Direct stimulation of pituitary prolactin release by glutamate

Login, Ivan S.

doi:10.1016/0024-3205(90)90158-n

Cited by 60 publications

(40 citation statements)

References 19 publications

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“…Testosterone may have decreased the number of pituitary NMDA receptors, which may explain both the lack of NMDA effect in adult males and the abolition of the inhibitory effect in prepubertal rats treated with high doses of testosterone. In contrast with present experiments developed in males, glutamate stimulated PRL release by pituitary cells from adult but not from prepubertal female rats (25), which confirmed the role of gonadal secretion in the NMDA effects in PRL secretion.…”

Section: Discussionsupporting

confidence: 51%

Interactions between N-methyl-D-aspartate, nitric oxide and serotonin in the control of prolactin secretion in prepubertal male rats

Aguilar

Tena‐Sempere²,

Aguilar³

et al. 1997

European Journal of Endocrinology

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The role of N-methyl-D-aspartate (NMDA) in the control of prolactin (PRL) secretion was analysed in prepubertal male rats. In experiment 1, males of different ages were decapitated after administration of NMDA or vehicle. In experiment 2, 30-day-old males were killed at different times after administration of vehicle, NMDA, MK-801 (a non-competitive NMDA antagonist) or NMDA plus MK-801. In experiment 3, 23-day-old males were sham-orchidectomized or orchidectomized. Orchidectomized males were or were not implanted with Silastic capsules containing different amounts of testosterone. On day 30, the animals were decapitated after administration of vehicle, NMDA or MK-801. In experiment 4, 30-day-old male rats were decapitated after being injected with vehicle, NMDA, N wnitro-L-arginine methyl ester (NAME) (an inhibitor of nitric oxide (NO) synthase), or NMDA plus NAME. Serum PRL concentrations, and dopamine pituitary and hypothalamic content were measured. In experiment 5, males pretreated with vehicle or NAME were killed after administration of the precursor of serotonin synthesis 5-hydroxytryptophan (5-HTP), the 5-HT 1 receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) or the 5-HT 2 agonist (Ϯ)2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI). Finally, the effects of NMDA, NAME and sodium nitroprusside (SNP) were tested in dispersed adenohypophyseal cells. We found that: (i) antagonism of NMDA receptors with MK-801 decreased PRL secretion in intact, orchidectomized and orchidectomized-testosterone treated male rats; (ii) NMDA inhibited PRL release in vivo through an increase in dopamine release and this effect was potentiated by NAME and prevented by testosterone; (iii) NMDA inhibited PRL secretion in vitro and this effect was observed in presence of both SNP and NAME; (iv) NAME blocked the stimulatory effects of 5-HTP and DOI on PRL secretion. We conclude that endogenous glutamate stimulates PRL release and that NO might have a pivotal role in the mechanisms involved in the control of PRL release, inhibiting the release of dopamine and modulating the effects of NMDA and 5-HT. European Journal of Endocrinology 137 99-106

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Section: Discussionsupporting

confidence: 51%

Interactions between N-methyl-D-aspartate, nitric oxide and serotonin in the control of prolactin secretion in prepubertal male rats

Aguilar

Tena‐Sempere²,

Aguilar³

et al. 1997

European Journal of Endocrinology

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“…The analogue of phencyclidine, ketamine, directly reduces the basal release of prolactin. 27 Because the present data are entirely in vitro, they should not be confused or admixed with separate clinical data. Nevertheless, the present in vitro data are at least consistent with the clinical data on this topic.…”

Section: Discussionmentioning

confidence: 89%

Dopamine receptor contribution to the action of PCP, LSD and ketamine psychotomimetics

2005

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Although phencyclidine and ketamine are used to model a hypoglutamate theory of schizophrenia, their selectivity for NMDA receptors has been questioned. To determine the affinities of phencyclidine, ketamine, dizocilpine and LSD for the functional high-affinity state of the dopamine D2 receptor, D2 High , their dissociation constants (K i ) were obtained on [ 3 H]domperidone binding to human cloned dopamine D2 receptors. Phencyclidine had a high affinity for D2 High with a K i of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a K i of 313 nM, as labeled by [ 3 H]dizocilpine on rat striatal tissue. Ketamine also had a high affinity for D2 High with a K i of 55 nM, an affinity higher than its 3100 nM K i for the NMDA sites. Dizocilpine had a K i of 0.3 nM at D2 High , but a K d of 1.8 nM at the NMDA receptor. LSD had a K i of 2 nM at D2 High . Because the psychotomimetics had higher potency at D2 High than at the NMDA site, the psychotomimetic action of these drugs must have a major contribution from D2 agonism. Because these drugs have a combined action on both dopamine receptors and NMDA receptors, these drugs, when given in vivo, test a combined hyperdopamine and hypoglutamate theory of psychosis. Keywords: dopamine receptor; phencyclidine; domperidone; ketamine; NMDA receptors; psychotomimetics While the clinical anti-dopaminergic actions of antipsychotic drugs are compatible with the hyperdopamine hypothesis of psychosis and schizophrenia, 1,2 the psychoses caused by glutamate antagonists such as phencyclidine or ketamine suggest a hypo-glutamate component in psychosis. [3][4][5] However, phencyclidine also lowers plasma prolactin 6 and elicits rotation, 7 suggesting a direct or indirect dopaminemimetic action of phencyclidine.Although phencyclidine and ketamine are not selective for glutamate NMDA receptors, 8 the precise affinities of these drugs for dopamine D2 receptors need to be clarified in order to determine their dopaminergic and non-dopaminergic components of action. More specifically, although phencyclidine had a dissociation constant of 37 000 nM at the D2 receptor in rat striatal homogenate, 8 phencyclidine had a dissociation constant of 1.3 nM for the functional high-affinity site of the cloned D2 receptor, or the D2 High receptor. 9 This apparent discrepancy may be resolved by the recent finding that dopamine itself has a dissociation constant of 3000 nM when competing vs [ 3 H]raclopride at striatal D2 receptors, but has a dissociation constant of 1.5 nM at the D2 High receptor when the link between dopamine D1 and D2 receptors is blocked by the D1 antagonist SCH23390. 10 The link between D1 and D2 receptors arises from several sources, including the colocalization of dopamine D1 and D2 receptors in at least 50% of the medium spiny neurons in the striatum, the cooperation and mutual potentiation of D1 and D2 agonists on various behaviors, and the biochemical conversion of D2 receptors from their functional high-affinity state, D2 High , into their low-affinity state, D2 Lo...

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“…route was chosen to examine the effects of NBQX within the central nervous system (CNS), while systemic injection was chosen in the previous report [37]. Glutamate receptor immunostaining in the anterior pituitary has also been reported [39,40], and glutamate has been reported to enhance prolactin release directly from perifused anterior pituitary cells in vitro [41], suggesting that direct modulation by glutamate in the anterior pituitary is also possible. Systemic injection of NBQX might affect dopamine neuron in the ME thorough two ways: through the direct action of NBQX in the ME and through indirect action mediated by NBQXinduced prolactin release at the pituitary level.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Stress-Induced Adrenocorticotropin and Prolactin Secretion Mediating Hypophysiotropic Factors by Antagonist of AMPA Type Glutamate Receptor

Kusakawa

Tohei

Jaroenporn

et al. 2007

Journal of Reproduction and Development

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Abstract. Glutamate is the dominant excitatory neurotransmitter in a large number of physiological processes including neuroendocrine regulation. Some pharmacological studies have shown that different subtypes of glutamate receptor, such as the N-methyl-D-aspartic acid (NMDA) and α-amino-3-hydroxy-5-methy-4-isoxazolepropionic acid (AMPA) receptors, are involved in stress-induced adrenocorticotropin (ACTH) and prolactin secretion. However, the roles of the respective glutamate receptors and the mechanism of ACTH and prolactin secretion during stress via these receptors have not been investigated in detail. In the present study, we evaluated the role of AMPA-type glutamate receptor in ACTH and prolactin regulation under restraint stress in adult male rats. Male rats pretreated with a selective AMPA receptor antagonist, 2, 3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX; 50 µg), through a lateral ventricle cannula were stressed by immobilization. Administration of NBQX inhibited ACTH and prolactin secretion in response to restraint stress. However, NBQX had no significant effects on the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis, as measured by the accumulation of 3, 4-dihydroxyphenylalanine (DOPA). In addition, administration of NBQX suppressed stress-induced prolactin secretion in the male rats pretreated with α-MT, an inhibitor of dopamine synthesis, and infused with dopamine solution (2.5 µg/200 µl/10 min). These results indicated that the effects of NBQX on prolactin secretion might be mediated by non-dopamine mechanisms. The contents of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in the median eminence (ME) of the male rats decreased during restraint stress; however, the fluctuations in CRH and AVP were eliminated by NBQX administration. These results suggest that stress-induced ACTH and prolactin release mediated by neurotransmission via AMPA receptors might be partly attributable to hypophysiotropic regulatory factors in the hypothalamus. Key words: Adrenocorticotropin (ACTH), α-Amino-3-hydroxy-5-methy-4-isoxazolepropionic acid (AMPA), Prolactin, Rat, Stress (J. Reprod. Dev. 53: [545][546][547][548][549][550][551][552][553][554] 2007) he excitatory amino acid glutamate is the primary mediator of excitatory synaptic transmission in the central nervous system [1,2].

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Direct stimulation of pituitary prolactin release by glutamate

Cited by 60 publications

References 19 publications

Interactions between N-methyl-D-aspartate, nitric oxide and serotonin in the control of prolactin secretion in prepubertal male rats

Interactions between N-methyl-D-aspartate, nitric oxide and serotonin in the control of prolactin secretion in prepubertal male rats

Dopamine receptor contribution to the action of PCP, LSD and ketamine psychotomimetics

Inhibition of Stress-Induced Adrenocorticotropin and Prolactin Secretion Mediating Hypophysiotropic Factors by Antagonist of AMPA Type Glutamate Receptor

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