Physiopharmacological interactions between stress hormones and central serotonergic systems

Chaouloff, Francis

doi:10.1016/0165-0173(93)90005-k

Cited by 464 publications

(245 citation statements)

References 301 publications

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“…Exposure to stressful stimuli leads to activation of several neurotransmitter and endocrine systems of which the hypothalamic-pituitaryadrenocortical (HPA) axis is the key hormonal component (Chaouloff, 1993). Acute stress has been shown to reduce the expression of BDNF mRNA in the hippocampus (Smith et al, 1995), while numerous studies have documented that both chronic and acute stress paradigms decrease the expression of hippocampal BDNF mRNA in animals (Smith et al, 1995;Vaidya et al, 1997;Nibuya et al, 1999;Duman, 2004;Duman and Monteggia, 2006).…”

Section: Stressmentioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

679

458

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Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are two seemingly distinct signaling systems that play regulatory roles in many neuronal functions including survival, neurogenesis, and synaptic plasticity. A common feature of the two systems is their ability to regulate the development and plasticity of neural circuits involved in mood disorders such as depression and anxiety. BDNF promotes the survival and differentiation of 5-HT neurons. Conversely, administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression. There is also evidence for synergism between the two systems in affective behaviors and genetic epitasis between BDNF and the serotonin transporter genes.

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Section: Stressmentioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

679

458

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“…Thus, the NE and indoleamine responses can be independently manipulated, and must involve distinct mechanisms. The brain content of tryptophan increases in response to a large variety of stimuli, including several psychotropic drugs, increases in body temperature and several different stressors [39][40][41][42][43]. In our experience, increases in brain tryptophan are a very sensitive index of an animal's state of health.…”

Section: 12mentioning

confidence: 99%

Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

284

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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“…Similarly, many studies using post-mortem tissue assays and microdialysis indicate that footshock and other stressors increase the release of serotonin in terminal regions (see Bliss et al 1972;Rueter et al 1997). In addition, SSRI agents, and other manipulations that increase serotonin neurotransmission, activate the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (Chaouloff 1993;Fuller and Snoody 1990), known to be activated during stress (Cannon 1935;Selye 1956). It should be noted, however, that it is unlikely that activation of the HPA axis is involved in stress-induced reinstatement.…”

Section: For Reviews)mentioning

confidence: 99%

“…21, NO. 3 nervous system (Chaouloff 1993;Fuller and Snoody 1990), known to be activated during stress (Cannon 1935;Selye 1956). It should be noted, however, that it is unlikely that activation of the HPA axis is involved in stress-induced reinstatement.…”

mentioning

confidence: 99%

Effects of Naltrexone and Fluoxetine on Alcohol Self-Administration and Reinstatement of Alcohol Seeking Induced by Priming Injections of Alcohol and Exposure to Stress

Lê

Poulos

Harding

et al. 1999

Neuropsychopharmacology

217

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We have recently shown that priming injections of alcohol and footshock stress reinstate alcohol seeking in drug-free rats. Here we tested whether naltrexone and fluoxetine, two drugs used in the treatment of alcohol dependence, would affect reinstatement of alcohol seeking induced by these events. We also determined the effects of these drugs on alcohol self-administration during the maintenance phase. Rats were trained to press a lever for a 12% w/v alcohol solution. After stable drug-taking behavior was obtained, lever pressing for alcohol was extinguished. Reinstatement of drug seeking was then determined after priming injections of alcohol (0.24-0.96 g/kg) Studies with laboratory rats have shown mu opioid antagonists and selective serotonin reuptake inhibitors (SSRIs) decrease alcohol self-administration in a number of experimental procedures (Amit et al. 1991; Herz 1997;Lê et al. 1996). The preferentially mu opioid receptor antagonist, naltrexone, and SSRI agents such as fluoxetine also have been shown to decrease relapse to alcohol in humans (Naranjo and Sellers 1989;O'Malley et al. 1992;Sellers et al. 1992;Volpicelli et al. 1992). It is important to note, however, that several studies failed to find that SSRIs decrease rates of relapse (Zernig et al. 1997). In addition, although naltrexone has been found to decrease rates of relapse in alcoholics, a high proportion of these individuals relapse to alcohol during nal- Received September 25, 1998; revised February 11, 1999; accepted February 15, 1999. 436 A.D. Lê et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 3 trexone treatment (Volpicelli et al. 1997). Thus, it appears that while drugs such as naltrexone and fluoxetine consistently decrease alcohol consumption in laboratory animals, their clinical efficacy in humans is more variable.One important difference between the studies with humans versus the studies with laboratory animals is that those with humans concentrated on the relapse phase, while those with rats were done during the maintenance phase of the addiction process. Consequently, data on the effect of fluoxetine and naltrexone on relapse to alcohol seeking in preclinical models do not exist. In the present study, therefore, we used a reinstatement procedure, an animal model of relapse (Carroll and Comer 1996;Stewart and de Wit 1987), to study the effect of fluoxetine and naltrexone on relapse to drug seeking induced by reexposure to alcohol and exposure to a footshock stressor. Acute reexposure to alcohol (Bigelow et al. 1977;de Wit 1996;de Wit and Chutuape 1993;Hodgson et al. 1979;Ludwig et al. 1974) and exposure to stress (Brown et al. 1995;Cooper et al. 1992;Hore 1971) are regarded as two important factors for provoking relapse in humans.We have recently modified the reinstatement method, previously used to study factors involved in relapse to opioid and stimulant drugs in rats and monkeys, in order to determine factors involved in relapse to alcohol seeking in rats (Lê et al. 1998). We found that priming injections of alc...

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Physiopharmacological interactions between stress hormones and central serotonergic systems

Cited by 464 publications

References 301 publications

Interaction between BDNF and Serotonin: Role in Mood Disorders

Interaction between BDNF and Serotonin: Role in Mood Disorders

Effects of cytokines and infections on brain neurochemistry

Effects of Naltrexone and Fluoxetine on Alcohol Self-Administration and Reinstatement of Alcohol Seeking Induced by Priming Injections of Alcohol and Exposure to Stress

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