α&lt;sub&gt;2&lt;/sub&gt;-Adrenergic Receptors Are Involved in the Suppression of Luteinizing Hormone Release during Acute Fasting in the Ovariectomized Estradiol-Primed Rats

Cagampang, Felino R.; Ohkura, Satoshi; Tsukamura, Hiroko; Coen, Clive W.; Ota, Kei; Maeda, Kei‐ichiro

doi:10.1159/000126299

Cited by 32 publications

(16 citation statements)

References 21 publications

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“…Similarly, female NPY KO mice do not exhibit a suppression of LH levels after a fast (100), but we are not aware of any comparable data with DBH KO mice. Although these findings seem to indicate an essential role for NPY, it has also been reported that ICV administration of ␣-adrenergic antagonists is sufficient to prevent fasting-induced decreases in LH levels (27), consistent with crucial participation of ␣-adrenergic transmission. Perhaps both NPY and CA signaling are required.…”

Section: Control Of Lh Secretionmentioning

confidence: 77%

“…2) Energetic challenges such as food deprivation and diabetes increase release of NE and NPY in the forebrain (3,118,153,160,195,231). 3) Forebrain infusions of either NPY (30,177) or NE (27,241) inhibit LH secretion (Figs. 7 and 8), and studies using selective agonists and antagonists suggest that these effects are mediated by NPY Y5 and ␣-adrenergic receptors, respectively (27,177).…”

Section: Control Of Lh Secretionmentioning

confidence: 99%

“…3) Forebrain infusions of either NPY (30,177) or NE (27,241) inhibit LH secretion (Figs. 7 and 8), and studies using selective agonists and antagonists suggest that these effects are mediated by NPY Y5 and ␣-adrenergic receptors, respectively (27,177).…”

Section: Control Of Lh Secretionmentioning

confidence: 99%

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Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

228

166

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Natural selection has linked the physiological controls of energy balance and fertility such that reproduction is deferred during lean times, particularly in female mammals. In this way, an energetically costly process is confined to periods when sufficient food is available to support pregnancy and lactation. Even in the face of abundance, nutritional infertility ensues if energy intake fails to keep pace with expenditure. A working hypothesis is proposed in which any activity or condition that limits the availability of oxidizable fuels (e.g., undereating, excessive energy expenditure, diabetes mellitus) can inhibit both gonadotropin-releasing hormone (GnRH)/luteinizing hormone secretion and female copulatory behaviors. Decreases in metabolic fuel availability appear to be detected by cells in the caudal hindbrain. Hindbrain neurons producing neuropeptide Y (NPY) and catecholamines (CA) then project to the forebrain where they contact GnRH neurons both directly and also indirectly via corticotropin-releasing hormone (CRH) neurons to inhibit GnRH secretion. In the case of estrous behavior, the best available evidence suggests that the inhibitory NPY/CA system acts primarily via CRH or urocortin projections to various forebrain loci that control sexual receptivity. Disruption of these signaling processes allows normal reproduction to proceed in the face of energetic deficits, indicating that the circuitry responds to energy deficits and that no signal is necessary to indicate that there is an adequate energy supply. While there is a large body of evidence to support this hypothesis, the data do not exclude nutritional inhibition of reproduction by other pathways and processes, and the full story will undoubtedly be more complex than this. luteinizing hormone; estrous behavior; corticotropin-releasing hormone; neuropeptide Y; hindbrain OF NECESSITY, the physiological controls of reproduction and energy balance are closely intertwined. Living creatures require a steady stream of oxidizable substrates to fuel their many energy-consuming activities, including reproduction. But in nature, energetic demands and opportunities for meal taking can be erratic and sometimes unpredictable, necessitating the existence of physiological and behavioral strategies to maximize chances of individual survival and permit propagation of the species (21,22,200,208).A need to eat constantly is obviated by the presence of internal caloric buffers that store glycogen and fatty acids and provide sustenance in between meals and during brief fasts. When food is abundant, animals adjust their intakes to meet all demands and keep their storage depots full (or overfull in an increasing number of cases). However, a more likely scenario in nature and during human evolution is that food can be scarce or have a very high acquisition cost. In that case, animals adjust their energetic priorities, i.e., how they partition and use the available metabolic fuels (Fig.

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Section: Control Of Lh Secretionmentioning

confidence: 77%

Section: Control Of Lh Secretionmentioning

confidence: 99%

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Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

228

166

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“…The neural pathways that relay information on insufficient energy stores to GnRH neurons included many signals. Different neuropeptides and neurotransmitters [such as NPY, adrenaline via ␣ 2 -adrenergic receptors, corticotropinreleasing hormone (CRH), leptin, ciliary neurotropic factor (CNTF), ␥-aminobutyric acid, and opioids] have been implicated in the effects of fasting on pituitary secretion (8,32,38,39,40,44).…”

Section: Discussionmentioning

confidence: 99%

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Pinilla¹,

Fernández²,

Vigo³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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] is a gastrointestinal secreted molecule recently shown to be involved in the control of food intake with agonistic activity on neuropeptide Y (NPY) receptor subtypes Y2 and Y5. Notably, PYY-(3-36) has been recently demonstrated as putative regulator of gonadotropin secretion in the rat. However, the "reproductive" facet of this factor remains to be fully elucidated. In this context, we report herein our analyses of the influence of the nutritional status on the effects of PYY-(3-36) upon GnRH and gonadotropin secretion. The major findings of our study are 1) the stimulatory effect of central administration of PYY-(3-36) on LH secretion was significantly enhanced after fasting and blocked by a GnRH antagonist; 2) besides central effects, PYY-(3-36) elicited LH and FSH secretion directly at the pituitary level, a response that is also augmented by fasting; 3) PYY-(3-36) inhibited GnRH secretion by hypothalamic fragments from male rats fed ad libitum, whereas a significant stimulatory effect was observed after fasting; and 4) the increase in the gonadotropin responsiveness to PYY-(3-36) in fasting was not associated with changes in the expression of Y2 and Y5 receptor genes at hypothalamus and/or pituitary. In conclusion, our study extends our previous observations suggesting a relevant, mostly stimulatory, role of PYY-(3-36) in the control of gonadotropin secretion. Strikingly, such an effect was significantly enhanced by fasting. Considering the proposed decrease in PYY-(3-36) levels after fasting, the possibility that reduced PYY-(3-36) secretion might contribute to defective function of the gonadotropic axis after food deprivation merits further investigation.polypeptide YY-(3-36); gonadotropin-releasing hormone; luteinizing hormone; follicle-stimulating hormone; fasting; pituitary ALTHOUGH IT IS KNOWN that conditions of negative energy balance are frequently linked to lack of puberty onset and reproductive failure, at the moment the mechanisms involved in fitting the reproductive function to body energy stores remain incompletely defined. Compelling evidence has recently demonstrated that central and peripheral endocrine signals governing energy homeostasis, such as the adipocytederived hormone leptin, the stomach-derived hormone ghrelin, orexins, and neuropeptide Y (NPY), are also involved in the control of reproductive function by acting at different levels of hypothalamic-pituitary-gonadal axis.In this context, it has been demonstrated that NPY, a member of the pancreatic polypeptide family (54), is involved in the control of food intake, reproductive function, and pituitary secretion (26,27,30,33). In rats, central administration of NPY advances puberty (43), whereas immunoneutralization of NPY reduced the magnitude of the LH surge during the afternoon of first proestrus (42). A facilitatory role of NPY on the onset of puberty has been also reported in the female rhesus monkey (23) and in chicks (18). Secretion of NPY to portal vasculature is increased on the afternoon of proestrus and serves to amplify...

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“…The MA dose (2 μmol/rat) has previously been shown to suppress LH pulses, when injected into the 4V [13]. In addition, the dose for PVN injection was one third of the dose for intracerebroventricular injection of the α1-, α2-or β-adrenergic antagonist to block fasting-induced suppression of LH pulses [16] in E2-implanted ovariectommized rats. This treatment regimen resulted in the following eight groups: PVN vehicle+4V MA (n=6); PVN α1-antagonist+4V MA (n=5); PVN α2-antagonist+4V MA (n=5); PVN β-antagonist+4V MA (n=6); PVN vehicle+4V Saline (n=5); PVN α1-antagonist+4V saline (n=5); PVN α2-antagonist+4V saline (n=5); and PVN β-antagonist+4V saline (n=5).…”

Section: Drug Administration and Blood Samplingmentioning

confidence: 99%

Paraventricular .ALPHA.1- and .ALPHA.2-Adrenergic Receptors Mediate Hindbrain Lipoprivation-induced Suppression of Luteinizing Hormone Pulses in Female Rats

Sajapitak

Uenoyama

Yamada

et al. 2008

Journal of Reproduction and Development

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Abstract. Acute central lipoprivation suppresses pulsatile luteinizing hormone (LH) release and increases blood glucose levels through noradrenergic input to the hypothalamic paraventricular nucleus (PVN) in female rats. The present study was conducted to identify adrenergic receptor subtypes involved in central lipoprivation-induced suppression of pulsatile LH secretion and increases in plasma glucose levels in female rats. Acute hindbrain lipoprivation was produced by injection into the fourth cerebroventricle (4V) of 2-mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in estradiol-implanted ovariectomized rats. Two min before MA injection, α1-, α2-or β-adrenergic receptor antagonist was injected into the PVN. Injection of MA into the 4V suppresses pulsatile LH release in PVN vehicle-treated rats, whereas pretreatment of animals with injection of α1-or α2-adrenergic antagonist into the PVN blocked the effect of the 4V MA injection on LH pulses. β-Adrenergic antagonist did not affect MA-induced suppression of LH pulses. The counter-regulatory increase in plasma glucose levels after 4V MA injection was also partially blocked by pretreatment with α1-and α2-adrenergic receptor antagonists. These results suggest that α1-and α2-adrenergic receptors in the PVN mediate hindbrain lipoprivation-induced suppression of LH release and counterregulatory increases in plasma glucose levels in female rats. Key words: Adrenergic receptor, Energy sensing, Free fatty acid, Lipoprivation, Mercaptoacetate, Rat (J. Reprod. Dev. 54 : 198-202, 2008) nergy availability is one of the critical factors regulating gonadal function through control of gonadotropin release in mammals at various phases of reproduction, such as the onset of puberty and lactational anestrus [1][2][3][4]. Pulsatile luteinizing hormone (LH) release is suppressed by food restriction or acute food deprivation in rats [1,5,6]. Acute glucoprivation induced by peripheral injection of 2-deoxyglucose (2DG) also results in suppression of LH pulses [7].Glucose availability has been reported to be monitored by a specific sensor(s) located in the brain to regulate food intake [8]. The hindbrain may monitor glucose availability in rats to control food intake and LH release because 2DG injection into the fourth cerebroventricle (4V) increases food intake and suppresses LH release [9]. Glucokinase-immunoreactive ependymocytes in the hindbrain show an in vitro increase in intracellular Ca 2+ levels in response to altered extracellular glucose levels [10], suggesting that ependymocytes in the hindbrain play a role in glucose sensing. In addition, information concerning the glucose availability may partly be conveyed by noradrenergic ascending input into the hypothalamic paraventricular nucleus (PVN) [11].Peripheral and central inhibition of β-oxidation of fatty acids, another metabolic fuel, also suppresses pulsatile LH release in female rats [12,13], suggesting that the fatty acid is a metabolic signal controlling LH release. Our previous study demonstrated that fat...

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α<sub>2</sub>-Adrenergic Receptors Are Involved in the Suppression of Luteinizing Hormone Release during Acute Fasting in the Ovariectomized Estradiol-Primed Rats

Cited by 32 publications

References 21 publications

Neuroendocrinology of nutritional infertility

Neuroendocrinology of nutritional infertility

Stimulatory effect of PYY-(3–36) on gonadotropin secretion is potentiated in fasted rats

Paraventricular .ALPHA.1- and .ALPHA.2-Adrenergic Receptors Mediate Hindbrain Lipoprivation-induced Suppression of Luteinizing Hormone Pulses in Female Rats

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