Brain, behavior, and immunity
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Brain Behav. Immun. · May 2006
Randomized Controlled TrialPlacebo effects in laser-evoked pain potentials.
Placebo treatment may affect multiple components of pain, including inhibition of nociceptive input, automatic or deliberative appraisal of pain, or cognitive judgments involved in pain reporting. If placebo analgesia is due in part to an attenuation of early nociceptive processing, then pain-evoked event-related potentials (ERPs) should be reduced with placebo. In this study, we tested for placebo effects in P2 laser-evoked potentials at midline scalp electrodes. ⋯ However, we also found evidence that the very robust placebo-induced decreases in reported pain are not solely explained by early reductions in P2. N2 amplitude was affected by neither placebo nor reduction of laser intensity. These results suggest that placebo treatment affects early nociceptive processing, but that another component of placebo effects in reported pain occurs later, either in evaluation of pain or cognitive judgments about pain reports.
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Brain Behav. Immun. · Jan 2006
Randomized Controlled TrialBelief or Need? Accounting for individual variations in the neurochemistry of the placebo effect.
The activation of pain-suppressive, endogenous opioid neurotransmission after administration of a placebo with expectation of analgesia has been directly demonstrated in humans using molecular imaging techniques in recent work. Regional effects were described in the dorsolateral prefrontal cortex, pregenual anterior cingulate, anterior insula, and nucleus accumbens. However, it was also observed that the magnitude of these responses was subject to substantial individual and regional variation. ⋯ A model that included affective qualities of pain, the volume of algesic stimulus required to maintain pain over the experimental period within a moderate range, and the internal affective state of the volunteers contributed to 40-68% of the variance in the regional neurochemical responses to placebo. These initial data suggests that in the case of endogenous opioid mediated placebo analgesic responses, the individual experience of pain, in particular its affective elements, the internal affective state of the individuals during pain and a measure of sustained pain sensitivity are important factors contributing to the formation of a placebo effect. Further examination of individual variations in placebo responding will need to take into account the underlying process for which relief is required.
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The regulation of the innate immune response is critical for controlling inflammation and for the prevention and treatment of diseases. We recently demonstrated that the efferent vagus nerve inhibits pro-inflammatory cytokine release and protects against systemic inflammation, and termed this vagal function "the cholinergic anti-inflammatory pathway." The discovery that the innate immune response is regulated partially through this neural pathway provides a new understanding of the mechanisms that control inflammation. In this review, we outline the cholinergic anti-inflammatory pathway and summarize the current insights into the mechanisms of cholinergic modulation of inflammation. We also discuss possible clinical implications of vagus nerve stimulation and cholinergic modalities in the treatment of inflammatory diseases.
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Brain Behav. Immun. · Nov 2005
Comparative StudyThe effects of lipopolysaccharide and lithium chloride on the ingestion of a bitter-sweet taste: comparing intake and palatability.
Activation of the immune system with lipopolysaccharide (LPS) has been shown to result in decreased consumption of normally preferred substances while at the same time not affecting palatability. The present study examined the effects LPS administration on both intake and palatability of a relatively unpalatable bitter-sweet taste. Bitter is thought to signal a danger cue to an animal representing a potential toxin-containing food. ⋯ When the consummatory responses were examined, LPS-treatment produced an increase in active oral rejection relative to NaCl- and LiCl-treated groups on both conditioning days. The present study demonstrates that although both LPS- and LiCl-treatment result in similar conditioned avoidance using an intake measure, they do not elicit similar patterns of taste reactivity responding to intraoral infusions of the bitter-sweet taste. Furthermore, the present results suggest that immune activation with LPS-treatment results in increased rejection of a mildly aversive stimulus and supports the hypothesis that reorganization of behavioral priorities occurs during bacteria-induced sickness.
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Epidemiological data demonstrate an association between systemic low-grade inflammation defined as 2- to 3-fold increases in circulating inflammatory mediators and age-related decline in cognitive function. However, it is not known whether small elevations of circulating cytokine levels cause direct effects on human neuropsychological functions. We investigated changes in emotional, cognitive, and inflammatory parameters in an experimental in vivo model of low-grade inflammation. ⋯ The neutrophil count increased and the lymphocyte count declined. In this model, low-dose endotoxemia did not affect cognitive performance significantly but declarative memory performance was inversely correlated with cytokine increases. In conclusion, our findings demonstrate a negative association between circulating IL-6 and memory functions during very low-dose endotoxemia independently of physical stress symptoms, and the hypothalamo-pituitary-adrenal axis.