Interferon-α reduces catecholamine secretion from bovine adrenal chromaffin cells stimulated by acetylcholine

Tachikawa, Eiichi; Kondo, Yukiko; Takahashi, Masakuni; Kashimoto, Takeshi; Yanagihara, Nobuyuki; Toyohira, Yumiko; Izumi, Fujio

doi:10.1007/pl00005108

Cited by 10 publications

(22 citation statements)

References 44 publications

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“…4,44 A third hypothesis involves IFN-α causing chronic activation of neuroendocrine pathways, which interact with 5-HT neurons, via the hypothalamic-pituitary-adrenal axis. 2,34,38,45 Unlike the 5-HT results, we did not find reduced 5-HIAA levels after 14-day treatment, suggesting that 5-HT turnover was increased. This prompted us to investigate 5-HTT mRNA levels.…”

Section: Discussioncontrasting

confidence: 99%

“…17,37 Tachikawa et al reported that long-term (72-h) pretreatment with IFN-α decreases secretion of catecholamines from bovine adrenal chromaffin cells stimulated by acetylcholine. 38 Another hypothesis is that IFN-α reduces and facilitates metabolism of tryptophan, the precursor of 5-HT. 4,39 Immune stimulation reportedly results in tryptophan degradation.…”

Section: Discussionmentioning

confidence: 99%

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Chronic intraperitoneal injection of interferon‐α reduces serotonin levels in various regions of rat brain, but does not change levels of serotonin transporter mRNA, nitrite or nitrate

Sato¹,

Suzuki²,

Yokoyama³

et al. 2006

Psychiatry Clin Neurosci

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Interferon-α therapy is associated with a high rate of depression, but the pathophysiological mechanisms remain unclear. The purpose of the present study was to investigate the effects of i.p. administered interferon-α on monoaminergic neurotransmission in the brain. The levels of monoamines and associated metabolites were measured in various regions of the rat brain using a high-performance liquid chromatography-electrochemical detection system. The serotonin transporter mRNA levels were also measured using in situ hybridization. After 1 day, dopamine turnover was diminished in the cortex. Norepinephrine turnover was decreased in most regions tested after 4 days. However, these changes were transient. After 14 days, serotonin turnover was increased in the frontal cortex and hippocampus in rats given a dose of 20 000 IU/kg; in the frontal cortex, hippocampus, amygdala, thalamus, hypothalamus and brainstem in those on 200 000 IU/kg; and in the thalamus and hypothalamus in those on 2 000 000 IU/kg (all P < 0.05). However, 14-day treatment did not significantly change serotonin transporter mRNA levels. Next, the question of whether interferon-α affects monoamine levels via induction of nitric oxide (NO), was investigated. However, there were no changes in either NO 2 -or NO 3 -, as markers of NO production, in any brain regions after 14-day treatment. These results suggest that chronic peripheral administration of interferon-α induces metabolic changes in the central serotonin system. Further investigation is needed to determine exactly how this cytokine affects the central serotonin system and to assess whether a central serotonin abnormality is involved in interferon-induced depression.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic intraperitoneal injection of interferon‐α reduces serotonin levels in various regions of rat brain, but does not change levels of serotonin transporter mRNA, nitrite or nitrate

Sato¹,

Suzuki²,

Yokoyama³

et al. 2006

Psychiatry Clin Neurosci

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“…Similar prolonged exposure of bovine chromaffin cells to IFN-a resulted in a time-and concentration-dependent suppression in Ca 2? -influx and catecholamine release in response to acetylcholine (Tachikawa et al 1997). Two key observations led the authors to suggest that these actions resulted from an IFN-a-mediated suppression of nicotinic acetylcholine receptor expression; firstly, the reduction in secretion could be overcome by increased concentrations of acetylcholine, and secondly, IFN-a had no effect on secretion induced by K ?…”

Section: Interferonsmentioning

confidence: 98%

“…The CNS actions of IFN-a are particularly important because of the often-severe psychiatric side effects (depression and confusion) that accompany its use in antivirus or anti-tumour therapy (O'Brien et al 2004;Dafny and Yang 2005). This has led to considerable interest in IFN-a influence on various catecholaminergic systems including the adrenal medulla (Tachikawa et al 1997;Toyohira et al 1998).…”

Section: Interferonsmentioning

confidence: 98%

Cytokine Interactions with Adrenal Medullary Chromaffin Cells

et al. 2010

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It is generally accepted that a bi-directional or reciprocal interaction occurs between the immune and neuroendocrine systems, and that this relationship is important for the appropriate physiological functioning of both systems. Similarly, an imbalance in this relationship may contribute to a number of pathologies, most notably those relating to stress. The aim of this article is to consider the interaction of cytokines with the adrenal medulla, a potentially important player in this relationship. The chromaffin cells of the adrenal medulla release catecholamines and a range of biologically active peptides in response to a wide variety of stress-related signals. A growing body of evidence indicates that this stress response is influenced by, and in turn has influence upon, immune signalling. This brief review will focus primarily on the best-described adrenal medullary active cytokines, namely interferon-α, interleukin-6, interleukin-1α/β and tumour necrosis factor-α. In each case, three key issues will be addressed: the physiologically relevant source of the cytokine; the intracellular signalling events arising from activation of its receptor and finally the cellular consequences of such activation in terms of modulation of gene expression and the secretory output of the chromaffin cells.

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“…ACCs express receptors for cytokines that are systemically elevated during IBD, including tumor necrosis factor (TNF)-␣ and interleukin (IL)-6 (1,2,26,36,43). Furthermore, inflammatory mediators have been shown to alter I Ca and catecholamine secretion in ACCs in vitro (48,60). Given these findings, we hypothesized that I Ca is inhibited in ACCs during experimental colitis, similar to postganglionic sympathetic neurons (50).…”

mentioning

confidence: 99%