Regulation of the Central Nervous System-Pituitary-Adrenal Axis in Rats after Neonatal Treatment with Monosodium Glutamate

1988 ◽  
Vol 48 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Maria Magariños ◽  
Fernando Estivariz ◽  
Inés Morado ◽  
Alejandro F. De Nicola
1965 ◽  
Vol 13 (01) ◽  
pp. 235-243 ◽  
Author(s):  
O. N Lucas ◽  
L. B Jaques

SummaryL.S.D. was used as an emotional stress agent in rats in an attempt to evaluate the influence of the central nervous system in triggering spontaneous hemorrhage in rats treated with anticoagulants. L.A. was used to evaluate whether the hemorrhagic activity of L.S.D. was through the pituitary-adrenal axis. A high percentage of spontaneous hemorrhage was found when the emotional stress agent was combined with the anticoagulant. There was no mortality or hemorrhagic manifestation with anticoagulant alone or in the groups where the treatments were given alone as a control.


2018 ◽  
Author(s):  
Thomas O’Rourke ◽  
Cedric Boeckx

AbstractThe present paper highlights the prevalence of signals of positive selection on genes coding for glutamate receptors—most notably kainate and metabotropic receptors—in domesticated animals and anatomically modern humans. Relying on their expression in the central nervous system and phenotypes associated with mutations in these genes, we claim that regulatory changes in kainate and metabotropic receptor genes have led to alterations in limbic function and Hypothalamic-Pituitary-Adrenal axis regulation, with potential implications for the emergence of unique social behaviors and communicative abilities in (self-)domesticated species.


1998 ◽  
Vol 275 (2) ◽  
pp. R612-R618
Author(s):  
Teresa M. Reyes ◽  
Christopher L. Coe

The ability of both exogenous and endogenous glucocorticoids (GCs) to inhibit proinflammatory cytokine production was investigated in vivo. Specifically, we investigated the effects of elevated GC levels on interleukin (IL)-1-induced release of IL-6 into both blood and cerebrospinal fluid (CSF). Three experiments were conducted in rhesus macaques to elevate corticoid levels for at least 4 h before administration of IL-1β. The first study used dexamethasone pretreatment, the second utilized ACTH to stimulate endogenous cortisol release, while the third relied on a psychological challenge to stimulate the hypothalamic-pituitary-adrenal axis. Contrary to our a priori predictions, none of these treatments attenuated the IL-1-induced release of IL-6 into CSF. Additionally, the pattern in the blood response was similar, such that the IL-6 response was not blocked, although there was a trend toward a reduction of this response. These data indicated that the IL-1-induced IL-6 response is for the most part resistant to corticosteroid influence, such that even when a partial inhibition was sometimes evident in blood, cytokine release in the central nervous system was not affected.


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