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

Chabot, Jean‐Guy; Enjalbert, A; Pelletier, Georges; Dubois, Paul; Morel, Gérard

doi:10.1159/000124963

Cited by 68 publications

(22 citation statements)

References 30 publications

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“…In vitro NPY stimulation of GtH secretion from pituitary dispersed cells in the trout (Breton et al, 1990) suggests similarities with in vivo actions, as has also been postulated in mammals (Chabot et al, 1988). The most plausible hypothesis in mammals is that NPY is a component of an excitatory neural circuit responsible for the induction of preovulatory LH release (Sahu et al, 1989) mainly interacting with the LHRH system, on which it could have a dual action.…”

Section: Discussionmentioning

confidence: 54%

“…In gonadectomized rats, generally NPY had opposite in vivo and in vitro effects. It stimulated in vitro LH secretion (McDonald et al, 1985;Chabot et al, 1988), whereas it inhibited in vivo LH secretion (McDonald et al, 1985;Kerkerian et al, 1985;Crowley et al, 1985;Guy et al, 1988). This in vivo inhibitory effect can be suppressed by estrogen-progesterone treatment (Crowley et al, 1985) and was not apparent in intact animals, in which NPY stimulated in vivo LH secretion, but did not affect its in vitro release (RodriguezSierra, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y stimulates in vivo gonadotropin secretion in teleost fish

Breton¹,

Mikołajczyk²,

Popek³

et al. 1991

General and Comparative Endocrinology

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The effects of the neuropeptide Y (NPY), alone or in combination with a gonadotropinreleasing hormone analogue, D-Ala6+lesGly10-Pro9-Net LHRH (LHRHa), have been studied on the in vivo secretion of the maturational gonadotropin (GtH3 in the rainbow trout Oncorhynchus mykiss and the common carp Cyprinus carpio. Depending on the species, two routes of administration were used: in trout, intraperitoneal injection (20 p&g body wt); in carp, direct infusion (3 p&g body wt) into the third ventricle via a temporary brain cannula. In both cases NPY alone induced a twofold increase in GtH, secretion and peaked 2 to 4 hr after administration regardless of the route of injection. The plasma gonadotropin levels returned to basal within 8 hr. The relative increases (peaked secretion/basal secretion) did not differ with the route of injection. When the animals were first treated with NPY and then LHRHa (20 pg/kg) 1 hr later, the magnitude of the response to LHRHa was greater in the animals pretreated with NPY, indicating either a potentiation of LHRHa action by NPY or additive effects of the two peptides. The return to basal levels also took longer in fish receiving NPY tirst. NPY may act directly at tbe pituitary level or activate central neuromediatory systems. Q 195'1 Academic Press, Inc.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y stimulates in vivo gonadotropin secretion in teleost fish

Breton¹,

Mikołajczyk²,

Popek³

et al. 1991

General and Comparative Endocrinology

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“…A direct effect of NPY on pituitary function is plausible in that studies in rats have demonstrated a subpopulation of NPY neurons, located in the arcuate nucleus, that project to fenestrated capillaries within the median eminence [75]. In addition, NPY is found in significant concentrations in hypophyseal portal blood [76], the pituitary expresses Y5 receptors [77, 78], and NPY can modify hormone release from primary pituitary cultures [79]. …”

Section: Discussionmentioning

confidence: 99%

Expression Analysis of Hypothalamic and Pituitary Components of the Growth Hormone Axis in Fasted and Streptozotocin-Treated Neuropeptide Y (NPY)-Intact (NPY<sup>+/+</sup>) and NPY-Knockout (NPY<sup> –/–</sup>) Mice

et al. 2005

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In the fasted and the streptozotocin (STZ)-induced diabetic male rat, hypothalamic growth hormone (GH)-releasing hormone (GHRH) mRNA levels, and pulsatile GH release are decreased. These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY^+/+) and NPY-knockout (NPY^–/–) mice by ribonuclease protection assay. In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. Under fed conditions the GH axis of NPY^+/+ and NPY^–/– did not differ. In the NPY^+/+ mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. In the NPY^–/– mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. Fasting resulted in an overall increase in circulating GH, which reached significance in the fasted NPY^–/– mouse. Induction of diabetes in NPY^+/+ mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. Induction of diabetes in NPY^+/+ and NPY^–/– mice, using a multiple, low-dose, STZ paradigm (5 consecutive daily injections of 40 mg/kg), did not alter body weight, hypothalamic neuropeptide expression or pituitary receptor expression, with the exception that sst2 mRNA levels were suppressed and GH levels did rise in the NPY^–/– mouse. These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. In contrast to the rat, fasting clearly did not suppress circulating GH levels in mice, but resulted in an overall rise in mean GH levels, similar to that observed in other mammalian species. The fact that many of the fasting-induced changes in the GH axis were observed in the high-dose STZ-treated mice, but were not observed in the multiple, low-dose paradigm, suggests STZ-mediated modulation of GH axis function is dependent on the severity of the catabolic state and not hyperglycemia.

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“…The situation with regard to the direct action of NPY on gonadotropes is controversial. An ability of NPY to stimulate LH release has been reported by some workers [7, 8], but not others [9, 10]. Oxytocin antagonist and NPY antiserum have been observed to inhibit production of the LH surge in vivo [2, 11, 12, 13], suggesting an actual physiological role.…”

Section: Introductionmentioning

confidence: 97%

Release of Luteinizing Hormone from the Anterior Pituitary Gland in vitro Can Be Concurrently Regulated by at Least Three Peptides: Gonadotropin-Releasing Hormone, Oxytocin and Neuropeptide Y

2001

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Normal action of the female ovulatory cycle is dependent on a surge of luteinizing hormone (LH) from the pituitary. Regulation of the levels of LH is therefore vital to reproductive function. It has long been established that gonadotropin-releasing hormone (GnRH) is an important component of the regulatory processes. Other peptides, including oxytocin and neuropeptide Y (NPY), have also been observed to affect LH activities. However, the possibility of the concurrent actions of these peptides has rarely been considered despite their documented presence in the hypophyseal blood during pro-oestrus. In this study, the direct effects of oxytocin and NPY on LH release were studied, as well as the effects of both peptides simultaneously. Also, pituitaries were stimulated with GnRH, and the effects of pre-exposure of the pituitary tissue to oxytocin or NPY were investigated. Further, the effect of oxytocin and NPY together on GnRH stimulation of LH release was determined. Anterior pituitaries were collected from adult female rats on the morning of pro-oestrus. Hemipituitaries were cut in two and placed in a chamber of a perifusion system. The pituitary tissue was perifused with medium alone, oxytocin and NPY, separately or in combination, for 2 h after an initial 100-min equilibration period with no peptide present. Fractions of eluate were collected and LH was measured by radioimmunoassay. LH output was stimulated by both oxytocin (p < 0.01) and NPY (p < 0.02). Furthermore, the addition of NPY to oxytocin during the perifusion elicited a further increase in LH release (p < 0.05). The pituitary tissue was exposed to a 4-min pulse of GnRH after 220 min. Stimulation of LH release by GnRH was synergistically augmented by exposure of the tissue to either oxytocin (p < 0.01) or NPY (p < 0.05) for the immediately preceding 2 h. When NPY was added to oxytocin in the perifusion medium, stimulation of LH release by GnRH was increased even further (p < 0.05). Oxytocin also synergistically enhanced the effect of a second, primed GnRH pulse, whereas the effect of NPY was less robust. This study therefore demonstrated that LH release is modified in the presence of oxytocin, NPY or GnRH alone, and also that combinations of the peptides produce further variations in LH output. Therefore, the concentrations of LH that are present in vivo are likely to be at least partly the result of the co-ordinated effects of combinations of peptides acting on the pituitary.

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

Cited by 68 publications

References 30 publications

Neuropeptide Y stimulates in vivo gonadotropin secretion in teleost fish

Neuropeptide Y stimulates in vivo gonadotropin secretion in teleost fish

Expression Analysis of Hypothalamic and Pituitary Components of the Growth Hormone Axis in Fasted and Streptozotocin-Treated Neuropeptide Y (NPY)-Intact (NPY<sup>+/+</sup>) and NPY-Knockout (NPY<sup> –/–</sup>) Mice

Release of Luteinizing Hormone from the Anterior Pituitary Gland in vitro Can Be Concurrently Regulated by at Least Three Peptides: Gonadotropin-Releasing Hormone, Oxytocin and Neuropeptide Y

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