Central Administration of Antiserum to Vasoactive Intestinal Peptide Delays and Reduces Luteinizing Hormone and Prolactin Surges in Ovariectomized, Estrogen-Treated Rats

Beek, Eline M. van der; Swarts, Hans J. M.; Wiegant, V.M.

doi:10.1159/000054423

Cited by 79 publications

(37 citation statements)

References 40 publications

(61 reference statements)

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“…Interestingly, Chappell et al (2000) reported that cAMP levels in the anteroventral periven-tricular nucleus (AVPV) exhibit a diurnal rhythm that is markedly analogous to the rhythm of VIP. Third, aging affects the rhythm of VIP in the SCN (Krajnak et al, 1998a), and suppression of this rhythm in young rats leads to delayed and attenuated LH surges that are strikingly similar to those observed in middleaged (MA) female rats (Harney et al, 1996;van der Beek et al, 1999).…”

Section: Introductionmentioning

confidence: 75%

“…Several lines of evidence suggest that a diurnal pattern of vasoactive intestinal polypeptide (VIP) gene and protein expression, originating from the SCN, is an essential component of the constellation of stimulatory signals leading to the proper timing of preovulatory GnRH (Harney et al, 1996;Horvath et al, 1998;van der Beek et al, 1999) and that changes in the dynamics of this neuropeptide may contribute to age-related alterations in the pattern of GnRH secretion (Krajnak et al, 2001;Le et al, 2001). First, VIP neurons in the SCN directly innervate GnRH neurons in the rostral preoptic nucleus (rMPN) (van der Beek et al, 1997;Horvath et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Suppression of Vasoactive Intestinal Polypeptide in the Suprachiasmatic Nucleus Leads to Aging-Like Alterations in cAMP Rhythms and Activation of Gonadotropin-Releasing Hormone Neurons

Gerhold¹,

Rosewell²,

Wise³

2005

J. Neurosci.

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Input from the suprachiasmatic nucleus (SCN) to gonadotropin-releasing hormone (GnRH) neurons is critical to the occurrence of regular cyclic GnRH secretion. It is thought that an essential neuropeptide in the SCN that communicates this cyclic information to GnRH neurons is vasoactive intestinal polypeptide (VIP) and that it may act through cAMP. We tested the hypothesis that (1) aging involves a blunting of cAMP diurnal rhythmicity in the SCN; (2) administration of antisense oligonucleotides (anti-oligos) against VIP, which produces an aging-like pattern in VIP, would lead to an aging-like suppression of cAMP; and (3) this in turn would lead to inhibition of the steroid-induced activation of GnRH neurons. We measured cAMP concentrations in the SCN and rostral preoptic nucleus throughout the day in young and middle-aged rats that were ovariectomized (OVX) or OVX and treated with estradiol.Our results show that cAMP concentrations exhibit a diurnal rhythm in young rats, and that this rhythm is totally abolished by the time rats are middle age. Administration of antisense oligonucleotides against VIP or random oligos suppresses VIP concentrations and abolishes the cAMP rhythm, leading to significantly reduced activation of GnRH neurons. Together, these findings strongly suggest that the SCN conveys diurnal information to GnRH neurons by driving VIP-dependent cAMP rhythms. In addition, aging involves deterioration in this VIP-driven rhythmicity, which impacts the ability of steroids to induce GnRH neuronal activation.

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Section: Introductionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Suppression of Vasoactive Intestinal Polypeptide in the Suprachiasmatic Nucleus Leads to Aging-Like Alterations in cAMP Rhythms and Activation of Gonadotropin-Releasing Hormone Neurons

Gerhold¹,

Rosewell²,

Wise³

2005

J. Neurosci.

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“…For example, vasoactive intestinal peptide (VIP) 2 receptors that are positively coupled to adenylate cyclase are expressed by rat GnRH neurons (36). Central administration of an antiserum to VIP delays and attenuates the LH surge (37). Overexpression of PDE4D1 could inhibit the VIP-induced increase in cAMP.…”

Section: Discussionmentioning

confidence: 99%

Phosphodiesterase expression targeted to gonadotropin-releasing hormone neurons inhibits luteinizing hormone pulses in transgenic rats

Paruthiyil

Majdoubi

Conti

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Experiments in the GT1 gonadotropin-releasing hormone (GnRH) cell line have shown that the cAMP signaling pathway plays a central role in regulating the excitability of the cells. Lowering cAMP levels by expressing the constitutively active cAMP-specific phosphodiesterase PDE4D1 in GT1 cells inhibited spontaneous Ca 2؉ oscillations and intrinsic pulsatile GnRH secretion. To address the role of cAMP levels in endogenous GnRH neurons, we genetically targeted expression of PDE4D1 (P) to GnRH neurons in transgenic rats (R) by using the GnRH gene promoter͞enhancer regions (G). Three lines of transgenic rats, GPR-2, -4, and -5, were established. In situ hybridization and RT-PCR studies demonstrated that transgene expression was specifically targeted to GnRH neurons. Decreased fertility was observed in female but not in male rats from all three lines. The mean luteinizing hormone (LH) levels in ovariectomized rats were significantly reduced in the GPR-4 and -5 lines but not in the GPR-2 line. In castrated male and female GPR-4 rats, the LH pulse frequency was dramatically reduced. Six of twelve GPR-4 females studied did not ovulate and had polycystic ovaries. The remaining six females ovulated, but the magnitude of the preovulatory LH surge was inhibited by 63%. These findings support the hypothesis that cAMP signaling may play a central role in regulating excitability of GnRH neurons in vivo. The GPR-4 line of transgenic rats provides a genetic model for the understanding of the role of pulsatile gonadotropin release in follicular development.T he pulsatile release of gonadotropin-releasing hormone (GnRH) underlies reproductive function in male and female mammals. Understanding the molecular mechanisms regulating pulsatile GnRH secretion has been hampered by the low number of GnRH neurons and their scattered localization throughout the preoptic area in rodents. Further complicating the understanding of these questions is the complexity of the neural connectivity of GnRH neurons. The development of the highly differentiated GT1 GnRH neuronal cell lines (1) and the demonstration that pulsatile release was an intrinsic property of the cells provided a model to study molecular events underlying pulsatile GnRH release (2-4). However, one is always faced with the problem of translating findings from an immortalized cell line to the physiological setting. We have attempted to bridge observations made in GT1 cells regarding signaling events regulating GnRH pulsatility to the physiological setting by developing a transgenic rat model. We used an established genetic approach to alter the activity of a signaling pathway that could be used in parallel experiments in GT1 cells and transgenic rats. Transgenic rats, unlike transgenic mice, permit the reliable analysis of pulsatile luteinizing hormone (LH) release that closely mimics pulsatile GnRH release in castrated animals (5).The secretion of GnRH in GT1 neurons is stimulated by elevations in cAMP levels (6-8). The stimulation of GnRH secretion by elevated cAMP levels appears to...

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“…This hypothesis receives strong support and the spatial analysis focused our attention on an area defined by a population of vasoactive intestinal polypeptide (VIP) neurons. VIP neurons, fibers, and receptors are found in virtually every brain region that is known to be important for social behavior (22)(23)(24)(25), but with the exception of the VIP neuronal populations in the suprachiasmatic nucleus and tuberal hypothalamus, which regulate circadian rhythms and prolactin release, respectively (26,27), we know very little about the behavioral functions of VIP cell groups and their projection systems.…”

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confidence: 99%

An aggression-specific cell type in the anterior hypothalamus of finches

Goodson

Kelly

Kingsbury

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The anterior hypothalamus (AH) is a major integrator of neural processes related to aggression and defense, but cell types in the AH that selectively promote aggression are unknown. We here show that aggression is promoted in a very selective and potent manner by dorsal AH neurons that produce vasoactive intestinal polypeptide (VIP). Fos activity in a territorial finch, the violet-eared waxbill (Estrildidae: Uraeginthus granatina) is positively related to aggression in the dorsal AH, overlapping a population of VIP-producing neurons. VIP is known to promote territorial aggression in songbirds, and thus we used antisense oligonucleotides to selectively block AH VIP production in male and female waxbills. This manipulation virtually abolishes aggression, reducing the median number of displacements in a 3-min resident-intruder test from 38 in control subjects to 0 in antisense subjects. Notably, most antisense and control waxbills exhibit an agonistic response such as a threat or agonistic call within 2 s of intrusion. Thus, antisense subjects clearly classify intruders as offensive, but fail to attack. Other social and anxiety-like behaviors are not affected and VIP cell numbers correlate positively with aggression, suggesting that these cells selectively titrate aggression. Additional experiments in the gregarious zebra finch (Estrildidae: Taeniopygia guttata) underscore this functional specificity. Colony-housed finches exhibit significant reductions in aggression (primarily nest defense) following AH VIP knockdown, but no effects are observed for social preferences, pair bonding, courtship, maintenance behaviors, or anxiety-like behaviors. To our knowledge, these findings represent a unique identification of an aggression-specific cell type in the brain.neuropeptide | reproduction T he anterior hypothalamus (AH) is a hub of neural processes related to aggression and agonistic communication in taxa ranging from fish to mammals (1-9). The AH is strongly interconnected with the ventrolateral subnucleus of the ventromedial hypothalamus (VMHvl) (10), and both areas are overlapped by the "hypothalamic attack area," a region from which aggressive behavior is elicited by electrical stimulation in mammals (7,9,11,12). A comparable organization is found in birds, as demonstrated by both electrical stimulation (1, 8) and immediate early gene expression (13,14). The AH and VMHvl integrate information from many socially relevant forebrain regions and project to midbrain areas that regulate motivation and motor processes (10,(15)(16)(17). However, whereas recent studies in male mice show that overlapping but distinct neuronal populations of the VMHvl regulate fighting and mating (18), the neurochemical phenotypes of aggression-related neurons in the VMHvl and AH are largely unknown (7). AH vasopressin neurons that promote aggression in voles also influence affiliation (5), and the AH further regulates stress response and defense (12,14,19). Thus, the identification of AH neurons that selectively promote aggression requires t...

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Central Administration of Antiserum to Vasoactive Intestinal Peptide Delays and Reduces Luteinizing Hormone and Prolactin Surges in Ovariectomized, Estrogen-Treated Rats

Cited by 79 publications

References 40 publications

Suppression of Vasoactive Intestinal Polypeptide in the Suprachiasmatic Nucleus Leads to Aging-Like Alterations in cAMP Rhythms and Activation of Gonadotropin-Releasing Hormone Neurons

Suppression of Vasoactive Intestinal Polypeptide in the Suprachiasmatic Nucleus Leads to Aging-Like Alterations in cAMP Rhythms and Activation of Gonadotropin-Releasing Hormone Neurons

Phosphodiesterase expression targeted to gonadotropin-releasing hormone neurons inhibits luteinizing hormone pulses in transgenic rats

An aggression-specific cell type in the anterior hypothalamus of finches

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