Stimulation of prolactin release by vasoactive intestinal peptide (VIP)

Ruberg, Merle; Rotsztejn, W.H.; Arancibia, Sandor; Besson, J.; Enjalbert, A

doi:10.1016/0014-2999(78)90421-1

Cited by 161 publications

(49 citation statements)

References 4 publications

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“…These data suggest that the N-terminal 5 amino acids of the molecular sequence are required for binding or for recognition by VIP receptors in this preparation. Recent studies on [1251]VIP binding to brain membranes have reached similar conclusions 1211.…”

Section: Discussionmentioning

confidence: 71%

Adenylate cyclase of rat pituitary gland

et al. 1979

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Section: Discussionmentioning

confidence: 71%

Adenylate cyclase of rat pituitary gland

et al. 1979

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“…Of the peptides that are known to be present in the spinal cord, VIP appears to be one of the most efficacious in stimulating adenylate cyclase (13,14) in nonneuronal cells. In addition, VIP has been shown to act as a releasing agent (15,16) or a modulator of release for other hormones (17). PHI-27 and secretin were also examined for neurotrophic properties because of their close sequence homology (18) with VIP.…”

mentioning

confidence: 99%

Vasoactive intestinal peptide and electrical activity influence neuronal survival.

Brenneman¹,

Eiden²

1986

Proc. Natl. Acad. Sci. U.S.A.

232

107

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Blockade of electrical activity in dissociated spinal cord cultures results in a significant loss of neurons during a critical period in development. Decreases in neuronal cell numbers and '251-labeled tetanus toxin fixation produced by electrical blockade with tetrodotoxin (TTX) were prevented by addition ofvasoactive intestinal peptide (VIP) to the nutrient medium. The most effective concentration of VIP was 0.1 nM. At higher concentrations, the survival-enhancing effect of VIP on TTX-treated cultures was attenuated. Addition of the peptide alone had no significant effect on neuronal cell counts or tetanus toxin fixation. With the same experimental conditions, two closely related peptides, PHI-27 (peptide, histidylisoleucine amide) and secretin, were found not to increase the number of neurons in TTX-treated cultures. Interference with VIP action by VIP antiserum resulted in neuronal losses that were not significantly different from those observed after TTX treatment. VIP1..n, a fragment that inhibits VIP stimulation of adenylate cyclase, also produced a dose-dependent decrease in neuronal cell counts similar to that seen with TTX treatment. These data indicate that under conditions of electrical blockade a neurotrophic action of VIP on neuronal survival can be demonstrated.Most neural systems of mammalian embryos are comprised of significantly more neurons than are present at maturity (1). The regulation of the cell death that accounts for this paradoxical change during development is not understood. However, spontaneous electrical activity (2-4) and trophic substances (5,6) have been shown to influence neuronal cell death and have been hypothesized to be involved in a mechanism by which function determines the number of neurons that comprise a mature neural network.The relationship between electrical activity and trophic activity is only beginning to be explored, and it may be that there are multiple types of interaction. For example, spontaneous electrical activity may be linked to a mechanism by which neurons compete for trophic substances. Activity in this case may promote neuronal death by eliminating redundant neurons on the basis of their relative ability to obtain such trophic support. Evidence that supports this aspect of activity include observations that electrical blockade increases neuronal survival during developmental periods when neuronal death is normally occurring. Studies in vivo (3, 4) and with dissociated spinal cord cultures (7) support the existence of such a mechanism. In addition, a trophic substance or perhaps a trophic factor-releasing substance may be released during electrical activity. Activity in this case has the effect of promoting neuronal survival by stimulating the release of substances important for survival. In the present study, the possibility is examined that neuropeptides may be among the activity-dependent components that can influence neuronal survival during development.Numerous neuropeptides have been found in the developing nervous system. However, their ...

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“…This could explain the wellknown parallel increase in plasma prolactin, corticotropin, and growth hormone levels-for example, under certain types of stress-as being due to a concomitant release of PHI-like, CRFlike, and enkephalin-like peptides from the same nerve endings in the median eminence. A hypothetical mechanism for the coordinated release of these three anterior pituitary hormones is discussed.It has been shown that vasoactive intestinal polypeptide (VIP) (1, 2) causes release of prolactin from the anterior pituitary gland in vitro (3)(4)(5) and in vivo (6). Therefore, this peptide may represent a candidate for the prolactin-releasing factor (7,8).…”

mentioning

confidence: 99%

“…It has been shown that vasoactive intestinal polypeptide (VIP) (1, 2) causes release of prolactin from the anterior pituitary gland in vitro (3)(4)(5) and in vivo (6). Therefore, this peptide may represent a candidate for the prolactin-releasing factor (7,8).…”

mentioning

confidence: 99%

The PHI (PHI-27)/corticotropin-releasing factor/enkephalin immunoreactive hypothalamic neuron: possible morphological basis for integrated control of prolactin, corticotropin, and growth hormone secretion.

Hökfelt¹,

Fahrenkrug²,

Tatemoto³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

140

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By using the indirect immunofluorescence technique, one and the same neuron in the parvocellular part of the paraventricular nucleus has been shown to stain with antisera against three different peptides: PHI (PHI-27), corticotropin-releasing factor (CRF), and enkephalin. This could explain the wellknown parallel increase in plasma prolactin, corticotropin, and growth hormone levels-for example, under certain types of stress-as being due to a concomitant release of PHI-like, CRFlike, and enkephalin-like peptides from the same nerve endings in the median eminence. A hypothetical mechanism for the coordinated release of these three anterior pituitary hormones is discussed.It has been shown that vasoactive intestinal polypeptide (VIP) (1, 2) causes release of prolactin from the anterior pituitary gland in vitro (3)(4)(5) and in vivo (6). Therefore, this peptide may represent a candidate for the prolactin-releasing factor (7,8). However, immunohistochemical studies have so far revealed only single VIP-positive nerve fibers in the medial basal hypothalamus, including the median eminence (9-12), from which the hypothalamic-releasing hormone and inhibitory hormone are released into the hypophysial portal blood vessels for transport to the anterior pituitary. More recently it has been demonstrated that PHI-like immunoreactivity [PHI-27; the peptide (P) having NH2-terminal histidine (H) and COOH-terminal isoleucine (I) amide and 27 amino acid residues] (13) is present in a parvocellular paraventriculo-infundibular system, forming a dense fiber network around the portal capillaries (14). PHI has considerable structural similarities to VIP (13) and causes prolactin release, although it is less potent than VIP in this respect (unpublished data).In the present communication we report that at least part of the PHI immunoreactive neurons in the parvocellular periventricular hypothalamic nuclei contain two other peptides, one enkephalin-like peptide (15) In some cases the restaining technique of Tramu et aL (20) was used to investigate the presence of more than one compound in the same neuron. Briefly, after photography of the PHI staining patterns, removal of the coverslip, and rinsing in phosphate-buffered saline, the sections were immersed in acid potassium permanganate, rinsed, incubated with fluorescein isothiocyanate-conjugated antiserum (as control), and, if negative, incubated with enkephalin or CRF antiserum. This procedure was repeated and the final incubation was made with CRF or, alternatively, enkephalin antiserum. For control purposes the antisera were pretreated with an excess of the respective peptide (50 pug of peptide per ml of antiserum diluted

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Stimulation of prolactin release by vasoactive intestinal peptide (VIP)

Cited by 161 publications

References 4 publications

Adenylate cyclase of rat pituitary gland

Adenylate cyclase of rat pituitary gland

Vasoactive intestinal peptide and electrical activity influence neuronal survival.

The PHI (PHI-27)/corticotropin-releasing factor/enkephalin immunoreactive hypothalamic neuron: possible morphological basis for integrated control of prolactin, corticotropin, and growth hormone secretion.

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