Interleukin-1β inhibits long-term potentiation in the CA3 region of mouse hippocampal slices

Katsuki, Hiroshi; Nakai, Satoru; Hirai, Yoshikatsu; Akaji, K.; Kiso, Yoshiaki; Satoh, Masamichi

doi:10.1016/0014-2999(90)90099-r

Cited by 313 publications

(149 citation statements)

References 7 publications

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“…et al, 1993;Tancredi et al, 1990 . Interleukin-1b suppresses tetanus-or tetraethylammonium-induced long-term Ž potentiation in CA1, CA3, and dentate gyrus areas Coogan and O'Connor, 1999;Cunningham et al, 1996;Katsuki et . al., 1990 .…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide inhibits induction of long-term potentiation and depression in the rat hippocampal CA1 area

Jo¹,

Park²,

Lee³

et al. 2001

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide inhibits induction of long-term potentiation and depression in the rat hippocampal CA1 area

Jo¹,

Park²,

Lee³

et al. 2001

European Journal of Pharmacology

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“…In contrast, high levels of IL-1 can impair LTP, as demonstrated by several research groups. It has been shown that elevated levels of IL-1 can inhibit the expression of LTP in the CA 3 region of the hippocampus [44] . Similar results have been obtained in the CA1 region of the hippocampus [45] and in the dentate gyrus [46,47] .…”

Section: Effects Of Il-1 On Long-term Potentiation (Ltp) Il-1mentioning

confidence: 99%

Interleukin-1β with learning and memory

Huang

Sheng²

2010

Neurosci. Bull.

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Abstract:Interleukin-1 (IL-1) is one of the first cytokines ever described. It has long been recognized to play an important role in mediating inflammation and orchestrating the physiological and behavioral adjustments that occur during sickness.Recently, accumulating evidence has indicated that IL-1 also adversely affects cognitive function. Nevertheless, there are also some reports showing no effects or even beneficial effects of IL-1 on learning and memory. The relationship between IL-1 and cognitive impairment has not been clearly elucidated. Here we reviewed the evidence of both negative and positive effects of IL-1 on learning and memory, and the key factors that may affect the effects of IL-1 on learning and memory were discussed.

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“…On the other hand, after injuries such as cerebral ischemia, the induction and the over-expression of these molecules that occurs as a part of neuroinXammatory response may result in the impairment of synaptic plasticity and the associated neurodegeneration. Earlier studies demonstrated inhibitory eVects of IL-1 on the hippocampal long-term potentiation (LTP) [67]. The exact mechanisms of the inhibitory eVects of IL-1 on synaptic plasticity are not completely elucidated; however, in vitro studies performed on pharmacologically isolated NMDA receptors revealed that administration of IL-1 was associated with signiWcant decrease in NMDA receptor excitatory post-synaptic potentials [14,41].…”

Section: Cytokines and Brain Plasticitymentioning

confidence: 99%

Inflammation, plasticity and real-time imaging after cerebral ischemia

2009

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With an incidence of approximately 350 in 100,000, stroke is the third leading cause of death and a major cause of disability in industrialized countries. At present, although progress has been made in understanding the molecular pathways that lead to ischemic cell death, the current clinical treatments remain poorly eVective. There is mounting evidence that inXammation plays an important role in cerebral ischemia. Experimentally and clinically, brain response to ischemic injury is associated with an acute and prolonged inXammatory process characterized by the activation of resident glial cells, production of inXammatory cytokines as well as leukocyte and monocyte inWltration in the brain, events that may contribute to ischemic brain injury and aVect brain recovery and plasticity. However, whether the post-ischemic inXammatory response is deleterious or beneWcial to brain recovery is presently a matter of debate and controversies. Here, we summarize the current knowledge on the molecular mechanisms underlying post-ischemic neuronal plasticity and the potential role of inXammation in regenerative processes and functional recovery after stroke. Furthermore, because of the dynamic nature of the brain inXammatory response, we highlight the importance of the development of novel experimental approaches such as real-time imaging. Finally, we discuss the novel transgenic reporter mice models that have allowed us to visualize and to analyze the processes such as neuroinXammation and neuronal repair from the ischemic brains of live animals.

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Interleukin-1β inhibits long-term potentiation in the CA3 region of mouse hippocampal slices

Cited by 313 publications

References 7 publications

Lipopolysaccharide inhibits induction of long-term potentiation and depression in the rat hippocampal CA1 area

Lipopolysaccharide inhibits induction of long-term potentiation and depression in the rat hippocampal CA1 area

Interleukin-1β with learning and memory

Inflammation, plasticity and real-time imaging after cerebral ischemia

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