2009
DOI: 10.1016/j.bbi.2009.06.083
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78. Cytokine-induced depression: Effects of interleukin-1 beta and corticotropin-releasing factor antagonism on biochemical and behavioral indicators of “depression” in the rat

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“…Manipulating the signaling functions of cytokines and their receptors by altering downstream effector molecules may also provide information about relevant inflammatory pathways involved in depression. Recently, we reported that treatment with IL-1β increased the phosphorylation of p38 MAP kinase in rat frontal cortex (Loftis et al, 2009a,b), a kinase that activates specific intracellular signaling pathways and transcription factors leading to the increased production of proinflammatory modulators. Thus, use of a conditional p38 MAP kinase knockout mouse model may also be useful in testing novel therapeutic strategies for depression (Kim et al, 2008).…”
Section: Animal Models and Hypothesized Mechanisms Of Cytokine-inducementioning
confidence: 99%
“…Manipulating the signaling functions of cytokines and their receptors by altering downstream effector molecules may also provide information about relevant inflammatory pathways involved in depression. Recently, we reported that treatment with IL-1β increased the phosphorylation of p38 MAP kinase in rat frontal cortex (Loftis et al, 2009a,b), a kinase that activates specific intracellular signaling pathways and transcription factors leading to the increased production of proinflammatory modulators. Thus, use of a conditional p38 MAP kinase knockout mouse model may also be useful in testing novel therapeutic strategies for depression (Kim et al, 2008).…”
Section: Animal Models and Hypothesized Mechanisms Of Cytokine-inducementioning
confidence: 99%