Endogenous Excitatory Amino Acids Are Involved in Stress-Induced Adrenocorticotropin and Catecholamine Release

Jezová, D; Tokarev, D; Rusnak, Milan

doi:10.1159/000127021

Cited by 53 publications

(22 citation statements)

References 23 publications

(25 reference statements)

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“…Under pentobarbital anesthesia indwelling cannulas were inserted into the tail artery for blood sampling and for drug injections, if appropriate, as previously described [14]. Treatments and blood sampling were performed 24 h later.…”

Section: Methodsmentioning

confidence: 99%

Neurotoxic Lesions Induced by Monosodium Glutamate Result in Increased Adenopituitary Proopiomelanocortin Gene Expression and Decreased Corticosterone Clearance in Rats

Škultétyová

Kiss²,

Ježová³

1998

Neuroendocrinology

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Hypothalamic-pituitary-adrenocortical function in rats with brain lesions induced by neonatal monosodium glutamate (MSG) treatment (4 mg/g, 5 administrations, i.p.) was evaluated in the present study. Using in situ hybridization we found increased proopiomelanocortin (POMC) mRNA levels in the adenopituitary and normal corticotropin-releasing hormone mRNA levels in the hypothalamic paraventricular nucleus in MSG-treated rats. The total content of pituitary adrenocorticotropin (ACTH) was not changed, while pituitary ACTH concentration was higher in MSG-treated compared to control rats. The number of ACTH-immunostained cells per a constant area of adenohypophysial section, as measured by immunohistochemistry, was unchanged indicating that no significant condensation of corticotropes occurred. Basal plasma ACTH concentrations were not different, whereas morning corticosterone levels were elevated in rats with MSG treatment. While ACTH response to stress stimuli was similar in both groups of rats, corticosterone response to exogenous ACTH (500 ng/kg, i.v., Synacthen), short-lasting handling and immobilization was of the same magnitude but prolonged in MSG-treated rats. Based on the decline of [³H]corticosterone in plasma, a decreased corticosterone clearance rate was found in MSG-treated rats. These findings suggest that MSG treatment results in increased POMC gene expression per corticotrope of the atrophic pituitary resulting in maintenance of normal pituitary ACTH stores and plasma ACTH levels. Elevated basal levels of corticosterone in plasma as well as prolonged corticosterone responses to stimulations in rats treated with MSG seem to be due to a decreased clearance rate of corticosterone.

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Section: Methodsmentioning

confidence: 99%

Neurotoxic Lesions Induced by Monosodium Glutamate Result in Increased Adenopituitary Proopiomelanocortin Gene Expression and Decreased Corticosterone Clearance in Rats

Škultétyová

Kiss²,

Ježová³

1998

Neuroendocrinology

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“…Glutamate is a well-known excitatory neurotransmitter, and known to be responsible for the fast excitatory input to magnocellular and parvocellular neurons in the PVN, where CRF is released [3]. In rats, glutamate injection into the third ventricle elevated plasma ACTH levels [38], and its agonists had similar effects as endogenous glutamate [39,40]. Excessive accumulation of glutamate in the extracellular spaces may lead to excessive activation of glutamate receptors in the hypothalamic nuclei.…”

Section: Adrenal Responsementioning

confidence: 99%

Chronic Administration of Monosodium Glutamate under Chronic Variable Stress Impaired Hypothalamic-Pituitary-Adrenal Axis Function in Rats

Seo

Ham

Jin

et al. 2010

Korean J Physiol Pharmacol

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The hypothalamic-pituitary-adrenal (HPA) axis is the primary endocrine system to respond to stress. The HPA axis may be affected by increased level of corticotrophin-releasing factors under chronic stress and by chronic administration of monosodium glutamate (MSG). The purpose of this study was to investigate whether chronic MSG administration aggravates chronic variable stress (CVS)-induced behavioral and hormonal changes. Twenty-four adult male Sprague-Dawley rats, weighing 200∼ 220 g, were divided into 4 groups as follows: water administration (CON), MSG (3 g/kg) administration (MSG), CVS, and CVS with MSG (3 g/kg) administration (CVS＋ MSG). In addition, for the purpose of comparing the effect on plasma corticosterone levels between chronic stress and daily care or acute stress, 2 groups were added at the end of the experiment; the 2 new groups were as follows: naïve mice (n=7) and mice exposed to restraint stress for 2 h just before decapitation (A-Str, n=7). In an open field test performed after the experiment, the CVS＋ MSG group significant decrease in activity. The increase in relative adrenal weights in the CVS and CVS＋ MSG group was significantly greater than those in the CON and/or MSG groups. In spite of the increase in the relative adrenal weight, there was a significant decrease in the plasma corticosterone levels in the CVS＋ MSG group as compared to all other groups, except the naïve group. These results suggest that impaired HPA axis function as well as the decrease in the behavioral activity in adult rats can be induced by chronic MSG administration under CVS rather than CVS alone.

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“…Stress-induced changes in glutamate receptor gene expression [26]support the suggestion that glutamate receptor activation is involved in the stress response and potentially participates in triggering hormone release to stress stimuli. Indeed, our previous pharmacological studies have brought supportive evidence for a role of endogenous EAA in stress-induced catecholamine and ACTH release [12, 13]. …”

Section: Discussionmentioning

confidence: 94%

“…Thus, administration of glutamate receptor agonists, particularly in high doses, is followed by a rapid rise in PRL [3, 4, 5, 6]and ACTH levels [7, 8, 9, 10, 11]. There are only few data indicating a role of endogenous EAA [12, 13]. On the other hand, regulatory effects of glutamate on luteinizing hormone and follicle-stimulating hormone are well documented [for reviews see ref.…”

Section: Introductionmentioning

confidence: 99%

“…As to the neuroendocrine response during stress, acute pretreatment with a racemic form of dizocilpine (MK-801), a noncompetitive NMDA receptor blocker, was found to inhibit immobilization stress-induced ACTH and particularly epinephrine release [12]. Dizocilpine was effective to induce a slight inhibition of ACTH secretion during stress only in a dose which also elevated basal hormone levels.…”

Section: Introductionmentioning

confidence: 99%

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Simultaneous Blockade of Two Glutamate Receptor Subtypes (NMDA and AMPA) Results in Stressor-Specific Inhibition of Prolactin and Corticotropin Release

1999

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Many neurons express simultaneously two or more isotypes of glutamate receptors, so that pharmacological modulation of more than one receptor may be necessary to reveal the role of glutamate in mediating physiological processes. The present studies were aimed at evaluating involvement of endogenous glutamate in triggering plasma prolactin (PRL) and adrenocorticotropic hormone (ACTH) levels in response to three different stress stimuli (footshock, immobilization and ether stress). Blockade of glutamate receptor subtypes was achieved by the administration of the NMDA antagonist dizocilpine (MK-801, 0.2 mg/kg) and the selective AMPA antagonist GYKI 52466 (10 mg/kg). Rats were pretreated for 4–5 days and then exposed to stressful stimulation. Basal hormone levels were not affected by the antagonists. In male rats, combined, but not separate blockade of NMDA and AMPA/kainate subtypes of glutamate receptors prevented the rise in plasma PRL in response to footshock stress. In female rats, footshock-induced PRL release was inhibited even by separate blockade of NMDA receptors by dizocilpine, suggesting that the PRL system of females is more sensitive to the effect of NMDA antagonists than that of males. None of the treatments affected PRL release during immobilization or ether stress. Simultaneous blockade of NMDA and AMPA receptor subtypes resulted in a mild inhibition of immobilization-induced ACTH release without any effect on ACTH response to footshock or ether stress. The data suggest that involvement of glutamatergic pathways in neuroendocrine response during stress is selective for discrete stress stimuli and stress hormones. In addition a concerted action of glutamate on both NMDA and non-NMDA receptor subtypes is involved in the control of PRL release during footshock stress.

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Endogenous Excitatory Amino Acids Are Involved in Stress-Induced Adrenocorticotropin and Catecholamine Release

Cited by 53 publications

References 23 publications

Neurotoxic Lesions Induced by Monosodium Glutamate Result in Increased Adenopituitary Proopiomelanocortin Gene Expression and Decreased Corticosterone Clearance in Rats

Neurotoxic Lesions Induced by Monosodium Glutamate Result in Increased Adenopituitary Proopiomelanocortin Gene Expression and Decreased Corticosterone Clearance in Rats

Chronic Administration of Monosodium Glutamate under Chronic Variable Stress Impaired Hypothalamic-Pituitary-Adrenal Axis Function in Rats

Simultaneous Blockade of Two Glutamate Receptor Subtypes (NMDA and AMPA) Results in Stressor-Specific Inhibition of Prolactin and Corticotropin Release

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