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Interleukin-1 beta induces hyperpolarization and modulates synaptic inhibition in preoptic and anterior hypothalamic neurons

Academic Article
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Overview

authors

  • Tabarean, Iustin
  • Korn, Henri
  • Bartfai, Tamas

publication date

  • 2006

journal

  • Neuroscience  Journal

abstract

  • Most of the inflammatory effects of the cytokine interleukin 1beta (IL-1beta) are mediated by induction of cyclooxygenase (COX)2 and the subsequent synthesis and release of prostaglandin E2. This transcription-dependent process takes 45-60 min, but IL-1beta, a well-characterized endogenous pyrogen also exerts faster neuronal actions in the preoptic area/anterior hypothalamus. Here, we have studied the fast (1-3 min) signaling by IL-1beta using whole-cell patch clamp recordings in preoptic area/anterior hypothalamus neurons. Exposure to IL-1beta (0.1-1 nM) hyperpolarized a subset ( approximately 20%) of preoptic area/anterior hypothalamus neurons, decreased their input resistance and reduced their firing rate. These effects were associated with an increased frequency of bicuculline-sensitive spontaneous inhibitory postsynaptic currents and putative miniature inhibitory postsynaptic currents, strongly suggesting a presynaptic mechanism of action. These effects require the type 1 interleukin 1 receptor (IL-1R1), and the adapter protein myeloid differentiation primary response protein (MyD88), since they were not observed in cultures obtained from IL-1R1 (-/-) or from MyD88 (-/-) mice. Ceramide, a second messenger of the IL-1R1-dependent fast signaling cascade, is produced by IL-1R1-MyD88-mediated activation of the neutral sphingomyelinase. C2-ceramide, its cell penetrating analog, also increased the frequency of miniature inhibitory postsynaptic currents in a subset of cells. Both IL-1beta and ceramide reduced the delayed rectifier and the A-type K(+) currents in preoptic area/anterior hypothalamus neurons. The latter effect may account in part for the increased spontaneous inhibitory postsynaptic current frequency as suggested by experiments with the A-type K(+) channel blockers 4-aminopyridine. Taken together our data suggest that IL-1beta inhibits the activity of preoptic area/anterior hypothalamus neurons by increasing the presynaptic release of GABA.

subject areas

  • Analysis of Variance
  • Animals
  • Bicuculline
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Dose-Response Relationship, Radiation
  • Drug Interactions
  • Electric Stimulation
  • Embryo, Mammalian
  • Enzyme Inhibitors
  • Excitatory Amino Acid Antagonists
  • GABA Antagonists
  • Hypothalamus
  • Interleukin-1beta
  • Membrane Potentials
  • Mice
  • Mice, Knockout
  • Myeloid Differentiation Factor 88
  • Neural Inhibition
  • Neurons
  • Patch-Clamp Techniques
  • Potassium Channel Blockers
  • Receptors, Interleukin-1
  • Sodium Channel Blockers
  • Sphingosine
  • Synapses
  • Tetrodotoxin
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Research

keywords

  • GABAergic modulation
  • Src kinase
  • ceramide
  • mini-IPSCs
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Identity

International Standard Serial Number (ISSN)

  • 0306-4522

Digital Object Identifier (DOI)

  • 10.1016/j.neuroscience.2006.05.007

PubMed ID

  • 16777343
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Additional Document Info

start page

  • 1685

end page

  • 1695

volume

  • 141

issue

  • 4

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