Effect of N-methyl-D,L-aspartate on isolated rat somatotrophs

Lindstrom, Peter A.

doi:10.1210/en.131.4.1903

Cited by 18 publications

(14 citation statements)

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“…Gluta¬ mate receptors have been identified in lactotrophs (23) and either KA or NMDA stimulate directly LH, FSH and GH secretion by perifused adenohypophyseal cells (24,25), which indicates that the pituitary gland is a possible site of action of NMDA and KA. Gluta¬ mate receptors have been identified in lactotrophs (23) and either KA or NMDA stimulate directly LH, FSH and GH secretion by perifused adenohypophyseal cells (24,25), which indicates that the pituitary gland is a possible site of action of NMDA and KA.…”

Section: Discussionmentioning

confidence: 98%

Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats

Pinilla

Gonzalez²,

Tena‐Sempere³

et al. 1996

European Journal of Endocrinology

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The control of prolactin (PRL) secretion by N-methyl-D-aspartate (NMDA) and kainic acid (KA), agonists of NMDA and kainate receptors, and the interactions between NMDA and KA with nitric oxide (NO) were analysed in prepubertal female rats. For this purpose, serum PRL concentrations and hypothalamic and pituitary dopamine (DA) and serotonin (5-HT) concentrations were measured in females injected with NMDA, KA or two blockers of NO synthase: Nw-nitro-L-arginine methyl ester (NAME) and Nw-nitro-L-arginine (NA). Also, the effects of combined administration of NMDA and KA with the blockers of NO synthase were analyzed. We found that PRL release was inhibited 15 min after NMDA and KA administration, an effect probably mediated through the release of hypothalamic DA, as shown by the higher pituitary DA concentrations after NMDA or KA administration. The inhibitory effect of NMDA was preceded by an increase in serum PRL levels, observed at 5 and 10 min after NMDA administration. Nw-Nitro-L-arginine methyl ester alone inhibited prolactin secretion, and both NAME and NA abolished the inhibitory effect of KA, but not that of NMDA. We conclude that administration of NMDA exerted a dual action on PRL secretion: initially DA release was inhibited, leading to an increase in PRL secretion that in turn stimulated DA release and decreased serum PRL concentrations. Kainic acid also inhibited PRL secretion by releasing DA, an effect blocked by NO synthase inhibitors.

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Section: Discussionmentioning

confidence: 98%

Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats

Pinilla

Gonzalez²,

Tena‐Sempere³

et al. 1996

European Journal of Endocrinology

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“…Some of the actions of glutamate on the somatotropic axis may also be exerted at the hypophysial level. Ionotropic and metabotropic glutamate receptors are expressed by anterior pituitary cells (Bhat et al ., 1995; Caruso et al ., 2004) and N ‐methyl‐ D ‐aspartic acid (NMDA), kainate and glutamate can stimulate dose‐dependently GH secretion from perifused somatotrophs (Lindstrom & Ohlsson, 1992; Niimi et al ., 1994). Several lines of evidence also indicate that glutamate exerts central actions on GH secretion in which GHRH neurons play a crucial role.…”

Section: Discussionmentioning

confidence: 99%

Presence of vesicular glutamate transporter‐2 in hypophysiotropic somatostatin but not growth hormone‐releasing hormone neurons of the male rat

Hrabovszky

Túri

Liposits

2005

Eur J of Neuroscience

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Recent evidence indicates that hypophysiotropic gonadotropin-releasing hormone (GnRH), corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH) neurons of the adult male rat express mRNA and immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. In the present study, we investigated the issue of whether these glutamatergic features are shared by growth hormone-releasing hormone (GHRH) neurons of the hypothalamic arcuate nucleus (ARH) and somatostatin (SS) neurons of the anterior periventricular nucleus (PVa), the two parvicellular neurosecretory systems that regulate anterior pituitary somatotrophs. Dual-label in situ hybridization studies revealed relatively few cells that expressed VGLUT2 mRNA in the ARH; the GHRH neurons were devoid of VGLUT2 hybridization signal. In contrast, VGLUT2 mRNA was expressed abundantly in the PVa; virtually all (97.5 +/- 0.4%) SS neurons showed labelling for VGLUT2 mRNA. In accordance with these hybridization results, dual-label immunofluorescent studies followed by confocal laser microscopic analysis of the median eminence established the absence of VGLUT2 immunoreactivity in GHRH terminals and its presence in many neurosecretory SS terminals. The GHRH terminals, in turn, were immunoreactive for the vesicular gamma-aminobutyric acid (GABA) transporter, used in these studies as a marker for GABA-ergic neuronal phenotype. Together, these results suggest the paradoxic cosecretion of the excitatory amino acid neurotransmitter glutamate with the inhibitory peptide SS and the cosecretion of the inhibitory amino acid neurotransmitter GABA with the stimulatory peptide GHRH. The mechanisms of action of intrinsic amino acids in hypophysiotropic neurosecretory systems require clarification.

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“…Results of in vitro studies revealed additional direct hypophysial actions of glutamate on luteinising hormone (25), GH (26, 27) and prolactin (28, 29) secretion from the adenohypophysis and on vasopressin release from the neurohypophysis (30).…”

Section: Glutamate Regulates Endocrine Functions Via Binding To Hypotmentioning

confidence: 99%

Novel Aspects of Glutamatergic Signalling in the Neuroendocrine System

Hrabovszky

Liposits

2008

J Neuroendocrinology

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Glutamate is the principal neurotransmitter of excitatory synaptic transmission in the neuroendocrine hypothalamusIn addition to participating in normal cell metabolism, L-glutamate acts as the primary mediator of excitatory synaptic transmission in the central nervous system (1, 2). Its major contribution to the synaptic regulation of hypothalamic neuroendocrine systems has been shown by (i) the demonstration of glutamatergic asymmetric synapses on the cell bodies and dendrites of hypothalamic neurosecretory neurones, (ii) the finding of increased intracellular Ca 2+ in medial hypothalamic neurones grown in monolayer, in response to glutamate and the non-NMDA glutamate receptor agonists kainate and quisqualate, and finally (iii) the observation that the non-NMDA glutamate antagonist CNQX decreased the electrically stimulated and spontaneous excitatory postsynaptic potentials in acute hypothalamic slice preparations (3). Ionotropic and metabotropic receptors mediate glutamate actionsGlutamate receptors that form cation channels fall into the category of ionotropic receptors. Based on their binding affinities for prototypical ligands, they are further categorised as kainate, AMPA and NMDA receptors (4-7). Metabotropic glutamate receptors (mGluR1-8), in turn, comprise a unique family of G-protein coupled receptors that can be classified into three groups (groups I-III) based on G-protein coupling specificity and sequence similarity (7-10). Journal of NeuroendocrinologyCorrespondence to: Zsolt Liposits, Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, P.O. Box 67, 1450 Budapest, Hungary (e-mail: liposits@koki.hu).L-glutamate, the main excitatory neurotransmitter, influences virtually all neurones of the neuroendocrine hypothalamus via synaptic mechanisms. Vesicular glutamate transporters (VGLUT1-3), which selectively accumulate L-glutamate into synaptic vesicles, provide markers with which to visualise glutamatergic neurones in histological preparations; excitatory neurones in the endocrine hypothalamus synthesise the VGLUT2 isoform. Results of recent dual-label in situ hybridisation studies indicate that glutamatergic neurones in the preoptic area and the hypothalamic paraventricular, supraoptic and periventricular nuclei include parvocellular and magnocellular neurosecretory neurones which secrete peptide neurohormones into the bloodstream to regulate endocrine functions. Neurosecretory terminals of GnRH, TRH, CRF-, somatostatin-, oxytocin-and vasopressin-secreting neurones contain VGLUT2 immunoreactivity, suggesting the co-release of glutamate with hypophysiotrophic peptides. The presence of VGLUT2 also indicates glutamate secretion from non-neuronal endocrine cells, including gonadotrophs and thyrotrophs of the anterior pituitary. Results of in vitro studies show that ionotropic glutamate receptor analogues can elicit hormone secretion at neuroendocrine ⁄ endocrine release sites. Structural constituents of the median eminence, adenohypophysis and neurohypophysis contain elements of glut...

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Effect of N-methyl-D,L-aspartate on isolated rat somatotrophs

Cited by 18 publications

References 0 publications

Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats

Effects of N-methyl-d-aspartate and kainic acid on prolactin secretion in prepubertal female rats

Presence of vesicular glutamate transporter‐2 in hypophysiotropic somatostatin but not growth hormone‐releasing hormone neurons of the male rat

Novel Aspects of Glutamatergic Signalling in the Neuroendocrine System

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