Interleukin-1β (IL-1β) and tumour necrosis factor (TNF) inhibit long-term potentiation in the rat dentate gyrus in vitro

Cunningham, Alan; Murray, Carol; O’Neill, Luke A.J.; Lynch, Marina A.; O’Connor, John

doi:10.1016/0304-3940(95)12252-4

Cited by 394 publications

(254 citation statements)

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“…(Barrientos et al, 2002). Consistent with these data, IL-1β potently inhibits long-term potentiation (LTP), a form of synaptic strengthening thought to underlie many forms of memory (Cunningham et al, 1996). …”

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confidence: 63%

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

et al. 2007

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The intra-hippocampal administration of interleukin-1β (IL-1β) as well as the induction of elevated but physiological levels of IL-1β within the hippocampus interferes with the formation of long-term memory. There is evidence suggesting that the induction of prostaglandin (PG) formation by IL-1β is involved in impairments in working and spatial memory following IL-1β. The present experiments extend these findings by showing that PGs are responsible for memory deficits in contextual fear conditioning that occur following IL-1β injection into the dorsal hippocampus. Cyclooxygenase (COX) inhibition blocked the disruption in contextual fear conditioning produced by IL-1β and COX inhibition alone also disrupted contextual memory, suggesting an inverted Ushaped relationship between PG levels and memory. In addition to demonstrating the necessity of PGs in IL-1β mediated memory deficits, we also show that PGs injected directly into the dorsal hippocampus are sufficient to impair context memory and significantly reduce post-conditioning levels of BDNF within the hippocampus, suggesting a possible mechanism for the memory-impairing effects of PGs. Keywords memory; brain derived neurotrophic factor; cyclooxygenase; EP receptorThe pro-inflammatory cytokine interleukin-1β (IL-1β) exerts powerful central and peripheral actions. Recently, there has been considerable interest in its influence within the brain on learning and memory. This interest initially derived in part from findings that Alzheimer's disease and AIDS-related dementia are associated with elevated brain levels of IL-1β (Griffen et al., 1989;Lombardi et al., 1999). More direct evidence implicating IL-1β in learning and memory has come from animal studies. Manipulations that increase levels of IL-1β within the hippocampus have been shown to impair memory formation. These manipulations include the injection of the gram-negative bacterial component lipopolysaccharide (LPS;Pugh et al. 1998), social isolation stress (Pugh et al., 1999), and aging (Gemma et al., 2005). The blockade of IL-1 receptors and/or the inhibition of IL-1 synthesis prevents these memory impairments, supporting the conclusion that they are mediated by IL-1β (Pugh et al. 1998;Pugh et al., 1999;Gemma et al., 2005). Moreover, direct injection of IL-1β into the dorsal hippocampus Tel.: +1 303 492 9616; fax: +1 303 492 2967., E-mail address: amy.hein@colorado.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Barrientos et al., 2002). Consistent with these data, IL-1β potently inhibits long-term potentiation (LTP), a form of synaptic strengthenin...

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confidence: 63%

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

et al. 2007

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“…suggested (Markowska et al, 1996;Frick et al, 1997). LTP could also be moderated by changes in endogenous cytokines such as TNF-α and IL-1β (Cunningham et al, 1996;Butler et al, 2004) as a direct consequence of exercise (Ang et al, 2004). Both TNF-α and IL-1β are known to inhibit LTP.…”

Section: Discussionmentioning

confidence: 99%

Alterations in spatial learning and memory after forced exercise

et al. 2006

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A B S T R A C TExercise has been shown to influence learning and memory. Most studies were performed with a voluntary running paradigm (e.g. running wheel) in mice. However, such effects of exercise on learning and memory are less well demonstrated using a forced running paradigm (e.g. treadmill). The present study was designed to examine the effects of 12 weeks of forced treadmill running on learning and memory performance in rats. We have previously shown that forced running resulted in qualitative and quantitative changes in the cholinergic neurons of the horizontal diagonal band of Broca (HDB) in the septum. This study was conducted in order to determine whether or not these changes occur simultaneously with enhanced learning and memory. The one-day version of the Morris water maze (MWM) test [Frick, K.M., Stillner, E.T., Berger-Sweeney, J., 2000. Mice are not little rats: species differences in a one-day water maze task. NeuroReport 11, 3461-3465] was used to test spatial learning and memory after the exercise period. Our data showed that runners displayed better spatial learning and memory when compared to nonrunners. This was evidently shown by a reduction in the time required for spatial acquisition (p < 0.05) and superior probe trial performance (p < 0.05). A shorter distance swam by the runners also suggested improved learning over the nonrunners (p < 0.05). In an attempt to revalidate our earlier quantitative results, we used design-based stereology (DBS) to estimate the number of cholinergic neuronal profile population in the medial septum and diagonal band (MSDB).We confirmed that forced running increased the cholinergic neuronal profile subpopulation in the HDB (Coefficient of Error < 0.2). Taken together, these results indicate that forced exercise could influence learning and memory with a concomitant increase in the number of cholinergic neurons in the HDB.⁎ Corresponding authors. E.-T. Ang is to be contacted at

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“…In the early 90s exogenous application of TNF-α was shown to have inhibitory effects on synaptic plasticity and long-term potentiation (LTP), an electrophysiological correlate of learning and memory [37,38]. Later it was shown that the JNK and p38 MAP kinase played an important role in this inhibitory effect on LTP [39,40].…”

Section: Tnf-α and Synaptic Plasticitymentioning

confidence: 99%

Targeting tumour necrosis factor-α in hypoxia and synaptic signalling

O’Connor

2013

Ir J Med Sci

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Tumor necrosis factor (TNF)-α is a proinflammatory cytokine, which is synthesised and released in the brain by astrocytes, microglia and neurons in response to numerous internal and external stimuli. It is involved in many physiological and pathophysiological processes such as gene transcription, cell proliferation, apoptosis, synaptic signalling and neuroprotection. The complex actions of TNF-α in the brain are under intense investigation. TNF-α has the ability to induce selective necrosis of some cells whilst sparing others and this has led researchers to discover multiple activated signalling cascades. In many human diseases including acute stroke and inflammation and those involving hypoxia, levels of TNF-α are increased throughout different brain regions. TNF-α signalling may also have several positive and negative effects on neuronal function including glutamatergic synaptic transmission and plasticity. Exogenous TNF-α may also exacerbate the neuronal response to hypoxia. This review will summarise the actions of TNF-α in the central nervous system on synaptic signalling and its effects during hypoxia.

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Interleukin-1β (IL-1β) and tumour necrosis factor (TNF) inhibit long-term potentiation in the rat dentate gyrus in vitro

Cited by 394 publications

References 17 publications

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

Alterations in spatial learning and memory after forced exercise

Targeting tumour necrosis factor-α in hypoxia and synaptic signalling

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