TY - JOUR
T1 - Vasoactive intestinal peptide is a hypothalamic prolactin-releasing neuropeptide in the turkey (Meleagris gallopavo)
AU - El Halawani, M. E.
AU - Silsby, J. L.
AU - Mauro, L. J.
N1 - Funding Information:
’ Minnesota Agricultural Experiment Station Scientific Journal Article 17,266. Supported by USDA Grant88-37242-3845.
PY - 1990/4
Y1 - 1990/4
N2 - The hypothesis that vasoactive intestinal peptide (VIP) functions as a hypothalmic prolactin (PRL)-releasing peptide in the turkey was tested by determining the effects of hypothalamic VIP immunoneutralization and pituitary VIP receptor blockade on hypothalamic extract (HE)-induced PRL secretion from dispersed anterior pituitaries. Incubation of cells with porcine VIP (pVIP; 0.5 or 10 nM) significantly stimulated PRL secretion. This effect was inhibited in a dose-related manner by 1-hr preincubation of pVIP with a VIP antisera ( A S; 1:500-1:50,000). Likewise, HE (0.3 equivalent)-stimulated PRL secretion was inhibited by preincubation with VIP A S (P < 0.0001). A 96-98% reduction in PRL secretion was obtained from cells cultured with HE, that was previously incubated with 1 500 dilution of antiserum. Pretreatment of pituitary cells for 15 min with [4Cl-d-Phe6,Leu17] VIP, a VIP receptor antagonist (10-5 M), significantly depressed the PRL response to 0.5 nM VIP (9.9 ± 0.5 μg/500,000 cells vs 4.9 ± 0.1 μg/500,000 cells; 22.4 ± 0.9 μg/500,000 cells vs 14.7 ± 0.4 μg/500,000 cells) or 0.3 eq HE (8.8 ± 0.6 μg/500,000 cells vs 5.2 ± 0.2 μg/500,000 cells; 15.3 ± 0.3 μg/500,000 cells vs 8.2 ± 0.2 μg/500,000 cells). These results suggest that hypothalamic stimulation of PRL secretion appears to be mediated by receptors specific for VIP and that VIP is an endogenous hypothalamic PRL-releasing peptide in the turkey.
AB - The hypothesis that vasoactive intestinal peptide (VIP) functions as a hypothalmic prolactin (PRL)-releasing peptide in the turkey was tested by determining the effects of hypothalamic VIP immunoneutralization and pituitary VIP receptor blockade on hypothalamic extract (HE)-induced PRL secretion from dispersed anterior pituitaries. Incubation of cells with porcine VIP (pVIP; 0.5 or 10 nM) significantly stimulated PRL secretion. This effect was inhibited in a dose-related manner by 1-hr preincubation of pVIP with a VIP antisera ( A S; 1:500-1:50,000). Likewise, HE (0.3 equivalent)-stimulated PRL secretion was inhibited by preincubation with VIP A S (P < 0.0001). A 96-98% reduction in PRL secretion was obtained from cells cultured with HE, that was previously incubated with 1 500 dilution of antiserum. Pretreatment of pituitary cells for 15 min with [4Cl-d-Phe6,Leu17] VIP, a VIP receptor antagonist (10-5 M), significantly depressed the PRL response to 0.5 nM VIP (9.9 ± 0.5 μg/500,000 cells vs 4.9 ± 0.1 μg/500,000 cells; 22.4 ± 0.9 μg/500,000 cells vs 14.7 ± 0.4 μg/500,000 cells) or 0.3 eq HE (8.8 ± 0.6 μg/500,000 cells vs 5.2 ± 0.2 μg/500,000 cells; 15.3 ± 0.3 μg/500,000 cells vs 8.2 ± 0.2 μg/500,000 cells). These results suggest that hypothalamic stimulation of PRL secretion appears to be mediated by receptors specific for VIP and that VIP is an endogenous hypothalamic PRL-releasing peptide in the turkey.
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U2 - 10.1016/0016-6480(90)90048-Q
DO - 10.1016/0016-6480(90)90048-Q
M3 - Article
C2 - 2158920
AN - SCOPUS:0025263823
SN - 0016-6480
VL - 78
SP - 66
EP - 73
JO - General and Comparative Endocrinology
JF - General and Comparative Endocrinology
IS - 1
ER -