Ultrastructural Evidence for Endogenous Somatostatin-Like Immunoreactivity in the Pituitary Gland

Morel, Gérard; Mesguich, Patrick; Dubois, M. P.; Dubois, Paul

doi:10.1159/000123470

Cited by 34 publications

(10 citation statements)

References 25 publications

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“…Moreover, the subcellular distribution resembled that previously observed with neuropeptides such as GnRH [23], TRH [28], CRF [24], GRF [27] and somatosta tin [26] in adenohypophyseal cells as well as that for TRH and NPY in the parenchymal cells of the frog intermediate lobe [29]. The presence of NPY-like immunoreactivity at the plasma membrane is difficult to observe, possibly because the molecule is rapidly internalized.…”

Section: Discussionsupporting

confidence: 79%

“…33. 38], TRH [28,29], CRF [16,24], somatostatin [25,26] and GRF [27], The biological significance of NPY-like immuno reactivity over the secretory granules is unclear. However, based on immunocytochemistry, such a localization has al ready been reported for GnRH [23], TRH [28], CRF [241.…”

Section: Discussionmentioning

confidence: 99%

“…However, based on immunocytochemistry, such a localization has al ready been reported for GnRH [23], TRH [28], CRF [241. GRF [2] and somatostatin [26].…”

Section: Discussionmentioning

confidence: 99%

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Evidence for a Direct Action of Neuropeptide Y in the Rat Pituitary Gland

et al. 1988

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Neuropeptide Y (NPY) has recently been localized in the rat hypothalamus. In order to evaluate the putative effects of NPY on pituitary function, its action was examined on anterior pituitary cells in culture. Also, an immunocytochemical method was used with the aim of localizing endogenous NPY-like material at the cellular and subcellular levels of the pituitary gland. In vitro studies using dispersed anterior pituitary cells indicated that NPY (10^–6 to 10^–9M) increased the secretion of luteinizing hormone, growth hormone and prolactin, whereas β-lipotropin hormone and thyrotropin secretions were not affected. The presence of endogenous NPY was demonstrated in gonadotrophs, somatotrophs, corticotrophs and some lactotrophs, but not in thyrotrophs. In immunoreactive cells, NPY-like material was detected in the cytoplasmic matrix, in the secretory granules and in the nucleus distributed primarily in the euchromatin, in the vicinity of the heterochromatin. NPY-like immunoreactivity was also observed at the plasma membrane but only scarcely. These biochemical and immunocytochemical results indicate that NPY may play a direct regulatory role in adenohypophyseal secretion.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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Evidence for a Direct Action of Neuropeptide Y in the Rat Pituitary Gland

et al. 1988

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“…It has been postulated that one of somatostatin's func tions is to temporarily block the release of stored intracellular GH, while allowing GH to accumulate in an immediately re leasable pool; withdrawal of the somatostatin block permits dis charge of this releasable pool [32]. Moreover, previous studies have reported the presence of somatostatin in the somatotroph secretory granules [33], Whether this peptide is increased in the pituitary of the obese rat and therefore may interfere with GH release remains to be determined. In addition, alterations of so matotroph GRF a n d /o r somatostatin receptors or changes in the postreceptorial events could be involved in the anomaly of the GH release.…”

Section: Discussionmentioning

confidence: 99%

Decreased Pituitary Growth Hormone Response to Growth Hormone-Releasing Factor in Cafeteria-Fed Rats: Dietary and Obesity Effects

Renier

Gaudreau²,

Hajjad³

et al. 1990

Neuroendocrinology

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The in vivo and in vitro growth hormone (GH) responsiveness to growth hormone-releasing factor [rGRF(l-29)NH2] was evaluated in a dietary obese rat model. Sprague-Dawley rats were divided into two groups after weaning. The control group received a semisynthetic defined diet, and the cafeteria-fed group was maintained on a mixed energy-rich palatable diet. After 2 months of diet, the cafeteria-fed rats were divided into two groups, according to their degree of weight gain compared to controls: group I: 0%; group II: 24%. After 5 months of diet, the weight increase was, respectively, in groups I and II, 12 and 41%, as compared to controls. Under pentobarbital anesthesia, rGRF(l-29)NH2 was injected intravenously in two consecutive doses of 0.8 and 4.0 µg/kg body weight into the control and cafeteria-fed rats. After 2 months of diet, a significant decrease of basal GH levels and GH peak response to the 4.0 µg/kg rGRF dose was observed in both cafeteria-fed rat groups as compared to the control group. After 5 months of diet, basal GH levels decreased in both cafeteria-fed groups. However, a significantly blunted GH response to both doses of rGRF occurred only in group II. After 5 months of diet, perifused anterior pituitary cells of control and cafeteria-fed rats were challenged with increasing concentrations of rGRF (6.25, 25 and 100 pM). The basal GH secretion was similar in all groups but the stimulated GH release in response to 25 and 100 pM GRF, expressed as peak value, was depressed in group II, compared to controls. Epididymal fat pad weights were significantly increased in group II 5-month-old rats, compared to controls (p < 0.05). A positive linear correlation was found between fat pad weight and body weight (r = 0.68, p < 0.01). In addition, the peak GH response to 4.0 µg/kg body weight of rGRF was inversely correlated with the total body weight (r = –0.57, p < 0.05) and the fat pad weight (r = –0.71 p < 0.02) in all the cafeteria-fed rats. These data demonstrate an in vivo decreased basal and stimulated GH response to rGRF and an alteration of the GH-stimulated release at the pituitary level in an obese cafeteria rat model and suggest that obesity and/or a cafeteria diet blunts the GH response.

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“…In secretory granules, other peptides have been detected [23,25,27,28], and binding sites have been characterized for some of these peptides [ 19,48],…”

Section: Discussionmentioning

confidence: 99%

Effect of Corticotropin-Releasing Factor on the Release and Synthesis of Prolactin

Morel

Enjalbert

Proulx³

et al. 1989

Neuroendocrinology

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Corticotropin-releasing factor (CRF) has been characterized on the basis of its intrinsic activity to release corticotropin from cultured rat anterior pituitary cells. Injected in intact rats, CRF increases adrenocorticotropic hormone (ACTH) release. Endogenous CRF-like immunoreactivity was detected in the cytoplasm and nucleus of corticotrophs. Using an antirat CRF serum, a similar location of CRF-like immunoreactivity was observed in lactotrophs: cytoplasmic matrix, secretory granules, nucleus and, to a lesser degree, the plasma membrane level were stained. One injection of CRF increased the plasma ACTH concentration 4-fold after 15 min, while plasma prolactin (PRL) increased 2.7-fold 5 min after injection. In vitro, incubation of female pituitary cells with rat CRF (10^–10–10^–8M) had no significant effect on PRL secretion. In contrast, after 4 days of in vitro pretreatment with 17β-estradiol (10^–9M), rat CRF stimulated PRL secretion by 42%. In situ hybridization of whole pituitary slices showed that rat CRF injection significantly increased the labeling of corticotrophs using an ACTH-cDNA probe, but had no significant effect on the labeling of lactotrophs using a PRL riboprobe. These results indicate that CRF is a factor which can modulate PRL release but not the synthesis of PRL.

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Ultrastructural Evidence for Endogenous Somatostatin-Like Immunoreactivity in the Pituitary Gland

Cited by 34 publications

References 25 publications

Evidence for a Direct Action of Neuropeptide Y in the Rat Pituitary Gland

Evidence for a Direct Action of Neuropeptide Y in the Rat Pituitary Gland

Decreased Pituitary Growth Hormone Response to Growth Hormone-Releasing Factor in Cafeteria-Fed Rats: Dietary and Obesity Effects

Effect of Corticotropin-Releasing Factor on the Release and Synthesis of Prolactin

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