Dexamethasone suppression of the effects of cocaine on adrenocortical secretion in Lewis and fischer rats

Simar, M. Renée; Saphier, D.; Goeders, Nicholas E.

doi:10.1016/s0306-4530(96)00049-2

Cited by 11 publications

(7 citation statements)

References 33 publications

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“…It might thus be argued that corticosterone availability at the anterior pituitary in Lewis rats does not need to reach the same concentrations as it does in the Fischer rats in order to inhibit further activation of the HPA axis. This contention is consistent with the finding that, in males, central administration of dexamethasone blunts cocaine-induced corticosterone secretion to a greater extent in the Lewis than in the Fischer rat (Simar et al, 1997).…”

Section: Discussionsupporting

confidence: 91%

Differential Impact of Audiogenic Stressors on Lewis and Fischer Rats: Behavioral, Neurochemical, and Endocrine Variations

Michaud

McLean

Keith

et al. 2003

Neuropsychopharmacol

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Exposure to intense noise can trigger a cascade of neuroendocrine events reminiscent of a stress response, including activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. Using male Fischer and Lewis rats, which exhibit differences in their corticosterone response to stressors, this investigation assessed effects of acute noise exposure on neurochemical and neuroendocrine responses. In response to the noise exposure, Fischer rats displayed greater plasma adrenocorticotropin-releasing hormone (ACTH) and corticosterone responses than their Lewis counterparts. However, both strains responded with similar increases of plasma prolactin, suggesting that strain differences in the HPA response were not likely because of differences in noise perception. Post-mortem analyses revealed that noise exposure induced strain-dependent variations of corticotropin-releasing hormone (CRH) across several brain regions. These effects were evident irrespective of whether the rats were noise exposed in a familiar (home cage) or unfamiliar environment. In vivo, dynamic assessment of immunoreactive (ir)-CRH at the pituitary gland revealed that noise exposure elicited an immediate rise in ir-CRH among Fischer rats, relative to the delayed response in Lewis rats. Similarly, the rise in local interstitial corticosterone was more rapid and pronounced in Fischer rats. In contrast to these differences, ir-CRH released at the central nucleus of the amygdala (CeA) was gradual and protracted following noise exposure in both strains. Behaviorally, the Fischer rats displayed an active stress response, whereas the Lewis strain adopted freezing as a defensive style. The role of CRH in the genesis of the overall straindependent response to stressors is discussed.

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Section: Discussionsupporting

confidence: 91%

Differential Impact of Audiogenic Stressors on Lewis and Fischer Rats: Behavioral, Neurochemical, and Endocrine Variations

Michaud

McLean

Keith

et al. 2003

Neuropsychopharmacol

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“…Corticosteroids clearly play an important role in regulating autoimmune disease expression, 1,3,4 and they also appear to be involved in regulating susceptibility to addiction. 54,55 For example, central administration of dexamethasone produces feedback inhibition of cocaine‐induced corticosteroid production, and, notably, LEW rats are more sensitive to dexamethasone suppression of cocaine‐induced corticosteroid production than are F344 rats. 54,55 In other words, corticosteroids appear to modulate sensitivity to drug addiction.…”

Section: Susceptibility To Drug Addiction and Hpa Axis Abnormalities mentioning

confidence: 99%

“…54,55 For example, central administration of dexamethasone produces feedback inhibition of cocaine‐induced corticosteroid production, and, notably, LEW rats are more sensitive to dexamethasone suppression of cocaine‐induced corticosteroid production than are F344 rats. 54,55 In other words, corticosteroids appear to modulate sensitivity to drug addiction. Of relevance to these observations, both autoimmune‐disease‐prone and addiction‐prone LEW and DA rats, in striking contrast to relatively resistant F344, BN, and most other inbred rat strains, show marked abnormalities in hypothalamic‐pituitary‐adrenal (HPA) axis function.…”

Section: Susceptibility To Drug Addiction and Hpa Axis Abnormalities mentioning

confidence: 99%

Susceptibility to Autoimmune Disease and Drug Addiction in Inbred Rats: Are There Mechanistic Factors in Common Related to Abnormalities in Hypothalamic‐Pituitary‐Adrenal Axis and Stress Response Function?

Wilder

Griffiths

Cannon

et al. 2000

Annals of the New York Academy of Sciences

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A BSTRACT : DA and LEW inbred rats are extraordinarily susceptible to a wide range of experimental autoimmune diseases. These diseases include rheumatoid arthritis models such as collagen-induced arthritis (CIA) and adjuvantinduced arthritis (AIA), multiple sclerosis models such as myelin-basic-protein (MBP)-induced experimental autoimmune encephalomyelitis (MBP-EAE), and autoimmune uveitis models such as retinal S antigen (SAG) and interphotoreceptor-retinoid-binding-protein (IRBP) -induced experimental autoimmune uveitis (SAG-EAU and IRBP-EAU, respectively). DA and LEW rats are also addiction-prone to various drugs of abuse, such as cocaine. Moreover, they exhibit a variety of behavioral and biochemical characteristics that appear to be related to their susceptibility to addiction. By contrast, F344 and BN rats show quite different phenotypes. They are relatively resistant to CIA, AIA, MBP-EAE, SAG-EAU, and IRBP-EAU, and they are relatively resistant to addiction. Interestingly, both DA and LEW rats, in contrast to F344 and BN rats, have abnormalities in hypothalamic-pituitary-adrenal (HPA) axis function. For example, circadian production of corticosteroids is very abnormal in DA and LEW rats; that is, they exhibit minimal circadian variation in corticosterone levels. Since corticosteroids potentially have significant influences on immune function and autoimmune disease susceptibility and may also influence sensitivity to drugs of abuse, we have begun to dissect genetic control of these various phenotypic differences, focusing initially on the regulation of autoimmune disease expression. Using genomewide scanning techniques involving F2 crosses of DA ؋ F344 (CIA and AIA), DA ؋ BN (CIA), and LEW ؋ F344 [IRBP-EAU and streptococcal-cell-wall arthritis (SCWA)], we have d Address for correspondence: Ronald L. Wilder, M.D., Ph.D., Chief, Inflammatory Joint Diseases Section, ARB, NIAMS, NIH, Bldg. 10, Room 9N240, Bethesda, Maryland 20892. Voice: 301-496-6499; fax: 301-402-0012. wilderr@exchange.nih.gov 785 WILDER et al. : AUTOIMMUNE DISEASE & DRUG ADDICTION identified, to date, 14 genomic regions [quantitative trait loci (QTL)] that regulate disease expression in these crosses. Development and analysis of QTLcongenic rats involving these loci are in progress and should permit us to address the relationships among autoimmune disease susceptibility, drug addiction, and HPA axis and stress response function. These initial data, however, indicate that the genetic control of the autoimmune disease traits is highly complex.

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“…In addition, investigators also reported that different doses of dexamethasone suppress corticosterone secretion and this synthetic corticoid induces a decrease in body weight, adrenal weight and plasma ACTH in rats (19,20). Thus, dexamethasone is found to have an adverse effect on the adrenal cortex, as it either suppresses the action of corticotrophin releasing factor (CRF) at the level of the pituitary, thereby reducing the sensitivity of the adrenal to ACTH (56), or inhibits corticosterone secretion from the adrenals, although ACTH synthesis by adrenohypophysis is unaffected (57).…”

Section: Discussionmentioning

confidence: 98%

“…Dexamethasone also results in a prompt and potent inhibition of proliferative activity of adrenocortical cells, as assessed by the counting of metaphase arrested cells in the adrenal of rats (17,18). Dexamethasone has been also found to decrease body weight, adrenal weight (19) and suppress the nocturnal increase in corticosterone secretion in both male and female rat (20). Investigation also indicates that glucocorticoids influence serotonin and melatonin synthesis in rat (21).…”

Section: Introductionmentioning

confidence: 90%

Adrenal corticoids induce pineal gland stimulation associated with adrenocortical inhibition of karyomorphology cell proliferation and hormone milieu in male mice (mus musculus)

Bandyopadhyay¹

2010

Acta Endo (Buc)

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Background. Pineal and adrenocortical cell morphology, dynamics, hormonal analysis and function in response to both natural and synthetic corticoids awaits in depth investigation in mammals.Aim. To investigate the pineal responsiveness to corticoid treatment from combined morphological and hormonal studies in postpubertal male mice.Material and methods. Three groups, each with 14 mice were used as control (C) or treated with the natural corticoid, hydrocortisone (HYC) at a dose of 4 mg/100 g.b.w. and synthetic corticoid, dexamethasone (DEX) at a dose of 4 mg/100 g.b.w. for ten consecutive days.Results. The treatment induced inverse changes in pineal-adrenocortical karyomorphology, cell proliferation (mitotic percentage M%) and hormonal milieu. Whereas both these corticoids caused pineal stimulation as evidenced from significantly increased nuclear diameter (μm) values (C 3.35 ± 0.05, HYC 4.77 ± 0.02, DEX 4.59 ± 0.04, p<0.001) and cell proliferation (M%) (C 1.11 ± 0.09, HYC 1.59 ± 0.07, DEX 1.44 ± 0.05, p<0.01), the changes induced in adrenocortical nuclear diameter in all the zones (p<0.001), cell proliferation (M%) (C 1.38 ± 0.05, HYC 0.53 ± 0.06, DEX 0.70 ± 0.05, p<0.001) and decreased content of adrenal corticosterone (C 0.24 ± 0.03, HYC 0.13 ± 0.01, p<0.001 DEX 0.15 ± 0.02, p<0.01) were those of adrenocortical inhibition.Conclusion. There exists an inverse relationship between the pineal and adrenocortical functions in post pubertal male mice (Mus musculus).

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Dexamethasone suppression of the effects of cocaine on adrenocortical secretion in Lewis and fischer rats

Cited by 11 publications

References 33 publications

Differential Impact of Audiogenic Stressors on Lewis and Fischer Rats: Behavioral, Neurochemical, and Endocrine Variations

Differential Impact of Audiogenic Stressors on Lewis and Fischer Rats: Behavioral, Neurochemical, and Endocrine Variations

Susceptibility to Autoimmune Disease and Drug Addiction in Inbred Rats: Are There Mechanistic Factors in Common Related to Abnormalities in Hypothalamic‐Pituitary‐Adrenal Axis and Stress Response Function?

Adrenal corticoids induce pineal gland stimulation associated with adrenocortical inhibition of karyomorphology cell proliferation and hormone milieu in male mice (mus musculus)

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