Effect of Intraventricular Glutamate on ACTH Release

Makara, G. B.; Stark, E.

doi:10.1159/000122400

Cited by 47 publications

(33 citation statements)

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“…Thus, direct injection of glutamate into the PVN caused CRH release from the median eminence and consequent increase in serum ACTH and CS levels [34,35].…”

Section: Direct Adrenergic and Glutamate Stimulation Of The Hypothalamusmentioning

confidence: 99%

The Role of the Amygdala in Regulating the Hypothalamic-Pituitary-Adrenal Axis

Weidenfeld¹,

Ovadia²

2017

The Amygdala - Where Emotions Shape Perception, Learning and Memories

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We investigated the regulatory role of the amygdala upon the function of the hypothalamic-pituitary-adrenal (HPA) axis as measured by median eminence corticotrophin releasing hormone (CRH) content and serum levels of adrenocorticotrophic hormone (ACTH) and corticosterone. Our indings showed that (1) lesions of the central amygdala inhibited the HPA axis responses to a variety of stressful stimuli. (2) Depletion of norepinephrine or serotonin in the amygdala and hypothalamus and local injections of norepinephrine and serotonin receptor antagonists into the central amygdala inhibited the HPA axis responses to neural stress. Norepinephrine and serotonin agonists injected into the amygdala caused an increase in HPA axis activity. The activation of the amygdala facilitated the in vivo release of serotonin from the paraventricular nucleus following electrical stimulation of the brainstem raphe nuclei. (3) Electrical stimulation of the amygdala impaired the glucocorticoid negative feedback action following neural stressful stimuli probably via a decrease in hippocampal corticosteroid receptors.

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“…Thus, direct injection of glutamate into the PVN caused CRH release from the median eminence and consequent increase in serum ACTH and CS levels [34,35].…”

Section: Direct Adrenergic and Glutamate Stimulation Of The Hypothalamusmentioning

confidence: 99%

The Role of the Amygdala in Regulating the Hypothalamic-Pituitary-Adrenal Axis

Weidenfeld¹,

Ovadia²

2017

The Amygdala - Where Emotions Shape Perception, Learning and Memories

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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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“…Recently we considered another possibility, namely that this gas might play a role in the ability of N-methyl-D-aspartate (NMDA) receptor activation to activate this same axis. The rationale for this hypothesis was based on three facts: first, that activation of NMDA receptors releases NO [18,[54][55][56][57]; second, that in the rat, peripheral [58] and central [59] injection of NMDA stimulates ACTH secretion; and third, that NMDA is reported to release CRF from isolated hypothalamic tissue [60]. It therefore seemed reasonable to pro-pose that activation of NMDA receptors could stimulate CRF neurons, and hence increase plasma ACTH levels, through an NO-dependent pathway.…”

Section: Role Of No In N-methyl-d-aspartate-induced Activation Of Thementioning

confidence: 99%

Role of Nitric Oxide and Carbon Monoxide in Modulating the ACTH Response to Immune and Nonimmune Signals

Rivier

1998

Neuroimmunomodulation

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The role played by nitric oxide (NO) and carbon monoxide (CO) was explored in the adult male rat by determining whether antagonizing the activity of the enzymes responsible for the formation of these gases altered the response of the hypothalamic-pituitary-adrenal (HPA) axis to immune (cytokines) or nonimmune (mild electroshocks) signals. The arginine derivative N_ωnitro-L-arginine-methylester (L-NAME), which inhibits all three NO synthase (NOS) isoforms [inducible (i), endothelial (e) and neuronal (n)] significantly augments the ACTH response to blood-borne cytokines, but decreases it in rats exposed to shocks or other physico-emotional stresses. The effect of L-NAME in both models is mimicked by L-nitroarginine (L-NNA) and L-nitromethylarginine (L-NMMA), which block constitutive (e and n) forms of NOS, but not by aminoguanidine (which blocks iNOS) or 7-nitroindazole (which specifically blocks nNOS). Despite the ability of L-NAME to markedly augment the stimulatory effect of vasopressin on ACTH secretion, removal of this peptide does not interfere with the interaction between L-NAME and systemically administered interleukin-1β (IL-1β). In contrast, blockade of prostaglandin formation prevents both the stimulatory effect of IL-1β on ACTH release, and its potentiation by L-NAME. In contrast to the investigation of the importance of endogenous NO, studies focused on the role of CO remain scarce. Our preliminary results suggest that while blockade of the formation of this gas decreases the ACTH response to various stimuli, it also significantly interferes with the effect of L-NAME in rats systemically administered cytokines, and further decreases the ACTH response to shocks in animals also injected with arginine analogs. These results indicate the possible presence of functional interactions between NO and CO in regulating the activity of the HPA axis. Our present working hypothesis is that in the presence of elevated circulating cytokine levels, endogenous NO acts presynaptically to inhibit the release of ACTH secretagogues from nerve terminals in the infundibulum. As the acute ACTH response to these immune proteins is believed to primarily depend on events taking place within the median eminence, blockade of NO formation results in exaggerated ACTH release. During exposure to shocks and other nonimmune stresses, on the other hand, increased ACTH secretion is primarily due to activation of hypothalamic neurons. In this case, because of the stimulatory influence of endogenous NO on hypothalamic perikarya that manufacture corticotropin-releasing factor (CRF) and/or of the afferents to these neurons, blockade of NOS activity blunts CRF production, and consequently ACTH release. What remains undetermined is the net effect of the opposite influences of NO during long-term exposure to immune or nonimmune stress. Finally, it is possible that the conflicting results reported by investigators who study the role of NO and CO in isolated cell preparations may reflect, at least in part, these opposite effects of NO o...

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Effect of Intraventricular Glutamate on ACTH Release

Cited by 47 publications

References 0 publications

The Role of the Amygdala in Regulating the Hypothalamic-Pituitary-Adrenal Axis

The Role of the Amygdala in Regulating the Hypothalamic-Pituitary-Adrenal Axis

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

Role of Nitric Oxide and Carbon Monoxide in Modulating the ACTH Response to Immune and Nonimmune Signals

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