Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia

Rabey, J. M.; Scharf, M; Oberman, Z; Zohar, Motti; Graff, Eran

doi:10.1016/0006-3223(90)90525-7

Cited by 24 publications

(15 citation statements)

References 39 publications

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“…Endogenous glucocorticoids or treatment with synthetic glucocorticoids (e.g., dexamethasone) negatively regulate their secretion, and dexamethasone-mediated negative feedback resistance is often observed in these disorders (Rabey et al, 1990;Pariante et al, 1995;Plocka-Lewandowska et al, 2001). This disruption of the HPA system is related to some of the depressive symptoms, including cognitive deficits (Steckler et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…Disruption of the HPA system is often observed in several stress-related neuropsychiatric disorders showing PFC cognitive deficits such as depression, schizophrenia, and Parkinson's disease (Rabey et al, 1990;Deutch, 1993;Dolan et al, 1994;Fibiger, 1995;Pariante et al, 1995;Drevets et al, 1997;PlockaLewandowska et al, 2001). In addition, depression frequently occurs in patients suffering from a stroke induced in the PFC, and a large number of these patients exhibit HPA disruption (Lipsey et al, 1985;Robinson et al, 1987).…”

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confidence: 99%

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Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Mizoguchi¹,

Ishige²,

Takeda³

et al. 2004

J. Neurosci.

174

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Glucocorticoid hormones are important in the maintenance of many brain functions. Although their receptors are distributed abundantly throughout the brain, including the prefrontal cortex (PFC), it is not clear how glucocorticoid functions, particularly with regard to cognitive processing in the PFC. There is evidence of PFC cognitive deficits such as working memory impairment in several stressrelated neuropsychiatric disorders, including depression, schizophrenia, and Parkinson's disease. Disruption of the hypothalamopituitary-adrenal (HPA) system, which is characterized by attenuated glucocorticoid negative feedback, is also observed. In rats, chronic stress induces working memory impairment as a result of decreased dopaminergic transmission in the PFC. These chronically stressed rats also show HPA disruption; this is caused in part by a reduced glucocorticoid response in the PFC. These findings implicate reduced glucocorticoid actions in working memory impairment. In the present study, we examined the effects of the suppression of endogenous glucocorticoids by adrenalectomy (ADX) on working memory in rats and explored the involvement of PFC dopaminergic activities in memory. The ADX impaired working memory, decreased dopamine release, and upregulated D 1 receptors in the PFC. These dysfunctions were prevented by corticosterone replacement that reproduced normal physiological plasma levels, indicating that suppression of glucocorticoids causes these dysfunctions. Moreover, the ADX-induced working memory impairment was ameliorated by intra-PFC infusions of a D 1 receptor agonist, SKF 81297. Thus, suppression of glucocorticoids impaired working memory through a D 1 receptormediated hypodopaminergic mechanism in the PFC. This finding indicates that endogenous glucocorticoids are essential for maintaining PFC cognitive function and suggests that HPA disruption contributes to PFC cognitive deficits.

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Mizoguchi¹,

Ishige²,

Takeda³

et al. 2004

J. Neurosci.

174

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“…Parkinsonian patients do indeed exhibit an increase in cortisol levels and/or alterations in their circadian pattern [13, 14, 15]. In other cases, basal levels are apparently not modified in patients but alterations in the hypothalamic adrenal axis involve defective response [16, 17, 18]. Parkinsonian animal models display some alterations in the hypothalamic adrenal axis and changes in cortisol regulation have been described in MPTP-treated dogs [19]and rats [20].…”

Section: Introductionmentioning

confidence: 99%

Circadian Determinations of Cortisol, Prolactin and Melatonin in Chronic Methyl-Phenyl-Tetrahydropyridine-Treated Monkeys

Barcia

Mora-Bautista²,

Sánchez-Bahillo³

et al. 2003

Neuroendocrinology

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The aim of this study was to investigate whether prolactin, melatonin and cortisol are altered in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys and if so, whether MPTP may alter the availability of these hormones in chronic experimental parkinsonism. Furthermore, vegetative and sleep disorders have been described in both parkinsonian patients and in MPTP chronic monkeys; these may result indirectly from concomitant hormonal variations. Seven adult male cynomolgus monkeys were used for this experiment. Five were treated with systemic doses of intravenous MPTP but not with L-DOPA or dopaminergic agonists. In their 3rd year of parkinsonism, plasma samples were obtained day and night at 3-hour intervals. Sample collection was repeated three times for each animal. Prolactin, melatonin and cortisol concentrations were determined by enzyme immunoassay and compared with samples taken from the control group. Both MPTP-treated monkeys and the control group displayed a similar secretion pattern for the three hormones, except at several specific times when prolactin and melatonin showed significant differences. No changes were found for cortisol. The results suggest a possible alteration of hormonal metabolism in chronic MPTP parkinsonian monkeys.

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“…While higher plasma ACTH levels [75]and altered PRL and TSH responses to TRH [76]have been found in PD patients, other studies have shown that either basal or stimulated secretion of cortisol, PRL, TSH and GH remain unchanged [77, 78]. Certainly, the use of transgenic mouse models of PD will help to clarify these observations.…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Neuroendocrinology of Neurodegenerative Diseases

Aguilar

Frydman²,

Dupuis³

et al. 2003

Neuroendocrinology

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The nervous system plays a key role in the regulation of neuroendocrine axes and, in turn, the released neurohormones modulate the activity of different brain regions. Neurodegenerative diseases, which are known to affect specific neuronal populations, may provoke neuroendocrine dysfunctions that alter the intimate relationship between both systems. In addition, these modifications may influence the progression of the neurodegenerative process. In the present review, we summarise some of the endocrine changes characterising three major neurodegenerative diseases: Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Special attention is focused on the contribution of disease transgenic models to elucidate such alterations.

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Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia

Cited by 24 publications

References 39 publications

Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Endogenous Glucocorticoids Are Essential for Maintaining Prefrontal Cortical Cognitive Function

Circadian Determinations of Cortisol, Prolactin and Melatonin in Chronic Methyl-Phenyl-Tetrahydropyridine-Treated Monkeys

Neuroendocrinology of Neurodegenerative Diseases

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