RAPID INCREASE IN LHRH mRNA LEVELS FOLLOWING NMDA

Petersen, Sandra L.; McCrone, Sue; Keller, Mary L.; Gardner, Erin R.

doi:10.1210/endo-129-3-1679

Cited by 77 publications

(35 citation statements)

References 23 publications

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“…There are several alternative or complementary explanations. It is possible that changes in GnRH mRNA may occur more rapidly (e.g., within 15 min to 1 h), similar to what has been reported for effects of N -methyl-D , L -aspartate [42,64] , whereas in the current study, rats were euthanized 4 h after ifenprodil injection. Alternatively, GnRH mRNA may replenish pools of the GnRH peptides over a longer time course.…”

Section: Effects Of Ifenprodil On Lh Release Occur Independently Of Esupporting

confidence: 65%

NMDA Receptor Subunit NR2b: Effects on LH Release and GnRH Gene Expression in Young and Middle-Aged Female Rats, with Modulation by Estradiol

Maffucci¹,

Walker²,

Ikegami³

et al. 2007

Neuroendocrinology

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hypothalamus were quantified as indices of the reproductive axis. Results: Our results showed effects of ifenprodil on both endpoints. In OVX rats given cholesterol, neither age nor ifenprodil had any effects on LH release. In E 2 -treated rats, aging was associated with significant decreases in pulsatile LH release. Additionally, ifenprodil stimulated parameters of pulsatile LH release in both young and middle-aged animals. Ifenprodil had few effects on GnRH mRNA; the only significant effect of ifenprodil was found in the middle-aged, cholesterol group. Conclusion: Together, these findings support a role for the NR2b subunit of the NMDAR in GnRH/ LH regulation. Because most of these effects were exhibited on pituitary LH release in the absence of a concomitant change in GnRH gene expression, it is likely that NMDA receptors containing the NR2b subunit play a role in GnRH-induced LH release, independent of de novo GnRH gene expression.

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Section: Effects Of Ifenprodil On Lh Release Occur Independently Of Esupporting

confidence: 65%

NMDA Receptor Subunit NR2b: Effects on LH Release and GnRH Gene Expression in Young and Middle-Aged Female Rats, with Modulation by Estradiol

Maffucci¹,

Walker²,

Ikegami³

et al. 2007

Neuroendocrinology

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“…concept that NMDA acts at a post-transcriptional level in GnRH neurons is supported further by the observation that treatment of rats with NMDA did not stimulate expression of cFos, a putative indicator of gene activation (transcription), in GnRH neurons (Saitoh et al, 1991;Lee et al, 1993). Furthermore, the rapidity with which NMDA stimulates acute increases in GnRH mRNA levels in adult rats (Petersen et al, 1991;Liaw and Barraclough, 1993;Gore and Roberts, 1994) indicates a more rapidly regulated mechanism than transcription, such as mRNA stability.…”

Section: Discussionmentioning

confidence: 94%

“…Our laboratory and others have reported previously that changes in the steroid or neurotransmitter environment can result in increases in cytoplasmic GnRH mRNA levels (Petersen et al, 1991(Petersen et al, , 1996Liaw and Barraclough, 1993;Roberts, 1994, 1995) independent of transcription of the GnRH gene Roberts, 1994, 1995). This suggests that GnRH mRNA levels are regulated to a large extent by a post-transcriptional mechanism such as mRNA stability.…”

mentioning

confidence: 83%

Gonadotropin-Releasing Hormone and NMDA Receptor Gene Expression and Colocalization Change during Puberty in Female Rats

et al. 1996

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During development, an increase in gonadotropin-releasing hormone (GnRH) release occurs that is critical for the initiation of puberty. This increase is attributable, at least in part, to activation of the GnRH neurosecretory system by inputs from neurotransmitters, such as glutamate, acting via NMDA receptors. We examined changes in GnRH and NMDA-R1 gene expression by RNase protection assay of preoptic area-anterior hypothalamic (POA-AH) dissections of female rats undergoing normal puberty or in which precocious puberty was induced by treatment with the glutamate agonist NMA. GnRH mRNA levels increased significantly throughout normal development; this was accelerated by treatment with NMA. NMDA-R1 mRNA levels increased only between P10 and P20. The acceleration of the elevation in GnRH mRNA levels by NMDA suggests that a stimulation of GnRH gene expression may be a rate-limiting factor for the onset of puberty. This is attributable to a posttranscriptional mechanism because GnRH primary transcript levels, an index of proGnRH gene transcription, were not observed to change during puberty. Alterations in the colocalization of GnRH neurons with the NMDA-R1 subunit during puberty also were assessed immunocytochemically. The percentage of GnRH neurons that double-labeled with NMDA-R1 was 2% in prepubertal rats and 3% in pubertal rats; this increased to 19% in postpubertal rats. Taken together, these studies suggest that an increase in glutamatergic input to GnRH neurons plays a role in the increase in GnRH release and gene expression that occurs at the initiation of puberty.

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“…Moreover, dualphenotype contacts were found on all medial GnRH neurons examined, but on few lateral GnRH neurons. This is a key finding because in rats the majority of medial, but not lateral, GnRH neurons contains functional NMDA receptors (Ottem et al, 2002), a glutamate receptor subtype that regulates GnRH synthesis (Petersen et al, 1991;Liaw and Barraclough, 1993;Gore and Roberts, 1994), and surge release (Brann and Mahesh, 1995). All midline GnRH neurons also contain GABA A receptors (Petersen et al, 1993;Petersen, unpublished) and GABA B receptors (Petersen et al, 2003).…”

Section: Discussionmentioning

confidence: 97%

Dual-Phenotype GABA/Glutamate Neurons in Adult Preoptic Area: Sexual Dimorphism and Function

Ottem¹,

Godwin²,

Krishnan³

et al. 2004

J. Neurosci.

186

168

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It is generally assumed that the inhibitory neurotransmitter GABA and the stimulatory neurotransmitter glutamate are released from different neurons in adults. However, this tenet has made it difficult to explain how the same afferent signals can cause opposite changes in GABA and glutamate release. Such reciprocal release is a central mechanism in the neural control of many physiological processes including activation of gonadotropin-releasing hormone (GnRH) neurons, the neural signal for ovulation. Activation of GnRH neurons requires simultaneous suppression of GABA and stimulation of glutamate release, each of which occurs in response to a daily photoperiodic signal, but only in the presence of estradiol (E 2 ). In rodents, E 2 and photoperiodic signals converge in the anteroventral periventricular nucleus (AVPV), but it is unclear how these signals differentially regulate GABA and glutamate secretion. We now report that nearly all neurons in the AVPV of female rats express both vesicular glutamate transporter 2 (VGLUT2), a marker of hypothalamic glutamatergic neurons, as well as glutamic acid decarboxylase and vesicular GABA transporter (VGAT), markers of GABAergic neurons. These dual-phenotype neurons are the main targets of E 2 in the region and are more than twice as numerous in females as in males. Moreover, dual-phenotype synaptic terminals contact GnRH neurons, and at the time of the surge, VGAT-containing vesicles decrease and VGLUT2-containing vesicles increase in these terminals. Thus, we propose a new model for ovulation that includes dual-phenotype GABA/glutamate neurons as central transducers of hormonal and neural signals to GnRH neurons.

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RAPID INCREASE IN LHRH mRNA LEVELS FOLLOWING NMDA

Cited by 77 publications

References 23 publications

NMDA Receptor Subunit NR2b: Effects on LH Release and GnRH Gene Expression in Young and Middle-Aged Female Rats, with Modulation by Estradiol

NMDA Receptor Subunit NR2b: Effects on LH Release and GnRH Gene Expression in Young and Middle-Aged Female Rats, with Modulation by Estradiol

Gonadotropin-Releasing Hormone and NMDA Receptor Gene Expression and Colocalization Change during Puberty in Female Rats

Dual-Phenotype GABA/Glutamate Neurons in Adult Preoptic Area: Sexual Dimorphism and Function

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