Decreased vasopressin content in parvocellular CRH neurosecretory system of Lewis rats

Whitnall, Mark H.; Anderson, Karen; Lane, Cynthia; Mougey, Edward H.; Neta, Ruth; Perlstein, Robert S.

doi:10.1097/00001756-199408150-00023

Cited by 16 publications

(5 citation statements)

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“…The alterations in parvocellular AVP/CRH colocalization in autoimmune models may represent a hypothalamic adaptation to moderate disease progression or, alternatively, decreased colocalization may dictate increased susceptibility to inflammation. 47…”

Section: Chronic Inflammatory Stress and Hpa Functionmentioning

confidence: 99%

Inflammatory Disease as Chronic Stress

Shanks

Harbuz

Jessop

et al. 1998

Annals of the New York Academy of Sciences

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It is now established that communication between the CNS and the immune system is bidirectional, that endocrine factors can alter immune function and that immune responses can alter both endocrine and CNS responses. In many respects CNS and endocrine responses to acute inflammation are similar to the changes associated with acute stress exposure. In contrast, during chronic inflammation associated with adjuvant induced arthritis (AA), although circulating levels of corticosterone are increased, the peptidergic regulation of the hypothalamus is different from that seen during acute stress. As the disease progresses, a paradoxical reduction occurs in CRH mRNA in the paraventricular nucleus (PVN), whereas PVN AVP mRNA increases. These data suggest that there is increased expression of AVP mRNA within the CRH cells of the PVN with an increased emphasis on AVP regulation of HPA output. Additionally, HPA function is altered during chronic inflammation such that responses to psychological stress (i.e. restraint) are significantly dampened, while responses to further inflammatory challenges are maintained. These data suggest that alterations in PVN peptide colocalization may be important in regulating the progression of peripheral inflammatory responses and that the effects of inflammation on the hypothalamus alter stress-responsive systems. In addition to the AA model, we have similarly observed alterations in PVN peptide mRNA expression with disease onset in the murine MRL lpr/lpr and MRL +/+ model of SLE. Disease onset in murine SLE is spontaneous and does not rely on exogenous application of adjuvant; however, decreased levels of CRH in the PVN were observed from early disease onset in this animal model. It is suggested that alterations in CRH regulation in response to either acute or chronic inflammation may contribute as etiological factors to both psychiatric (i.e. neuropsychiatric SLE) and stress-related disease.

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Section: Chronic Inflammatory Stress and Hpa Functionmentioning

confidence: 99%

Inflammatory Disease as Chronic Stress

Shanks

Harbuz

Jessop

et al. 1998

Annals of the New York Academy of Sciences

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“…For example, Lewis (LEW) rats self-administer alcohol, opiates, and cocaine more readily than Fischer 344 (F344) rats, although both strains are derived from the Sprague-Dawley line [11], Differences in HPA activity have also been documented between these two strains. LEW rats exhibit diminished HPA responses to a variety of stressors, including re straint, swim stress, ether, and open field exposure [22] compared to F344 rats, as well as to inflammatory stimuli [23][24][25], If an association exists between HPA axis re sponsiveness and vulnerability to self-administer, one ap proach for characterizing this relationship would be to study the neuroendocrine responses to cocaine in animals which have both distinctive HPA axis activity and selfadministration behavior. These experiments were de signed to compare the plasma CS and ACTH.…”

Section: Introductionmentioning

confidence: 99%

Differential Neuroendocrine and Behavioral Responses to Cocaine in Lewis and Fischer Rats

1996

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Lewis (LEW) and Fischer 344 (F344) rats differ in responsiveness of the hypothalamo-pituitary-adrenocortical (HPA) axis as well as in their behavioral responses to drugs of abuse. The present experiments were conducted to compare hypothalamic corticotropin-releasing factor (CRF), plasma adrenocorti-cotropic hormone (ACTH) and plasma corticosterone (CS) responses to cocaine (0–60 mg/kg, i.p.) in LEW and F344 rats. Acute administration of cocaine resulted in decreases in CRF and dose-related increases in CS and ACTH with significant differences observed between the strains. Cocaine also increased plasma norepinephrine concentrations. Although the CS response was increased in the F344 compared to LEW rats, the percent change in the CS response was markedly enhanced in LEW rats. Plasma ACTH concentrations as well as the percentage of the control response were dramatically increased at the 40 mg/kg cocaine dose in the LEW compared to F344 rats. Since cocaine-induced changes in HPA axis activity may contribute to behavioral responses to cocaine, another experiment was performed to compare the locomotor responses to novelty and to acute cocaine between LEW and F344 rats. Strain differences were not observed in the locomotor response to novelty or to cocaine. These data indicate that strain differences exist in the neuroendocrine response to acute cocaine exposure.

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“…One predisposing genetic trait of LEW appears to be a glucocorticosteroid insufficiency 2 . 19 Defective paraventricular neuroendocrine regulation by corticotropin releasing hormone (females) or vasopressin (males) is reported to be responsible 20 . Although alternative immunomodulatory consequences for glucocorticosteroids remain to be fully understood, 21 they are best known for their anti‐inflammatory actions, through suppressive control of Th1‐dependent/macrophage (Mφ)‐dependent effector response, upon which EAE progression is dependent.…”

Section: Discussionmentioning

confidence: 99%

NADPH diaphorase‐positive dendritic profiles in rat thymus are discrete from autofluorescent cells, immunoreactive for inducible nitric oxide synthase, and show strain‐specific abundance differences

1998

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Predisposition to autoimmune disorder in Lewis rats has been associated with abnormal hypothalamic regulation of circulating steroids, leading to inadequate suppression of T helper 1 (Th1) cell-mediated inflammatory reactions. In addition, autoimmune syndromes can be triggered within formerly resistant animals, following damage to the negative selection process of the thymus. A contribution to the autoimmune-susceptible phenotype may therefore derive from the status of thymic tolerance. One mechanism of intrathymic negative selection may involve nitric oxide. Because inducible nitric oxide synthase (iNOS) is known to be inhibitable by steroids, its expression might be different within strains having neuroendocrine disturbance. We report on a study to compare intrathymic iNOS expression in autoimmune-prone Lewis rats with other resistant strains. Interdigitating cells (IDC), darkly stained for diaphorase, were confirmed as immunoreactive for iNOS. They were located towards the medullary side of an accumulation of unstained, but autofluorescent cells (presumed to be macrophages) that circumscribes the corticomedullary zone. The role of iNOS+ IDC in the apoptotic deletion of T cells has been suggested by other studies. Despite the blunted steroidal condition reported for Lewis, nitrergic cell abundance was shown, by quantitative analysis of histochemical stain, to be on average approximately twofold lower compared with resistant strains (Fischer and Sprague-Dawley). This trend was evident in males and females, and confirmed by independent observers. We hypothesize that an intrathymic, iNOS-dependent mechanism may be important for the suppression of potentially autoreactive T-cell clones.

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Decreased vasopressin content in parvocellular CRH neurosecretory system of Lewis rats

Cited by 16 publications

References 0 publications

Inflammatory Disease as Chronic Stress

Inflammatory Disease as Chronic Stress

Differential Neuroendocrine and Behavioral Responses to Cocaine in Lewis and Fischer Rats

NADPH diaphorase‐positive dendritic profiles in rat thymus are discrete from autofluorescent cells, immunoreactive for inducible nitric oxide synthase, and show strain‐specific abundance differences

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