INCORPORATION OF 14C-LABELLED AMINO ACIDS INTO CORTICOTROPHIN-LIKE INTERMEDIATE LOBE PEPTIDE AND α-MELANOCYTE-STIMULATING HORMONE BY THE RAT PITUITARY NEUROINTERMEDIATE LOBE IN VITRO, AND THE IDENTIFICATION OF FOUR NEW PARS INTERMEDIA PEPTIDES

1976 ◽  
Vol 70 (2) ◽  
pp. 197-205 ◽  
Author(s):  
A. P. SCOTT ◽  
P. J. LOWRY ◽  
TJ. B. VAN WIMERSMA GREIDANUS

SUMMARY At least seven radioactive peptides, which fractionated on Biogel P6, were found in rat neurointermediate lobes after incubation for 6 h with [14C]proline. Only three of these could be tentatively identified; one as α-melanocyte-stimulating hormone (α-MSH) and two as forms of corticotrophin-like intermediate lobe peptide (CLIP). One other crossreacted partially with a β-melanocyte-stimulating hormone (β-MSH) antiserum, was acidically charged and eluted on Biogel P6 in roughly the same position as ACTH. The other three peptides showed no resemblance to α-MSH, CLIP, β-MSH or ACTH.

1976 ◽  
Vol 68 (2) ◽  
pp. 283-287 ◽  
Author(s):  
BRIDGET I. BAKER

SUMMARY Various agents were tested for their ability to oppose the stimulatory effect of dibutyryl cyclic AMP on the release of the melanocyte-stimulating hormone from the rat neuro-intermediate lobe in vitro. Only dopamine exhibited an inhibitory effect; serotonin, γ-aminobutyric acid, tocinoic acid, tocinamide, the tripeptide Pro-Leu-Gly-NH2 and dibutyryl cyclic GMP were all ineffective.


1989 ◽  
Vol 122 (1) ◽  
pp. 135-NP ◽  
Author(s):  
M. Lamacz ◽  
M. C. Tonon ◽  
F. Leboulenger ◽  
F. Héry ◽  
S. Idres ◽  
...  

ABSTRACT We have examined the presence of 5-hydroxytryptamine (serotonin; 5-HT) in the intermediate lobe of the frog pituitary and investigated the effect of exogenous 5-HT on α-melanocyte-stimulating hormone (α-MSH) release from the perifused neurointermediate lobe (NIL). Using a specific antiserum against 5-HT, the indirect immunofluorescence technique revealed the presence of 5-HT-like immunoreactivity (5-HT-LI) in discrete cells, generally gathered in small clusters among parenchymal cells, and in numerous neurites surrounding melanotrophic cells. At the electron microscopic level, using a silver-gold intensification procedure, 5-HT-LI was localized in dense-core secretory vesicles within specific pituitary cells which appear to be different from pituitary melanotrophs. Dense accumulation of gold particles was also observed in nerve fibres running between parenchymal cells. A combination of high-performance liquid chromatography analysis and electrochemical detection showed the presence of both 5-HT and its metabolite 5-hydroxyindol acetic acid (5-HIAA) in frog NIL extracts (534 ± 40 and 1245 ± 65 (s.e.m.) pg/mg wet tissue respectively). Administration of graded doses of 5-HT (from 1 to 30 μmol/l) to perifused frog NIL induced a dose-dependent inhibition of α-MSH release. Repeated pulses of 5-HT (10 μmol/l each) induced a reproducible inhibition of α-MSH without any desensitization phenomena. The inhibitory effect of 5-HT was partially blocked by the serotonergic antagonists methysergide and ICS-205-930 (10 μmol/l each). Concomitant administration of methysergide and ICS-205-930 (10 μmol/l each) totally abolished 5-HT-evoked inhibition of α-MSH. Fenfluramine, a releaser of 5-HT, induced a slight but significant reduction of α-MSH secretion. While 5-HT caused a marked inhibition of α-MSH release from intact NIL, 5-HT was devoid of effect on acutely dispersed pars intermedia cells suggesting that 5-HT does not exert a direct action on pituitary melanotrophs. We have examined the effect of specific dopaminergic, GABAergic and α-adrenergic antagonists on 5-HT-induced α-MSH inhibition. We observed that sulpiride and SR 95531 (10 μmol/l each) did not affect the response of NIL to 5-HT while yohimbine (10 μmol/l) suppressed the inhibitory action of 5-HT. Taken together, our results indicate that discrete cells of the frog pars intermedia contain the neurotransmitter 5-HT which may act locally to inhibit α-MSH release. Our data also suggest that the inhibitory effect of 5-HT is mediated via presynaptic stimulation of catecholamine (possibly norepinephrine) release from adrenergic nerve endings terminating in the intermediate lobe of the frog pituitary. Journal of Endocrinology (1989) 122, 135–146


1985 ◽  
Vol 106 (2) ◽  
pp. 189-195 ◽  
Author(s):  
W. Knepel ◽  
D. Nutto ◽  
M. Vlaskovska ◽  
Ch. Kittel

ABSTRACT The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells. J. Endocr. (1985) 106, 189–195


1970 ◽  
Vol 46 (2) ◽  
pp. 201-NP ◽  
Author(s):  
A. HOWE ◽  
A. J. THODY

SUMMARY The changes in the content of melanocyte-stimulating hormone (MSH) and histology of the neuro-intermediate (n.i.) lobe were followed in rats which drank 2% sodium chloride for periods from 1–15 days. The pars intermedia showed a biphasic response. During the initial phase of 1–4 days there was a rapid rise in the MSH content, by 153% in the first day, falling back to control level by 4 days. These fluctuations were paralleled by an increase in the normally small numbers of Type 2 cells and at the same time numerous Type I cells showed hypertrophy and degranulation. After 4 days on saline there was a second rise in the MSH content, which was still evident at 15 days; during this second period the number of Type 2 cells declined to normal levels. The degranulated Type 1 cells also disappeared, most of Type 1 being smaller in size and intensely PAS-positive. After the ingestion of saline it apparently takes several days before the pars intermedia adapts to a new level of activity. The likely significance of these changes and the possibility of a relationship between the pars intermedia and the neurohypophysis are discussed.


1986 ◽  
Vol 17 (5) ◽  
pp. 717-723 ◽  
Author(s):  
S. Adjeround ◽  
M.C. Tonon ◽  
M. Lamacz ◽  
E. Leneveu ◽  
M.E. Stoeckel ◽  
...  

1992 ◽  
Vol 3 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Fermlín C. Iturriza ◽  
César L. A. Gómez Dumm

Glucocorticoid receptor-like immunoreactivity (GCRI) was found in the normal pituitary pars intermedia (PI) when immunohistochemistry was used. Since in previous studies we described two kinds of cells in the denervated (grafted) PI, i.e., “light cells” (overactive cells which do not contain detectable melanocyte stimulating hormone) and “dark cells” (hypoactive cells which contain the hormone), it was decided to investigate whether different patterns of distribution of the receptors could be detected in the grafted gland when compared with the intact PI. Intact glands showed the receptors located in the nucleus. In transplanted glands, it was observed that light cells showed receptors in both the nuclei and the cytoplasm; on the other hand, dark cells displayed them in the nuclei only, as is the case in all cells of the normal PI.We had previously interpreted dark cells as dopamine-indifferent, whereas light cells were considered dopamine-sensitive. The changes in the distribution of GCR after denervation by grafting, which only affected the light cells, support the view of other authors that GCR of. the pars intermedia are under the influence of dopamine and reinforce our opinion that dark cells are dopamine-indifferent


1981 ◽  
Vol 97 (3) ◽  
pp. 343-351 ◽  
Author(s):  
F.J. H. Tilders ◽  
M. Post ◽  
S. Jackson ◽  
P.J. Lowry ◽  
P. G. Smelik

Abstract. The intermediate lobe of the rat pituitary gland produces a series of peptides related to ACTH and LPH. The spontaneous and isoproterenol-stimulated release of such peptides was studied during in vitro superfusion of rat neurointermediate lobes with Krebs-Ringer medium. Products released into the superfusion medium were quantified by direct measurement or after chromatography on Sephadex G-50. ACTH bioactivity was determined by use of adrenal cortical cell suspension assay. In addition, NH2-terminal ACTH, CO2H-terminal ACTH, α-MSH and β-endorphin radioimmunoassays were used. The results show that 1. neurointermediate lobes of rats secrete spontaneously various ACTH- and LPH-related peptides in amounts proportional to the amounts in which these peptides are found in extracts of the neurointermediate lobe; 2. the β-adrenergic agonist, isoproterenol, stimulated the spontaneous release of various peptides, including α-MSH, ACTH, CLIP, glycosylated CLIP, and β-endorphin-like peptides; 3. isoproterenol induced a dose-dependent (10−9–10−7 m), parallel increase in the release of α-MSH and ACTH following similar time courses and showing indentical EC50 values (about 10−8 m). Although the spontaneous release of α-MSH and ACTH from rat neurointermediate lobes is not strictly coupled under the conditions used in this study, isoproterenol seems to affect the spontaneous release of these peptides to the same relative extent.


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