Effects of Newcastle disease virus administration to mice on the metabolism of cerebral biogenic amines, plasma corticosterone, and lymphocyte proliferation

Dunn, Adrian J.; Powell, Marie Louise; Moreshead, William V.; Gaskin, Jack M.; Hall, Nicholas R.

doi:10.1016/0889-1591(87)90024-9

Cited by 75 publications

(18 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…More recent work has extended this observation to other viruses (see review by Silverman et al [155]). NDV administration also caused neurochemical changes; MHPG and MHPG:NE ratios, DOPAC and DOPAC:DA ratios, and 5-HIAA and 5-HIAA:5-HT ratios were all increased in a number of brain regions [156,157]. Tryptophan was also elevated in all regions of the brain.…”

Section: Neurochemical Responses To Infectionsmentioning

confidence: 95%

Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

285

169

View full text Add to dashboard Cite

Administration of cytokines to animals can elicit many effects on the brain, particularly neuroendocrine and behavioral effects. Cytokine administration also alters neurotransmission, which may underlie these effects. The most well studied effect is the activation of the hypothalamopituitary-adrenocortical (HPA) axis, especially that by interleukin-1 (IL-1). Peripheral and central administration of IL-1 also induces norepinephrine (NE) release in the brain, most markedly in the hypothalamus. Small changes in brain dopamine (DA) are occasionally observed, but these effects are not regionally selective. IL-1 also increases brain concentrations of tryptophan, and the metabolism of serotonin (5-HT) throughout the brain in a regionally nonselective manner. Increases of tryptophan and 5-HT, but not NE, are also elicited by IL-6, which also activates the HPA axis, although it is much less potent in these respects than IL-1. IL-2 has modest effects on DA, NE and 5-HT. Like IL-6, tumor necrosis factor-α (TNFα) activates the HPA axis, but affects NE and tryptophan only at high doses. The interferons (IFN's) induce fever and HPA axis activation in man, but such effects are weak or absent in rodents. The reported effects of IFN's on brain catecholamines and serotonin have been very varied. However, interferon-γ, and to a lesser extent, interferon-α, have profound effects on the catabolism of tryptophan, effectively reducing its concentration in plasma, and may thus limit brain 5-HT synthesis.Administration of endotoxin (LPS) elicits responses similar to those of IL-1. Bacterial and viral infections induce HPA activation, and also increase brain NE and 5-HT metabolism and brain tryptophan. Typically, there is also behavioral depression. These effects are strikingly similar to those of IL-1, suggesting that IL-1 secretion, which accompanies many infections, may mediate these responses. Studies with IL-1 antagonists, support this possibility, although in most cases the antagonism is incomplete, suggesting the existence of multiple mechanisms. Because LPS is known to stimulate the secretion of IL-1, IL-6 and TNFα, it seems likely that these cytokines mediate at least some of the responses, but studies with antagonists indicate that there are multiple mechanisms. The neurochemical responses to cytokines are likely to underlie the endocrine and behavioral responses. The NE response to IL-1 appears to be instrumental in the HPA activation, but other mechanisms exist. Neither the noradrenergic nor the serotonergic systems appear to be involved in the major behavioral responses. The significance of the serotonin response is unknown.

show abstract

Section: Neurochemical Responses To Infectionsmentioning

confidence: 95%

Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

285

169

View full text Add to dashboard Cite

show abstract

“…In turn, many infections reduce concentration of blood testosterone [149,160] by the different mechanisms, including: pathogen replication in testes, like it was found in male rabbit infected with myxoma virus [161]; or the inhibition of the 5 alpha-reductase enzyme and the activation of aromatase gene expression in male mice infected with Taenia crassiceps cysticerci [136]; or the reduction of responsiveness of hypothlamo-pituitary complex in male kittens who were infected with the feline leukemia virus [162]. Some pathogens, like influenza, Mengo virus and Newcastle virus, stimulate the pituitary-adrenal system [163][164][165], by which higher activity reduces male odor attraction [102]. And fifth, practically each infection activates the host immune system, including expression of the MHC genes [145,146], that are important links in the mechanism of male odor attraction [6,166].…”

Section: Parasite-induced Reduction Of Attractivenessmentioning

confidence: 99%

The Role of the Immune System in Behavioral Strategies of Reproduction

Мошкин

Gerlinskaya

Evsikov

2000

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. Since both reproduction and immunocompetence are costly, the negative reciprocal relationships between these functions were found in many species. Due to reproductive immunosuppression, some fraction of seasonally breeding populations of small mammals reproduces in the first breeding season, while others reproduce in the next one. Elevation of breeding efforts under the increased risk of mortality and the reproductive delay until recovery are the polar variants of mating behavior of parasitized individuals. However the parasite-induced changes of odor, visual or acoustic signals limit the mating success of the infected hosts. The direct influence of the immune system, regularly activated by infections, to chemicals signals can be answer to the question: why these signals are honest? Decrease of a strange infection risk by kin breeding can be a satisfactory strategy of an isolated population. Nevertheless, many species follow the inbreeding avoidance strategy, where the major histocompatibility complex (MHC) genes play key role in kin recognition. The advantage of MHC heterozygosity was found at the all steps of the breeding cycle; including mating choice, fertilization, pre-and postnatal development. So, the relationships between immune system and neuroendocrine regulation of behavior give proximate explanations of the evolutionary stable strategies of breeding behavior.

show abstract

“…These effects persist throughout the life of the animal and the resulting differences in HPA activity are associated with altered T-dependent antibody responses (Bhatnagar et al, 1992) and the incidence of age-related neuropathology . Immune activation elicits both HPA and central catecholamine alterations similar to those seen following stress (Blalock, 1984;Dunn et al, 1987Dunn et al, , 1989Zalcman et al, 1991;Anisman et al, 1993;Rivier et al, 1993;Stenzel-Poore et al, 1993). Furthermore, the immune and HPA systems are mutually regulatory, and these interactions partly determine the impact of stress on immune functioning (Munck et al, 1984;Irwin et al, 1990;Berkenbosch et al, 199 1;Anisman et al, 1993;.…”

mentioning

confidence: 99%

Neonatal endotoxin exposure alters the development of the hypothalamic- pituitary-adrenal axis: early illness and later responsivity to stress

1995

View full text Add to dashboard Cite

The long-term consequences of neonatal endotoxin exposure on hypothalamic-pituitary-adrenal axis (HPA) function were assessed in adult female and male Long-Evans rats. At 3 and 5 d of age, pups were administered endotoxin (Salmonella enteritidis, 0.05 mg/kg, i.p.) at a dose that provokes a rapid and sustained physiological response, but with no mortality. As adults, neonatally endotoxin-treated animals exhibited significantly greater adrenocorticotrophic hormone (ACTH) and corticosterone responses to restraint stress than controls. In addition, dexamethasone pretreatment was less effective in suppressing ACTH responses to restraint stress in endotoxin-treated animals than in controls, suggesting decreased negative-feedback sensitivity to glucocorticoids. Neonatal endotoxin treatment elevated resting-state median eminence levels of corticotropin-releasing hormone (CRH) and arginine vasopressin in adult male animals, and arginine vasopressin in both adult males and females. Neonatal exposure to endotoxin also increased CRH mRNA expression in the paraventricular nucleus of the hypothalamus of adult males, with no difference in females. Finally, glucocorticoid receptor density was reduced across a wide range of brain regions in the neonatal endotoxin-treated, adult animals. These data illustrate the interactive nature of immune and endocrine systems during development. It appears that endotoxin exposure during critical stages of development decreases glucocorticoid negative-feedback inhibition of ACTH secretagogue synthesis, thus increasing HPA responsiveness to stress. The implication of these findings is that exposure to gram-negative LPS in early life can alter the development of neural systems which govern endocrine responses to stress and may thereby predispose individuals to stress-related pathology.

show abstract

Effects of Newcastle disease virus administration to mice on the metabolism of cerebral biogenic amines, plasma corticosterone, and lymphocyte proliferation

Cited by 75 publications

References 30 publications

Effects of cytokines and infections on brain neurochemistry

Effects of cytokines and infections on brain neurochemistry

The Role of the Immune System in Behavioral Strategies of Reproduction

Neonatal endotoxin exposure alters the development of the hypothalamic- pituitary-adrenal axis: early illness and later responsivity to stress

Contact Info

Product

Resources

About