Functional mapping of neural sites mediating prolactin-induced hyperphagia in doves

Hnasko, Robert; Buntin, John D.

doi:10.1016/0006-8993(93)91436-v

Cited by 41 publications

(19 citation statements)

References 33 publications

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“…For instance, PRL-knockout mice have reduced rapid eye movement sleep [25] and PRL receptor-deficient mice have reduced body weight [26] which may be associated with changes in pancreatic islet cell function [27]. In addition, acute PRL treatment can induce feeding behavior in both rodents and doves [28, 29]. These effects of PRL on feeding and metabolism are especially interesting in light of our previous results which show that vrDDfs mice consume more food than control mice [6].…”

Section: Discussionmentioning

confidence: 99%

Genetic Disruption of Dopamine Production Results in Pituitary Adenomas and Severe Prolactinemia

Hnasko

Hnasko²,

Sotak³

et al. 2007

Neuroendocrinology

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Background: Dopamine release from tuberoinfundibular dopamine neurons into the median eminence activates dopamine-D2 receptors in the pituitary gland where it inhibits lactotroph function. Methods: We have previously described genetic dopamine-deficient mouse models which lack the ability to synthesize dopamine. Because these animals require daily treatment with 3,4-L-dihydroxyphenylalanine (L-dopa) to survive, it has not been possible to examine the consequences of chronic loss of dopamine on pituitary physiology. We use viral-mediated gene transfer to selectively restore dopamine to the dorsal striatum of dopamine-deficient mice which allows the mice to survive without L-dopa. Results: We find that mice chronically lacking tuberoinfundibular dopamine secrete large amounts of prolactin due to the development of severely enlarged pituitaries composed principally of hyperplastic hypertrophic lactotrophs and multifocal prolactinomas. In addition, these mice have elevated serum growth hormone levels and aged males develop hypertrophy of the seminal vesicles. Conclusion: Our observations are consistent with the hypothesis that hypothalamic dopamine is a critical inhibitor of lactotroph proliferation and suggest additional roles for dopamine in the regulation of pituitary function.

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Section: Discussionmentioning

confidence: 99%

Genetic Disruption of Dopamine Production Results in Pituitary Adenomas and Severe Prolactinemia

Hnasko

Hnasko²,

Sotak³

et al. 2007

Neuroendocrinology

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“…Collectively, these two studies showed that PRL can induce food intake responses in male doves when it is administered into three regions of the diencephalon: the preoptic area (POA), ventromedial hypothalamic nucleus (VMN), and tuberal hypothalamus (TU). However, the VMN was significantly more effective in mediating PRLinduced feeding responses than were the other two sites [22].…”

Section: Introductionmentioning

confidence: 97%

“…The amount of IgG administered at each injection represented the equivalent of that present in 0.2 pi of undi luted NRS or antiserum. The 50-ng dose of oPRL employed in this experiment had been previously shown to induce a greater food intake response than VMN injections of 2.5 of 25 ng oPRL [5,22] but is still below the threshold dose required to induce a detectable increase in food intake following intracerebroventricular injection [21], Treatments were scheduled twice daily at approximately 10.30 h and 17.30 h and continued for 5 consecutive days. Injections were delivered through a 5-pl Hamilton syringe with an attached 33-gauge infusion cannula assembly (Plastics One), which was screwed on to the nylon threads of the guide cannula.…”

Section: In Vivo Studiesmentioning

confidence: 99%

“…The brains were then sectioned, stained with thionin, and examined to determine cannula placement. Birds were discarded from the study if ink was detected in the cerebral ventricles, if cannula tips had crossed midline, or if can nula tips were found at a distance of 0.5 mm or more from the lateral edge of the VMN [22],…”

Section: In Vivo Studiesmentioning

confidence: 99%

“…Among those effects elicited by PRL administra tion, the increase in feeding behavior is particularly dra matic, with male birds showing approximately 100% increase in daily food intake in response to twice-daily i.c.v. infusions of PRL at a dose of 2 pg/bird [4], The sites of this action in the brain were further examined [5,22] by administering PRL to a variety of diencephalic brain loci that had been previously shown to contain PRL binding sites [19]. Collectively, these two studies showed that PRL can induce food intake responses in male doves when it is administered into three regions of the diencephalon: the preoptic area (POA), ventromedial hypothalamic nucleus (VMN), and tuberal hypothalamus (TU).…”

Section: Introductionmentioning

confidence: 99%

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Inhibitory Effects of Anti-Prolactin Receptor Antibodies on Prolactin Binding in Brain and Prolactin-Induced Feeding Behavior in Ring Doves

Kelly

Buntin

1995

Neuroendocrinology

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Although binding sites for prolactin (PRL) have been mapped and partially characterized in the brains of several species, there is as yet no direct evidence that the effects of intracranial PRL on brain function are receptor-mediated events. We addressed this question by testing whether antibodies generated against rat liver PRL receptors can effectively antagonize the ability of PRL to enhance feeding behavior in male ring doves (Streptopelia risoria). Both agents were administered directly to the ventromedial hypothalamic nucleus (VMN), which is an effective site of PRL action in promoting hyperphagia in this species. In the initial study, affinity-purified γ-globulin (IgG) from the receptor antiserum preparation was tested for its ability to compete with ¹²⁵I-ovine PRL for binding to receptors in rat liver, dove choroid plexus, and 6 PRL-sensitive dove brain regions using in vitro quantitative film autoradiogra-phy. Although the binding affinity of the anti-PRL receptor antibodies was at least 50 times lower in dove brain than in rat liver, a 40-50% inhibition of specifically bound ¹²⁵I-ovine PRL was observed in choroid plexus and in 5 of 6 brain regions with anti-receptor IgG concentrations of 5.8 × 10^-7M and 1.2 × 10^-6M, using sections incubated with normal rabbit serum (NRS) IgG as a control. In a second study, anti-PRL receptor IgG or NRS IgG (2.4 µg) was injected unilaterally into the VMN at 45-60 min prior to VMN injection of ovine PRL (50 ng) or saline vehicle. This procedure was repeated at twice-daily intervals for 5 days. When compared to the feeding behavior of PRL-injected birds given NRS IgG, anti-receptor antibody-treated animals showed a marked reduction in PRL-induced hyperphagia. The magnitude of this reduction was calculated to be approximately 50% after corrections were made for a mild hypophagia induced by the anti-receptor IgG treatment alone, as reflected in the feeding behavior of the anti-PRL receptor IgG + vehicle-treated group. These results suggest that PRL receptors in dove brain and rat liver exhibit structural similarities as well as differences and that the hyperphagia induced by intracranial injections of PRL is mediated, at least in part, by interactions with PRL receptors in the brain.

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Atlas of the neurons that express mRNA for the long form of the prolactin receptor in the forebrain of the female rat

1997

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Prolactin has a variety of important physiological effects on peripheral tissue and on the brain. The behavioral effects of prolactin include the induction of maternal behavior and increased food intake. Prolactin acts via its cognate receptors which have two forms, a short and a long form. The long form of the receptor is predominant in the preoptic area-hypothalamus and is positioned to support maternal behavior since this form is regulated across pregnancy and lactation (Nagano and Kelly [1994] J. Biol. Chem. 269:13337-13345; Sugiyama et al. [1994] J. Endocrinol. 141:325-333). By using in situ hybridization with [33P] labelled cRNA probe specific for the long form of the receptor mRNA(L-PRL mRNA) we have mapped, in brains from 2- and 21-day-old pregnant females, the neuroanatomical distribution of neurons expressing the long form of the receptor. Many neurons with high expression of L-PRL mRNA were located in the anteroventral periventricular nucleus, the medial preoptic area (MPO), specific subdivisions of the paraventricular and supraoptic nuclei, and in the arcuate and ventromedial nuclei. Labelled neurons were also found in limbic system structures such as the bed nucleus of stria terminalis (BST) and the medial nucleus of the amygdala, in a few thalamic nuclei, and in the central gray. All cells throughout the choroid plexus expressed high levels of L-PRL mRNA. The levels of L-PRL mRNA were higher in females on day 21 of pregnancy in the MPO and in the choroid plexus, than in females on day 2 of pregnancy; levels in the ventromedial nucleus of the hypothalamus (VMH) were unchanged across pregnancy. The neuroanatomical distribution of neurons expressing L-PRL mRNA may have special relevance for the mediation of maternal behavior, lactation, sexual behavior, and feeding.

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Functional mapping of neural sites mediating prolactin-induced hyperphagia in doves

Cited by 41 publications

References 33 publications

Genetic Disruption of Dopamine Production Results in Pituitary Adenomas and Severe Prolactinemia

Genetic Disruption of Dopamine Production Results in Pituitary Adenomas and Severe Prolactinemia

Inhibitory Effects of Anti-Prolactin Receptor Antibodies on Prolactin Binding in Brain and Prolactin-Induced Feeding Behavior in Ring Doves

Atlas of the neurons that express mRNA for the long form of the prolactin receptor in the forebrain of the female rat

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