Synthesis and Secretion of Vasoactive Intestinal Peptide by Rat Fetal Cerebral Cortical and Hypothalamic Cells in Culture*

Lorenzo, María Jesús López; Sánchez‐Franco, Franco; Frailes, Maria Teresa de los; Reichlin, Seymour; Fernandez, G.; Cacicedo, Lucinda

doi:10.1210/endo-125-4-1983

Cited by 23 publications

(12 citation statements)

References 43 publications

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“…The involvement of GHRH in NMDA effect was analyzed in experiments 6 and 7. In experiment 6, 30-day-old males were injected with saline, 250 or 500 µl of normal rabbit serum (NRS) or GHRH antiserum (kindly donated by Dr. F. Sanchez Franco, Madrid, Spain) [18]and with NMDA (15 mg/kg) 120 and 15 min, respectively, before sacrifice. The GHRH antiserum, administered at a dose of 750 µl, blocks, in adult animals (250–300 g), the effects of 1 µg of GHRH [19]and the minimal dose of antiserum selected, injected every 72 h between days 20 and 32 of life, significantly (p ≤ 0.01) inhibited body weight gain (weights on day 32: NRS 120 ± 4 g, GHRH antiserum 85 ± 3 g).…”

Section: Methodsmentioning

confidence: 99%

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Pinilla

González²,

Tena‐Sempere³

et al. 1999

Neuroendocrinology

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Activation of N-methyl-D,L-aspartic acid (NMDA) receptors stimulates growth hormone (GH) secretion. The mechanisms involved in this action are still a matter of debate. Present experiments were carried out to assess specifically: (1) the age-related changes in NMDA effects; (2) the physiological role of NMDA in pulsatile GH secretion; (3) the hypothalamic and/or pituitary actions of NMDA, and (4) the influence of gonadal function on NMDA-induced GH release. NMDA (15 mg/kg i.p.) stimulated GH secretion in neonatal, prepubertal and adult males, this effect being blocked by MK-801, a selective antagonist of NMDA receptors. In adult males, pulsatile GH secretion was abolished after administration of MK-801 and AP-5, antagonists of NMDA receptors. The stimulatory effect of NMDA on GH release was exerted at the hypothalamic level, since in vitro GH secretion was slightly inhibited in the presence of NMDA (0.5 mM). The increase in GH release after NMDA treatment cannot be explained through an increase in GHRH release, as the NMDA effect persisted in animals pretreated with GHRH antiserum and in those neonatally injected with mono- sodium glutamate, a drug that destroys GHRH neurons. In addition, NMDA-induced GH secretion was independent of testicular function since it remained after orchidectomy, testosterone replacement as well as after permanent damage of testicular function by neonatal administration of estrogens (500 µg on day 1 of life). We conclude that NMDA receptors play a physiological role stimulating GH secretion through a hypothalamic mechanism that is, at least partially, not GHRH-dependent, and is not modulated by testicular secretion.

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Section: Methodsmentioning

confidence: 99%

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Pinilla

González²,

Tena‐Sempere³

et al. 1999

Neuroendocrinology

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“…αMSH was measured using a RIA kit supplied by UCB Bioproducts (Belgium). VIP was quantified by a well-characterized RIA [34], using an antiserum against porcine VIP raised in our laboratory.…”

Section: Methodsmentioning

confidence: 99%

Direct Action of Serotonin on Prolactin, Growth Hormone, Corticotropin and Luteinizing Hormone Release in Cocultures of Anterior and Posterior Pituitary Lobes: Autocrine and/or Paracrine Action of Vasoactive Intestinal Peptide

et al. 1998

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There is extensive evidence that serotonin (5-HT) is implicated in the neuroendocrine control regulating the secretion of several anterior pituitary hormones. It has also been reported that the posterior pituitary is necessary for prolactin (PRL) response to 5-HT as well as to suckling, in which 5-HT implication has been demonstrated. As we have previously shown that vasoactive intestinal peptide (VIP) mediates through an autocrine or paracrine action the PRL release induced by insulin-like growth factor I, thyrotropin-releasing hormone (TRH) and dopamine withdrawal, the aim of the present work was to determine whether 5-HT has a direct action on pituitary secretion and to study the possible role of pituitary VIP in this situation. Cells from the anterior pituitary lobe (AP) were cultured either alone or together with cells from the posterior pituitary lobe (PP). As melanotropes from PP express glucocorticoid receptors in vitro, both AP cultures and cocultures of AP/PP cells were incubated in the presence or absence of corticosterone (0.1 µg/ml), thus designing four experimental conditions. Then both AP and mixed cultures were incubated with 5-HT (100 nM) for 20, 45 and 180. The release of PRL, growth hormone (GH), corticotropin (ACTH) and luteinizing hormone (LH) was stimulated by 5-HT, but only in cocultures of AP/PP cells preincubated with corticosterone, whereas follicle-stimulating hormone and thyroid-stimulating hormone release was not modified. As AP cultures did not show any response to 5-HT, both in the presence or absence of corticosterone, and as melanotropes are the main cellular type present in the PP cultures, we studied the response of α-melanocyte-stimulating hormone (αMSH) to 5-HT in PP cells cultured with or without corticosterone. Serotonin did not modify αMSH release either in the absence or the presence of corticosterone. VIP release was also stimulated by 5-HT in the cocultures, and the time response profile was only similar to that of PRL. In order to study whether pituitary VIP is implicated in 5-HT action, cocultures preincubated with corticosterone were incubated in the presence of 5-HT, a VIP-receptor antagonist (VIP-At) or simultaneously with 5-HT plus VIP-At. PRL response to 5-HT was abolished by the simultaneous presence of VIP-At, whereas GH, ACTH and LH response remained unchanged. These data demostrate that: (1) 5-HT stimulates the secretion of PRL, GH, ACTH, LH and VIP acting directly at pituitary level on PP, probably by releasing an unidentified mediator from melanotropes; (2) glucocorticoids make the response of AP cells to 5-HT possible due to the presence of PP cells in the coculture; (3) PRL response to 5-HT is mediated through an autocrine and/or paracrine action of VIP.

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“…IgGs were purified from VIP-As or pre-immune serum using DEAE-cellulose columns. Specificity of the VIP-As was previously tested and was shown to be completely specific [43]. …”

Section: Experimental Designmentioning

confidence: 99%

Involvement of Vasoactive Intestinal Peptide on Insulin-Like Growth Factor I-Induced Proliferation of Rat Pituitary Lactotropes in Primary Culture: Evidence for an Autocrine and/or Paracrine Regulatory System

Fernández

Sánchez‐Franco²,

Palacios³

et al. 2003

Neuroendocrinology

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In previous studies we demonstrated that insulin-like growth factor I (IGF-I) induces pituitary vasoactive intestinal peptide (VIP) gene expression and secretion, and that IGF-I-induced prolactin (PRL) release is mediated by VIP. In this study, we investigate the mitotropic action of IGF-I and VIP on pituitary lactotropes, and their possible interplay in this effect. Cultured male rat pituitary cells were treated with rhIGF-I (10^–7M) and/or VIP (10^–7M) for 48 h. 5-Bromo-2′-deoxyuridine (BrdU) (10 µM) was added for labeling proliferation of pituitary cells. BrdU-labeling indices indicative of the proliferation rate of lactotropes were determined by double-labeling immunofluorescence staining for PRL and BrdU. Treatment with either IGF-I or VIP increased BrdU-labeling indices of lactotropes, but there was no further increase upon combined incubation with both factors, suggesting an interaction between the signal transduction pathways of IGF-I and VIP. VIP antiserum partially suppressed IGF-I-induced BrdU-labeling indices of lactotropes. We also investigated the intracellular signal transduction pathways in the action of IGF-I and VIP on the proliferation of lactotropes. Treatment of pituitary cells with an inhibitor of the mitogen-activated protein kinase (MAPK) pathway completely abolished IGF-I-induced lactotrope proliferation, whereas it partially suppressed VIP-induced BrdU-labeling indices. The protein kinase A (PKA) inhibitor, which abolished the mitogenic action of VIP, markedly suppressed IGF-I-induced lactotrope proliferation. These results indicate that both IGF-I and VIP stimulate lactotrope proliferation, and that IGF-I-induced lactotrope proliferation is partially mediated by VIP produced locally. Also, this study suggests that interactions between MAPK and cyclic adenosine 3′,5′-monophosphate-PKA signaling pathways are implicated in the lactotrope proliferation induced by IGF-I and VIP.

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Synthesis and Secretion of Vasoactive Intestinal Peptide by Rat Fetal Cerebral Cortical and Hypothalamic Cells in Culture*

Cited by 23 publications

References 43 publications

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Direct Action of Serotonin on Prolactin, Growth Hormone, Corticotropin and Luteinizing Hormone Release in Cocultures of Anterior and Posterior Pituitary Lobes: Autocrine and/or Paracrine Action of Vasoactive Intestinal Peptide

Involvement of Vasoactive Intestinal Peptide on Insulin-Like Growth Factor I-Induced Proliferation of Rat Pituitary Lactotropes in Primary Culture: Evidence for an Autocrine and/or Paracrine Regulatory System

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