is present in both controls and
low-pH-adapted fish. The apparent loss of sensitivity of the MSH cells to
inhibitory concentrations of dopamine, therefore, must be caused by the
activation of the D1-like receptors and not by changes in the activity of
the D2-like receptor proper. Stimulatory concentrations of dopamine not
only quantitatively but also qualitatively enhanced the corticotropic
activity of the released alpha-MSH, as indicated by the elevated ratio of
diacetyl and monoacetyl alpha-MSH. This effect was mimicked by the D1-like
agonists SKF-38393 and 6-chloro APB, indicating that the D1-like receptor
activity is responsible for the enhancement of the di/mono ratio.
