Effects of interleukin-1β and mild stress on alterations of norepinephrine, dopamine and serotonin neurotransmission: a regional microdialysis study

Merali, Zul; Lacosta, Susan; Anisman, Hymie

doi:10.1016/s0006-8993(97)00312-0

Cited by 121 publications

(59 citation statements)

References 51 publications

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“…When they did occur, the anatomical patterns did not resemble those typical of stress responses, in which increases in the prefrontal cortex are far greater than in other brain regions. DA was not altered by ip IL-1β in microdialysates from the prefrontal cortex, nucleus accumbens or hippocampus [16]. IL-1β has also been reported to increase tyrosine hydroxylase activity in the median eminence of rats [22].…”

Section: Interleukin-1 (Il-1)mentioning

confidence: 85%

“…The interpretation of these catabolite studies as reflecting increased neurotransmitter release were supported by subsequent studies using microdialysis which can directly assess extracellular concentrations of neurotransmitters. Microdialysate NE from the hypothalamus was increased following peripheral IL-1 administration [14][15][16][17]. Complementary data were obtained from studies with push-pull cannulation [18], and by studies of NE turnover, using α-methyl-p-tyrosine (metyrosine) to inhibit tyrosine hydroxylase, measuring the consequent depletion of NE [19].…”

Section: Interleukin-1 (Il-1)mentioning

confidence: 93%

“…The maximal responses in the metabolite studies of NE activation occurred around 2 h following ip administration [8,9,26] in parallel with the increases in plasma ACTH and corticosterone [8,26]. The microdialysis studies indicated a similar time course [14][15][16][17]. The peak responses in tryptophan and 5-HIAA occur significantly later, typically around 4 h after IL-1 administration [8,9,26,33].…”

Section: 12mentioning

confidence: 99%

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Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

285

169

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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.

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Section: Interleukin-1 (Il-1)mentioning

confidence: 85%

Section: Interleukin-1 (Il-1)mentioning

confidence: 93%

Section: 12mentioning

confidence: 99%

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Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

285

169

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“…For example, IL-1, IL-2, and IL-6 alter dopaminergic activity in the PFC (34), and IL-1␤ increases PFC monoaminergic activity in response to mild stress (35). In turn, PFC dopaminergic function is altered in response to stress, and this alteration has been found to be asymmetric (36).…”

Section: Discussionmentioning

confidence: 99%

Affective style andin vivoimmune response: Neurobehavioral mechanisms

Rosenkranz

Jackson

Dalton

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

142

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Considerable evidence exists to support an association between psychological states and immune function. However, the mechanisms by which such states are instantiated in the brain and influence the immune system are poorly understood. The present study investigated relations among physiological measures of affective style, psychological well being, and immune function. Negative and positive affect were elicited by using an autobiographical writing task. Electroencephalography and affect-modulated eye-blink startle were used to measure trait and state negative affect. Participants were vaccinated for influenza, and antibody titers after the vaccine were assayed to provide an in vivo measure of immune function. Higher levels of right-prefrontal electroencephalographic activation and greater magnitude of the startle reflex reliably predicted poorer immune response. These data support the hypothesis that individuals characterized by a more negative affective style mount a weaker immune response and therefore may be at greater risk for illness than those with a more positive affective style.

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“…Administration of IL-6 and IL-1 results in elevation of vasopressin, cortisol, CRH, and ACTH (Brebner et al, 2000;Harbuz et al, 1992;Xu et al, 1999), which suggests a pivotal role of cytokines in HPA axis activation (Dentino et al, 1999). In rodents, treatment with IL-1 resulted in increased DA, NE, and 5-HT activity in the brain (Dunn & Swiergiel, 1999;Merali et al, 1997;Song et al, 1999).…”

Section: Neuroimmunementioning

confidence: 99%