Regulation of anterior pituitary galanin and vasoactive intestinal peptide by oestrogen and prolactin status

Hammond, P. J.; Khandan-Nia, N; Withers, Dominic J.; Jones, Philip; Ghatei, Mohammad A.; Bloom, S.R.

doi:10.1677/joe.0.1520211

Cited by 15 publications

(7 citation statements)

References 26 publications

(41 reference statements)

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“…Pituitary levels of prolactin mRNA and protein are markedly reduced in female GALKO mice (Wynick et al, 1998). Moreover, in addition to stimulating ethanol intake, GAL has a strong, stimulatory effect on the secretion of prolactin (Koshiyama et al, 1987; Ottlecz et al, 1988), which in turn can increase food intake (Cai et al, 1998; O’Halloran et al, 1991), and prolactin in E 2 -primed rats stimulates GAL (Hammond et al, 1997). Whereas there are no studies in female rats showing a causal effect of prolactin on ethanol intake, there is evidence that chronic consumption of ethanol increases circulating prolactin levels in females, while having no effect in males (Emanuele et al, 2001; Salonen and Huhtaniemi, 1990; Sanchis et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Galanin Knockout Mice Show Disturbances in Ethanol Consumption and Expression of Hypothalamic Peptides That Stimulate Ethanol Intake

Karatayev

Baylan

Weed

et al. 2009

Alcoholism Clin & Exp Res

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Background: There is growing evidence suggesting that hypothalamic galanin (GAL), which is known to stimulate intake of a fat-rich diet, has a role in promoting the consumption of ethanol. The present study further examined this possibility in GAL knockout (GALKO) mice.Methods: Two groups of female and male GALKO mice, compared to wild-type (WT) controls, were trained to voluntarily drink increasing concentrations of ethanol, while maintained on lab chow and water. They were examined in terms of their daily ethanol intake and preference, acute consumption of a high-fat diet, preference for flavored solutions, and expression of different peptides shown to stimulate ethanol intake.Results: In the GALKO mice compared to WT, the results revealed: (i) a 35 to 45% decrease in ethanol intake and preference, which was evident only at the highest (15%) ethanol concentration, was stronger in female than in male mice, and was seen with comparisons to littermate as well as nonlittermate WT mice; (ii) a 48% decrease in acute intake of a fat-rich diet, again stronger in female than male mice; (iii) no difference in consumption of sucrose or quinine solutions in preference tests; (iv) a total loss of GAL mRNA in the hypothalamic paraventricular nucleus (PVN) of female and male mice; and (v) a gender-specific change in mRNA levels of peptides in the perifornical lateral hypothalamus (PFLH), orexin and melanin-concentrating hormone, which are known to stimulate ethanol and food intake and were markedly decreased in females while increased in males.Conclusions: These results provide strong support for a physiological role of PVN GAL in stimulating the consumption of ethanol, as well as a fat-rich diet. Ablation of the GAL gene produced a behavioral phenotype, particularly in females, which may reflect the functional relationship of galanin to ovarian steroids. It also altered the peptides in the PFLH, with their reduced expression contributing to the larger behavioral effects observed in females and their increased expression attenuating these effects in males.

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Section: Discussionmentioning

confidence: 99%

Galanin Knockout Mice Show Disturbances in Ethanol Consumption and Expression of Hypothalamic Peptides That Stimulate Ethanol Intake

Karatayev

Baylan

Weed

et al. 2009

Alcoholism Clin & Exp Res

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“…In the pituitaries of randomly cycling female rats there are more galanin-containing cells and galanin mRNA than in the pituitaries of males [17, 42], the highest concentrations being seen on the morning of estrus and the lowest concentrations on the morning of diestrus. It has also been reported that estrogen stimulates galanin gene expression [16, 17, 43] and galanin release from the pituitary [18]. In addition, estrogen up-regulates the sensitivity of the pituitary to galanin in vivo [40].…”

Section: Discussionmentioning

confidence: 99%

Effects of Galanin and Leptin on Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Release from the Pituitary

Peters

Towler²,

Mason³

et al. 2008

Neuroendocrinology

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Background: A number of peptides regulate luteinizing hormone (LH) release. In some cases, these peptides exert an effect at the pituitary, to directly regulate LH release and/or to modulate the effects of gonadotropin-releasing hormone (GnRH). A link between nutrition and reproductive function is well established. In this study we investigated the effects of two peptides associated with appetite control, galanin and leptin, on the regulation of LH release from the pituitary. Methods: Using perifused anterior pituitary tissue from freely fed rats, we investigated the effect of galanin on basal LH release and GnRH-stimulated LH release from pituitaries in a high-estrogen (proestrus) and a low-estrogen (metestrus) environment. In addition, we examined the effect of galanin on LH release following GnRH self-priming. The effect of inhibiting protein synthesis, with cycloheximide, was also studied under these conditions. Finally, the effects of leptin alone and on a galanin-modulated LH response were investigated. Results: There was no detectable effect of leptin, either alone or in conjunction with galanin. We observed that galanin enhanced GnRH stimulation of LH secretion, an effect that was dependent on protein synthesis and on an estrogenized environment. In addition, importantly, galanin also enhanced the LH response in GnRH self-primed pulses. Conclusion: Our results provide further details on the effect of galanin on the LH surge, particularly the effect on the response to pulsatile GnRH and the effect of protein production, and thereby indicate a means by which appetite- and nutrition-related peptides may act on the ovulatory cycle at the pituitary.

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“…Several possibilities exist. It may be related to the known effects of E 2 and T 3 on the maintenance of lactotrope function and reactivity to TRH [1, 7, 35], and on the availability of pituitary paracrine/autocrine regulators such as VIP and galanin which stimulate basal PRL secretion [7]. E 2 or T 3 may also affect the receptor capacity, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…Among these factors, 17β-estradiol (E 2 ), thyroid hormones, and thyrotropin-releasing hormone (TRH) are known to affect both synthesis and secretion of PRL [1, 5, 6, 7, 8]. E 2 and triiodothyronine (T 3 ) have also been shown to influence lactotrope responses to PRL inhibitory and stimulatory factors [4, 7, 9]. In addition, acetylcholine (ACh), synthesized in the pituitary, has been implicated as a local regulator of pituitary function [10, 11, 12].…”

Section: Introductionmentioning

confidence: 99%

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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Acetylcholine (ACh), synthesized in the pituitary, can act locally to modulate pituitary function. We used rat primary anterior pituitary (AP) cells to investigate how ACh affects pituitary prolactin (PRL) secretion in the presence or absence of known PRL regulators: thyrotropin-releasing hormone (TRH), 17β-estradiol (E₂) and triiodothyronine (T₃). Cultured AP cells were prepared from ovariectomized rats and pretreated with diluent, 0.6 nM E₂, 10 nM T₃, or E₂ plus T₃ for 5 days, then challenged with various doses of ACh or muscarinic receptor agonists (oxotremorine or carbachol) and TRH (100 nM) for 20 min. Significant ACh (10^–5M) suppression of both basal and TRH-induced PRL secretion was not evident in diluent-, E₂- or T₃-pretreated cells, but observed only in cells pretreated with both E₂ and T₃. Moreover, in E₂ plus T₃-pretreated cells, oxotremorine and carbachol, like ACh (10^–7–10^–5M), suppressed both responses in a dose- related manner. Pertussis toxin (PTX; 100 ng/ml) as well as atropine (a muscarinic receptor antagonist; 1 mM) blocked these effects of cholinomimetics. ACh also inhibited both PRL responses elicited by drugs elevating intracellular cAMP (10 µM forskolin) or Ca²⁺ (1 µM Bay K-8644) in a PTX-sensitive manner. ACh inhibition of basal PRL secretion was unaltered by intracellular Ca²⁺ mobilization blockers, TMB-8 (100 µM) and thapsigargin (1 µM), but abrogated by the nitric oxide synthase inhibitor (300 µM L-NAME). ACh inhibition of TRH-induced PRL secretion was accentuated by TMB-8 and alleviated by thapsigargin or L-NAME. In summary, muscarinic inhibition of either basal or TRH-induced PRL secretion was augmented by E₂ and T₃, and involved the PTX-sensitive cAMP/Ca²⁺ pathways. Furthermore, nitric oxide mediated the basal rather than TRH-induced PRL response to ACh, whereas the intracellular Ca²⁺ mobilization concerned the TRH-induced rather than the basal PRL response to ACh. Thus, ACh synthesized in the AP appears to inhibit basal vs. TRH-induced PRL secretion via different mechanisms.

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Regulation of anterior pituitary galanin and vasoactive intestinal peptide by oestrogen and prolactin status

Cited by 15 publications

References 26 publications

Galanin Knockout Mice Show Disturbances in Ethanol Consumption and Expression of Hypothalamic Peptides That Stimulate Ethanol Intake

Galanin Knockout Mice Show Disturbances in Ethanol Consumption and Expression of Hypothalamic Peptides That Stimulate Ethanol Intake

Effects of Galanin and Leptin on Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Release from the Pituitary

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

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