{'fraction_non_alphanumeric': 0.048198408984557795, 'fraction_numerical': 0.024801123069723912, 'mean_word_length': 4.794037940379404, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Acid stress induces a D1-like dopamine receptor in pituitary MSH cells of Oreochromis mossambicus.

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.