LHRH release depends on Locus Coeruleus noradrenergic inputs to the medial preoptic area and median eminence

Martins-Afférri, Maristela Polachini; Ferreira-Silva, Isac Alexandre; Franci, Celso Rodrigues; Anselmo-Franci, Janete Aparecida

doi:10.1016/s0361-9230(03)00190-4

Cited by 31 publications

(22 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Subsequently the rising progesterone of proestrus would induce the noradrenaline release, which would induce GnRH, and consequently gonadotropin release. In fact we have shown an increase of FOS expression in LC during proestrus afternoon (Martins-Afferri et al 2003), which may represent an increase in noradrenaline release in POA, which is required for the release of these hormones.…”

Section: Locus Coeruleusmentioning

confidence: 66%

“…Data from our laboratory have demonstrated that electrolytic lesion of LC decreases noradrenaline content in medial POA and medial basal hypothalamus and blocks the preovulatory gonadotropin surges observed during proestrus as well as LH pulses (Anselmo-Franci et al 1999) and the steroidinduced surge in ovariectomized rats by decreasing GnRH release (Franci & Antunes-Rodrigues 1985, Anselmo-Franci et al 1997, 1999, Helena et al 2002, Martins-Afferri et al 2003 . Also, an increased number of FOS-immunoreactive (FOS-ir) neurons was observed in LC simultaneously with the preovulatory gonadotropin surges (Martins-Afferri et al 2003).…”

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Changes in α-estradiol receptor and progesterone receptor expression in the locus coeruleus and preoptic area throughout the rat estrous cycle

Helena¹,

Poletini²,

Sanvitto³

et al. 2006

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

We have previously shown that the locus coeruleus (LC) is essential for triggering surges of LH. Since LC neurons are responsive to estradiol, which induces progesterone receptor (PR) expression, this study aimed to investigate whether LC neurons express the -estradiol receptor ( ER) and PR as well as comparing such responses to that observed in the preoptic area (POA). Female rats were perfused at 10, 14 and 16 h on each day of the estrous cycle, and a blood sample was collected for estradiol, progesterone and LH measurements. ER-and PR immunoreactive (ir) neurons were detected in POA and LC by immunocytochemistry (ICC). Higher plasma estradiol levels were observed on the day of proestrus, when a smaller number of ER-ir POA neurons were detected. An increase in the number of ER-ir neurons were observed at 16 h of proestrus and estrus. The number of PR-ir neurons increased in POA only at 16 h of proestrus, and remained unchanged during all other days and times. The profile of ER-ir and PR-ir neurons in LC changed over the estrous cycle, with a lower expression on metestrus morning and reaching a peak on diestrus afternoon before declining on the day of proestrus. However, on estrus afternoon, ER-ir neurons increased, while PR-ir neurons decreased which may be related to the prolactin surge of estrus. These data show that LC neurons express ER and PR and seem to be more sensitive to variations in estradiol than POA. Also, the fluctuation in ER and PR observed for LC neurons seems to accompany the hormonal events that occur during the estrous cycle. This profile of ER and PR expression might be related to the ability of estradiol and progesterone in regulating the activity of LC neurons, which could be associated to the control mechanisms of LH and prolactin release.

show abstract

Section: Locus Coeruleusmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 96%

Changes in α-estradiol receptor and progesterone receptor expression in the locus coeruleus and preoptic area throughout the rat estrous cycle

Helena¹,

Poletini²,

Sanvitto³

et al. 2006

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In the study reported here, we investigated whether LC neurons of female rats display the same circadian profile of activity as those of male rats. Because estradiol exerts strong effects both on NE-biosynthetic enzyme dynamics in LC neurons (35,60,61) and on LC neuronal activity (38) in female rats, we characterized the LC neuronal activity in OVX rats and subsequently determined the role of clock-gene expression in the SCN on this rhythm.…”

mentioning

confidence: 99%

Knockdown of clock genes in the suprachiasmatic nucleus blocks prolactin surges and alters FRA expression in the locus coeruleus of female rats

Poletini¹,

McKee²,

Kennett³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Poletini MO, McKee DT, Kennett JE, Doster J, Freeman ME. Knockdown of clock genes in the suprachiasmatic nucleus blocks prolactin surges and alters FRA expression in the locus coeruleus of female rats. Am J Physiol Endocrinol Metab 293: E1325-E1334, 2007. First published August 28, 2007; doi:10.1152/ajpendo.00341.2007.-The nature of the circadian signal from the suprachiasmatic nucleus (SCN) required for prolactin (PRL) surges is unknown. Because the SCN neuronal circadian rhythm is determined by a feedback loop of Period (Per) 1, Per2, and circadian locomotor output cycles kaput (Clock) gene expressions, we investigated the effect of SCN rhythmicity on PRL surges by disrupting this loop. Because lesion of the locus coeruleus (LC) abolishes PRL surges and these neurons receive SCN projections, we investigated the role of SCN rhythmicity in the LC neuronal circadian rhythm as a possible component of the circadian mechanism regulating PRL surges. Cycling rats on proestrous day and estradiol-treated ovariectomized rats received injections of antisense or random-sequence deoxyoligonucleotide cocktails for clock genes (Per1, Per2, and Clock) in the SCN, and blood samples were taken for PRL measurements. The percentage of tyrosine hydroxylase-positive neurons immunoreactive to Fos-related antigen (FRA) was determined in ovariectomized rats submitted to the cocktail injections and in a 12:12-h light:dark (LD) or constant dark (DD) environment. The antisense cocktail abolished both the proestrous and the estradiolinduced PRL surges observed in the afternoon and the increase of FRA expression in the LC neurons at Zeitgeber time 14 in LD and at circadian time 14 in DD. Because SCN afferents and efferents were probably preserved, the SCN rhythmicity is essential for the magnitude of daily PRL surges in female rats as well as for LC neuronal circadian rhythm. SCN neurons therefore determine PRL secretory surges, possibly by modulating LC circadian neuronal activity. norepinephrine; PERIOD1; PERIOD2 IN FEMALE RATS, PROLACTIN (PRL) secretion has been proposed to result from synchronization among a circadian neural signal from the suprachiasmatic nucleus (SCN), both inhibitory and stimulatory neurotransmitter actions on the pituitary gland, and modulating effects of ovarian steroids (19). As a consequence of this synchronization, female rats display cyclical increases of PRL secretion characterized by two surges: the preovulatory surge of proestrous afternoon (64) and the secondary surge of estrous afternoon (12,70).The preovulatory surge of PRL depends on the levels of plasma ovarian steroids, because the increase of estradiol titers induces (45) and the increase of progesterone amplifies (76) this surge. Estradiol treatment in ovariectomized (OVX) rats induces daily PRL surges that occur at roughly the same time of day as the proestrous surge (13). Shifting of the light phase results in a coincident shift of the proestrous surge (10), and the estradiol-induced PRL surges of OVX rats free run in constant light (52), but the m...

show abstract

“…Similarly, it has recently been pointed out that LHRH release depends, at least in part, on LC noradrenergic inputs to the medial preoptic area and median eminence by activation of LHRH neurons (23). Furthermore, the LC appears to have an intrinsic cyclic activity which is amplified by ovarian steroids (23). Interaction of NMDA and noradrenaline, and noradrenaline and LHRH, appears to occur in different brain areas.…”

Section: Discussionmentioning

confidence: 96%

“…The activation by genital-somatosensory signals (22) of midbrain and brainstem noradrenergic neurons, which project to the mediobasal hypothalamus, promotes the release of LHRH from nerve terminals in the median eminence. Similarly, it has recently been pointed out that LHRH release depends, at least in part, on LC noradrenergic inputs to the medial preoptic area and median eminence by activation of LHRH neurons (23). Furthermore, the LC appears to have an intrinsic cyclic activity which is amplified by ovarian steroids (23).…”

Section: Discussionmentioning

confidence: 96%

Prazosin blocks the glutamatergic effects of N-methyl-D-aspartic acid on lordosis behavior and luteinizing hormone secretion in the estrogen-primed female rat

Landa

Cabrera

Gargiulo

2006

Braz J Med Biol Res

View full text Add to dashboard Cite

We have observed that intracerebroventricular (icv) injection of selective N-methyl-D-aspartic acid (NMDA)-type glutamatergic receptor antagonists inhibits lordosis in ovariectomized (OVX), estrogenprimed rats receiving progesterone or luteinizing hormone-releasing hormone (LHRH). When NMDA was injected into OVX estrogenprimed rats, it induced a significant increase in lordosis. The interaction between LHRH and glutamate was previously explored by us and another groups. The noradrenergic systems have a functional role in the regulation of LHRH release. The purpose of the present study was to explore the interaction between glutamatergic and noradrenergic transmission. The action of prazosin, an α1-and α2b-noradrenergic antagonist, was studied here by injecting it icv (1.75 and 3.5 µg/6 µL) prior to NMDA administration (1 µg/2 µL) in OVX estrogen-primed Sprague-Dawley rats (240-270 g). Rats manually restrained were injected over a period of 2 min, and tested 1.5 h later. The enhancing effect induced by NMDA on the lordosis/mount ratio at high doses (67.06 ± 3.28, N = 28) when compared to saline controls (6 and 2 µL, 16.59 ± 3.20, N = 27) was abolished by prazosin administration (17.04 ± 5.52, N = 17, and 9.33 ± 3.21, N = 20, P < 0.001 for both doses). Plasma LH levels decreased significantly only with the higher dose of prazosin (1.99 ± 0.24 ng/mL, N = 18, compared to saline-NMDA effect, 5.96 ± 2.01 ng/mL, N = 13, P < 0.05). Behavioral effects seem to be more sensitive to the α-blockade than hormonal effects. These findings strongly suggest that the facilitatory effects of NMDA on both lordosis and LH secretion in this model are mediated by α-noradrenergic transmission.

show abstract

LHRH release depends on Locus Coeruleus noradrenergic inputs to the medial preoptic area and median eminence

Cited by 31 publications

References 43 publications

Changes in α-estradiol receptor and progesterone receptor expression in the locus coeruleus and preoptic area throughout the rat estrous cycle

Changes in α-estradiol receptor and progesterone receptor expression in the locus coeruleus and preoptic area throughout the rat estrous cycle

Knockdown of clock genes in the suprachiasmatic nucleus blocks prolactin surges and alters FRA expression in the locus coeruleus of female rats

Prazosin blocks the glutamatergic effects of N-methyl-D-aspartic acid on lordosis behavior and luteinizing hormone secretion in the estrogen-primed female rat

Contact Info

Product

Resources

About