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Endocrinology Vol. 144, No. 7 2816-2821
Copyright © 2003 by The Endocrine Society

Neuropeptide W Acts in Brain to Control Prolactin, Corticosterone, and Growth Hormone Release

Jennifer R. Baker, Kara Cardinal, Cynthia Bober, Meghan M. Taylor and Willis K. Samson

Pharmacological and Physiological Sciences, St. Louis University School of Medicine, St. Louis, Missouri 63104

Address all correspondence and requests for reprints to: Willis K. Samson, Ph.D., Pharmacological and Physiological Science 1402 South Grand Boulevard, St. Louis University School of Medicine, St. Louis, Missouri 63104. E-mail: samsonwk{at}slu.edu.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
The endogenous, peptide ligand for the orphan receptors GPR7 and GPR8 was identified to be neuropeptide W (NPW). Because these receptors are expressed in brain and in particular in hypothalamus, we hypothesized that NPW might interact with neuroendocrine systems that control hormone release from the anterior pituitary gland. No significant effects of NPW were observed on the in vitro releases of prolactin (PRL), ACTH, or GH when log molar concentrations ranging from 1 pM to 100 nM NPW were incubated with dispersed anterior pituitary cells. However, NPW, when injected into the lateral cerebroventricle of conscious, unrestrained male rats, in a dose-related fashion elevated PRL and corticosterone and lowered GH levels in circulation. The threshold dose for all three effects was 1.0 nmol. We conclude that endogenous NPW may play a regulatory role in the organization of neuroendocrine signals accessing the anterior pituitary gland but does not itself act as a true releasing or inhibiting factor in the gland. Central administration of NPW23 also stimulated water drinking and food intake. The ability of exogenous peptide to decrease GH but stimulate PRL secretion and activate the hypothalamo-pituitary adrenal axis, together with the observed behavioral effects, suggests that endogenous NPW may play a role in the hypothalamic response to stress.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
IN 1995, O’DOWD et al. (1) cloned two novel genes that encoded opioid- and somatostatin-like receptors. Using Northern blot analysis, they identified the expression of these genes in human brain and demonstrated, by in situ hybridization histochemistry, the presence of gene transcripts in discrete hypothalamic areas of the mouse brain, suggesting a role for the endogenous ligands for these orphan receptors in neuroendocrine function (1). In 1999, this same group (2) reported an even wider distribution of GPR7 in rat brain than had been observed in mouse and human brain. Within the hypothalamus gene transcripts for these receptors were observed in the paraventricular (PVN) and supraoptic nuclei, the arcuate nucleus, and in the ventromedial and dorsomedial nuclei, as well as in the suprachiasmatic nuclei. All these nuclei are important contributors to the neuroendocrine regulation of anterior pituitary hormone secretion (3).

The endogenous ligand for these orphan receptors remained unidentified until 2002, when the Takeda group of Shimomura et al. (4) isolated and sequenced neuropeptide W (NPW). In fact, they identified two endogenous ligands, NPW-30 and NPW-23, the shorter form being the N-terminal sequence of the larger peptide, both of which bound with similar affinity to GPR7 and GPR8 (4). They also, predicting that these peptides would alter hypothalamic function, administered 10 nmol NPW23 intracerebroventricularly (icv) and demonstrated significant increases in food intake and prolactin secretion. No dose-response experiments were reported and the magnitude of the increase in food intake (3- to 4-fold) and prolactin secretion (2- to 3-fold) was not trivial, but certainly at such a high dose [~26 µg intracerebroventricularly (icv)] and in the absence of dose-response data not convincing. However, their preliminary data motivated us to examine the possibility that NPW might act in hypothalamus, or in the adenohypophysis, to alter anterior pituitary hormone release. We report here the ability of exogenous NPW23, when administered icv in conscious male rats, to significantly elevate circulating levels of prolactin (PRL) and corticosterone and to significantly lower plasma GH levels.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Animals
All procedures were approved by the University Animal Care and Use Committee. Adult, male Sprague Dawley rats (200–250 g, Harlan, Indianapolis, IN) were employed. Animals were housed individually under constant conditions (25 C; 12-h light, 12-h dark) and provided tap water and conventional lab chow ad libitum. In vivo experiments were begun 3–4 h after lights on.

In vitro experiments
Rats were killed by rapid decapitation. Anterior pituitary glands were collected into MEM (Life Technologies, Inc., Grand Island, NY) containing HEPES (20 mM, Fisher Scientific, Fair Lawn, NJ), 1% penicillin-streptomycin (Life Technologies, Inc.), 0.1% BSA (Sigma, St. Louis, MO), and 0.1% trypsin (Difco, Detroit, MI), and mechanically dispersed (5) until a single-cell suspension was obtained (37 C). Single-cell suspensions were aliquoted into polystyrene tubes (~200,000 cells/tube) and incubated for 3–4 d at 37 C in an atmosphere of 5% CO2/95% room air in DMEM (BioWhittaker, Inc., Walkersville, MD) containing 10% horse serum (Life Technologies, Inc.) and 1% penicillin-streptomycin. On the day of experimentation, cells were pelleted by centrifugation (600 x g, 10 min, room temperature), medium removed, and replaced with test medium [DMEM, 0.1% BSA, 1% penicillin-streptomycin, and 2.5 mM bacitracin (Sigma)] alone or medium containing log molar concentrations (1 pM to 100 nM) of NPW23, or 10 nM TRH, 10 nM CRH, or 10 nM GHRH alone or in combination with 100 nM NPW23 (all peptides purchased from Phoenix Pharmaceuticals, Inc., Belmont, CA). Incubations lasted 60 min and were terminated by centrifugation and collection of medium for subsequent determination of PRL, GH, and ACTH contents by RIA.

In vivo experiments
Under tribromoethanol anesthesia (2.5% in isotonic saline, 1 ml/100 g body weight ip injection; Sigma), rats were placed in a stereotaxic device and a 23-gauge stainless steel cannula (17 mm) implanted into the right lateral cerebroventricle as previously described (6). Minimally 5 d later, after the animals had returned to preimplantation body weights, an indwelling jugular vein cannula was implanted as previously described (7) again under tribromoethanol-induced anesthesia. The jugular cannula was exteriorized at the back of the neck and filled with heparinized saline (250 U/ml 0.9% NaCl) and tied shut. Rats remained in an isolated, quiet environment until the following day, when an extension tubing (PE-50) was attached to the jugular cannula to facilitate blood sampling and rats left undisturbed for 60 min. Then, an initial blood sample was withdrawn from the jugular vein without disturbing the animal. All blood samples (0.3 ml, into heparinized syringes) were removed from conscious, unrestrained rats and replaced with an equal volume of 0.9% NaCl (37 C). Blood samples were kept on ice before plasma was separated (3000 x g, 3 min) and stored at –20 C until hormone assays conducted. Immediately following the removal of the initial (0 time) blood sample, a 2-µl injection of isotonic saline vehicle alone or vehicle containing 0.3, 1.0, or 3.0 nmol NPW23 was conducted via the indwelling cerebroventricular cannula. Subsequent blood samples were removed 5, 10, 20, 30, and 60 min after icv injections. Each animal was employed only for one dose of test substance.

Feeding study.
The effect of icv administered NPW23 was examined in rats bearing a lateral cerebroventricular cannula, implanted minimally 1 wk earlier. Cannulated rats were placed in metabolic cages for a 4-d habituation period, during which time daily water and food consumptions and body weights were monitored. Food and water were available ad libitum at all times. On the day of experimentation, the animals were weighed before icv injection of 2 µl of saline vehicle or vehicle containing 3.0 nmol NPW23. Rats were returned to the metabolic cages and water bottles and food trays reintroduced 15 min later. Food and water intakes were monitored thereafter at 30-min intervals for 4 h and then again at 24 h.

RIAs.
PRL levels in incubation medium and plasma were determined using the kit materials provided by the National Hormone and Pituitary Program (rPRL-RP-3 standard). The minimum detectable hormone level in medium and plasma for PRL was 0.5 ng/ml (defined as <90% B/B0) and the interassay and intraassay coefficients of variability were less than 9%. GH levels were similarly measured using the material provided in the NIH kit (rGH-RP-2 standard, minimum detectable level: 0.5 ng/ml; interassay and intraassay coefficients of variability were less than 8%). ACTH content of incubation medium was determined using the commercial RIA kit (rat ACTH, Phoenix Pharmaceuticals, Inc.). All incubation samples were measured in the same ACTH assay (minimum detectable hormone level, 2 pg/tube; intraassay coefficient of variability less than 5%). Plasma corticosterone levels were determined according to the instructions of the commercial RIA kit (rat/mouse corticosterone, ICN Biomedicals, Inc., Costa Mesa, CA). The minimum detectable hormone level was 25 ng/ml, and the interassay and intraassay coefficients of variability were less than 10%.

Statistical analyses
Differences between treatment groups in the in vitro studies were analyzed by one-way ANOVA and Scheffé’s multiple comparison testing. Homogeneity of variance was established using the S test. Significance was assigned to results that occurred with less than 5% probability. For the in vivo experiments, data were similarly analyzed by ANOVA both within treatment groups across time and across treatment groups at any sampling time point.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
In vitro studies
NPW23 in log molar concentrations ranging from 1.0 pM to 100 nM failed to significantly alter PRL, GH, or ACTH release from dispersed anterior pituitary cells harvested from male rats (Table 1Go). Similarly, 100 nM NPW23 failed to alter the ability of the releasing factors to stimulate hormone release from these cells (Table 1Go).


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  		Table 1. Effect of NPW23 on hormone release from dispersed, anterior pituitary cells harvested from male rat donors

 
In vivo studies
Saline vehicle administration icv failed to significantly alter plasma PRL, GH, or corticosterone levels in conscious, unrestrained male rats. Similarly, the 0.3-nmol dose of NPW23 (Table 2Go) failed to alter circulating hormone levels. However, 1.0 nmol NPW23 stimulated an approximately 2-fold increase in plasma PRL levels (Fig. 1Go), which attained significance at 60 min (P < 0.05, vs. vehicle-injected controls, between group ANOVA). When the data were analyzed by within group ANOVA, a significant elevation in plasma PRL levels was observed (F = 3.38, P < 0.01) following icv injection of the 1.0-nmol dose. Following icv injection of the 3.0-nmol dose of NPW23, plasma PRL levels rose to levels 5- to 7-fold higher than those present in saline-injected controls. Compared with PRL levels present in control (between groups ANOVA) significant elevations were observed at all postinjection times in the 3.0-nmol dose group. When the PRL levels present in this group of animals were analyzed by within group ANOVA, a significant elevation in plasma PRL levels was observed as well (F = 3.84, P < 0.01). The stimulatory effect of centrally administered NPW23 on PRL secretion reached its peak at 20 min (P < 0.001 vs. control) and had all but resolved by 60 min (P < 0.05 vs. control).


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  		Table 2. Failure of 0.3 nmol NPW23 administration (icv) to significantly alter plasma hormone levels (ng/ml plasma, mean ± SEM) in conscious, male rats (n = 4)

 


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  		Figure 1. Central administration of NPW23 stimulates PRL secretion in conscious male rats. Group sizes are indicated in parentheses. *, P < 0.05; ***, P < 0.001 vs. control at that time point (between group ANOVA). a, P < 0.05 vs. preinjection levels (within group ANOVA).

 
Plasma corticosterone levels were determined as an indicator of the activity of the hypothalamo-pituitary-adrenal axis. Saline injection icv failed to alter basal corticosterone levels (Fig. 2Go). Although the 0.3-nmol dose of NPW23 was without effect, icv administration of 1.0 nmol NPW23 resulted in a significant, 2-fold elevation in plasma corticosterone levels. This elevation was significant already at 10 min after injection (P < 0.05, between group ANOVA). When the data were analyzed by within group ANOVA, a significant stimulatory effect of the 1.0-nmol dose of NPW23 was observed (F = 4.14, P < 0.01). The higher dose of NPW23 stimulated a 5-fold elevation in plasma corticosterone levels that was present (between group ANOVA) already at 5 min and peaked (P < 0.001) at 30 min following central peptide administration. Plasma corticosterone levels then began to fall but remained significantly elevated at 60 min (P < 0.01). When the data for the 3.0-nmol NPW23 dose were analyzed by within group ANOVA, a highly significant effect on plasma corticosterone levels (F = 9.49, P < 0.001) was observed.



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  		Figure 2. Central administration of NPW23 activates the hypothalamo-pituitary-adrenal axis in conscious male rats. Group sizes are indicated in parentheses. *, P < 0.05; **, P < 0.01; ***, P < 0.001 vs. control at that time point (between group ANOVA). a, P < 0.05; b, P < 0.01; c, P < 0.001 vs. preinjection levels (within group ANOVA).

 
In contrast to the effects of centrally administered NPW23 on PRL and corticosterone levels in plasma, GH levels were suppressed by icv administration of the peptide (Fig. 3Go). Although levels present in saline-injected controls did decline throughout the sampling period, this decrease was not statistically significant (within group ANOVA, F = 1.27, P = 0.29). On the other hand, plasma GH levels significantly declined in the animals receiving the 1.0-nmol dose of NPW23 (within group ANOVA, F = 2.93, P < 0.05) reaching their lowest point 30 min after peptide administration. A highly significant decrease in plasma GH levels was observed following central administration of the 3.0-nmol dose (within group ANOVA, F=5.01, P < 0.001). This effect was present already by 5 min and attained significance by 10 min (P < 0.01, between group ANOVA). GH levels remained significantly suppressed until the 60-min sampling period when levels in the 3.0-nmol dose group did not significantly differ from those observed before peptide injection (within group ANOVA) or in the saline-injected controls at that time point (between group ANOVA).



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  		Figure 3. Central administration of NPW23 inhibits GH release in conscious male rats. *, P < 0.05; **, P < 0.01 vs. control at that time point (between group ANOVA). a, P < 0.05; b, P < 0.01 vs. preinjection levels (within group ANOVA).

 
Feeding study.
Animals administered 3.0 nmol NPW23 icv consumed significantly more water during the first 120 min than did the control animals (Table 3Go). Similarly, these NPW23-treated animals consumed significantly more food during the initial 120 min of observation. These differences in food intake were apparent when the data were expressed as total food consumed per 100 g body weight (Table 3Go) or when simply expressed in terms of grams food consumed. No significant differences in water consumption or food intake were observed between the two groups thereafter.


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  		Table 3. Cumulative food and water intakes following icv injection of saline vehicle (n = 11) or vehicle containing 3.0 nmol NPW23 (n = 12) in sated, adult male rats

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The hypothalamic localization (2) of the receptors for NPW, GPR7 and GPR8, and the presence of the peptide in that region suggested to Shimomura et al. that the peptide might play a role in such diverse hypothalamic functions as the control of food intake and anterior pituitary function. Indeed, they (4) reported significant elevation in food intake and PRL secretion when a relatively high dose of NPW was infused into brain. Their preliminary data, together with the previously published localization studies (2), led us to hypothesize that NPW might act in brain to alter the neuroendocrine regulation of the secretion of several anterior pituitary hormones. Because the receptors have been reported to be present in human pituitary gland (1), we examined the possibility that NPW might act directly within the gland to alter hormone release. However, no significant effects of a wide concentration range of NPW23 were observed when PRL, GH, and ACTH release was examined. In addition, our studies indicate that NPW23 does not interact with GHRH-stimulated GH secretion, CRH-stimulated ACTH release, or TRH-induced PRL secretion. Thus, we do not think that the results we obtained following central administration of the peptide reflected spillover of NPW23 into the portal circulation.

We observed a general increase in the activity of the rats following central administration of NPW23, including increased locomotion and grooming. We also observed that, like the report of the Shimomura group (4), food intake was stimulated by NPW23, at a dose lower than that employed in their original study. Furthermore, we report that water consumption also was stimulated by icv administration of 3.0 nmol NPW23, something not reported by Shimomura et al. (4). We cannot conclude whether the effect of NPW23 on water consumption was unique or secondary to increased solute ingestion as a result of feeding; however, the time course of food and water consumption overlapped, suggesting that the water intake occurred before any absorption of solute from the digestive tract. It will be important in the future to study the effect of central administration of NPW23 in ad libitum-fed and -watered animals on water drinking when food is not provided during the testing period and in animals stimulated to drink by water restriction. Behavioral testing will be required as well to ensure that the increased water and food intakes were not merely a reflection of generalized increases in spontaneous locomotor activity. This is a distinct possibility because the magnitude of stimulation of feeding and drinking is certainly not remarkable compared with the effects of central administration of even lower doses of neuropeptide Y or angiotensin II, respectively. Finally, it is possible that the increased feeding is a reflection of the increased plasma corticosterone levels, which might inhibit central CRH release resulting in a loss of the anorexic effect of CRH; however, this is unlikely because it appears that the NPW injected acted to increase CRH release.

Our findings indicate that exogenous NPW23 can act in brain to alter the neuroendocrine regulation of PRL, GH, and ACTH release. These data differ from those of the Takeda group (4) with regards PRL secretion in that we were able to demonstrate an elevation of PRL levels in conscious rats that was dose related and more pronounced than they observed with an even higher dose of peptide. It is not clear from their report (4) whether or not their animals were anesthetized during their study. The presence of GPR7 in hypothalamic PVN (2) suggests that our observed action of NPW to stimulate PRL secretion may have been due to a stimulatory effect of the peptide on TRH release into the median eminence. Alternatively, GPR7 is present in the arcuate nucleus as well (2), and the ability of NPW to raise PRL levels may be explained by an action to inhibit the activity of tubero-infundibular dopamine neurons in these regions, thus removing physiologic inhibition of PRL secretion. We currently are examining that latter possibility using the experimental approach employed by us in the past to uncover a role for dopamine withdrawal in PRL secretion subsequent to central peptide administration (8).

The profound elevation in plasma corticosterone levels suggests that centrally administered NPW activates the hypothalamo-pituitary-adrenal axis. Because GPR7 is present in the PVN (2), it is possible that this action of NPW is mediated via an increase in the activity of CRH neurons that project to the median eminence. We are examining that possibility now using established in vivo models (9). Alternatively, the rapid increase in plasma corticosterone levels may reflect the ability of centrally administered NPW23 to activate sympathetic outflow and therefore exert neural control over adrenal function.

Both the elevation in plasma PRL and corticosterone levels suggest a role for NPW in the organization of the hypothalamic response to stress. Unlike in humans where stress elevates GH concentrations in circulation (3), the acute effect of stress in rats is inhibitory (10). Thus, all three neuroendocrine components of the stress response in rats (elevated PRL and corticosterone and lowered GH levels) were observed following central administration of NPW23. In addition, the behavioral responses observed mirror those reported in behavioral models of stress. In conclusion, we have identified novel, dose-related actions of the newly described, endogenous ligand for the orphan receptors GPR7 and GPR8. These pharmacologic effects are now being examined for physiological significance with the hypothesis that endogenous NPW is a necessary signaling molecule for the expression of the hypothalamic response to stress.


   Acknowledgments
 
The authors acknowledge the generous contributions of Dr. A. Parlow and the NIH NIDDK National Hormone and Pituitary Program for the PRL and GH assay reagents.


   Footnotes
 
This work was supported by NIH Grant HL-66023 (to W.K.S.) and a fellowship awarded by the American Heart Association (to M.M.T.).

Abbreviations: icv, Intracerebroventricular(ly); NPW, neuropeptide W; PRL, prolactin; PVN, paraventricular nucleus.

Received December 17, 2002.

Accepted for publication March 17, 2003.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. O’Dowd BF, Scheideler MA, Nguyen T, Cheng R, Rasmussen JS, Marchese A, Zastawny R, Heng HHQ, Tsui LC, Shi X, Asa S, Puy L, George SR 1995 The cloning and chromosomal mapping of two novel human opioid-somatostatin-like receptor genes, GPR7 and GPR8, expressed in discrete areas of the brain. Genomics 28:84–91[CrossRef][Medline]
  2. Lee DK, Nguyen T, Porter CA, Cheng R, George SR, O’Dowd BF 1999 Two related G protein-coupled receptors: the distribution of GPR7 in rat brain and the absence of GPR8 in rodents. Mol Brain Res 71:96–103[Medline]
  3. Reichlin S 1998 Neuroendocrinology. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams textbook of endocrinology. 9th ed. Philadelphia: Saunders; 165–248
  4. Shimomura Y, Harada M, Goto M, Sugo T, Matsumoto Y, Abe M, Watanabe T, Asami T, Kitada C, Mori M, Onda H, Fujino M 2002 Identification of neuropeptide W as the endogenous ligand for orphan G-protein coupled receptors GPR7 and GPR8. J Biol Chem 277:35826–35832[Abstract/Free Full Text]
  5. Samson WK, Said SI, Snyder GS, McCann SM 1979 In vitro stimulation of prolactin release by vasoactive intestinal polypeptide. Peptides 1:325–332
  6. Samson WK, Murphy TC, Resch ZT 1998 Central mechanisms for the hypertensive effects of preproadrenomedullin-derived peptides in conscious rats. Am J Physiol 274:R1505–R1509
  7. Harms PG, Ojeda SR 1974 A rapid and simple procedure for chronic cannulation of the rat jugular vein. J Appl Physiol 36:391–392[Free Full Text]
  8. Samson WK, Bianchi R, Mogg R 1988 Evidence for a dopaminergic mechanism for the prolactin inhibitory effect of atrial natriuretic factor. Neuroendocrinology 47:268–270[Medline]
  9. Samson WK, Taylor MM, Folwell M, Ferguson AV 2002 Orexin actions in hypothalamic paraventricular nucleus: physiological consequences and cellular correlates. Regul Pept 104:97–103[CrossRef][Medline]
  10. Rivier C, Vale W 1985 Involvement of corticotropin-releasing factor and somatostatin in stress-induced inhibition of growth hormone secretion in the rat. Endocrinology 117:2478–2482[Abstract]



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