2009
DOI: 10.1038/aps.2009.37
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Neuronal nicotinic receptors as novel targets for inflammation and neuroprotection: mechanistic considerations and clinical relevance

Abstract: A number of studies have confirmed the potential for neuronal nicotinic acetylcholine receptor (NNR)-mediated neuroprotection and, more recently, its anti-inflammatory effects. The mechanistic overlap between these pathways and the ubiquitous effects observed following diverse insults suggest that NNRs modulate fundamental pathways involved in cell survival. These results have wide-reaching implications for the design of experimental therapeutics that regulate inflammatory and anti-apoptotic responses through … Show more

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Cited by 34 publications
(21 citation statements)
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References 102 publications
(146 reference statements)
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“…To date there are no approved drugs specific for the treatment of sepsis, a costly illness that is poorly understood (Deutschman and Tracey, 2014). It is known that severe sepsis involves a flood of cytokine production, including TNFa, interleukin-1b, interleukin-10, interferon gamma, and HMGB1 (Bencherif, 2009;Bencherif et al, 2011), in which HMGB1 is a late lethal mediator of sepsis (Kim et al, 2014b). This flood of cytokines involves the participation of intracellular and extracellular "danger signals" that activate inflammasomes to mediate the release of these cytokines and involves both P2X7 receptors and a7 nAChRs (Deutschman and Tracey, 2014).…”
Section: G A7 Nicotinic Acetylcholine Receptors and The Immune Connementioning
confidence: 99%
“…To date there are no approved drugs specific for the treatment of sepsis, a costly illness that is poorly understood (Deutschman and Tracey, 2014). It is known that severe sepsis involves a flood of cytokine production, including TNFa, interleukin-1b, interleukin-10, interferon gamma, and HMGB1 (Bencherif, 2009;Bencherif et al, 2011), in which HMGB1 is a late lethal mediator of sepsis (Kim et al, 2014b). This flood of cytokines involves the participation of intracellular and extracellular "danger signals" that activate inflammasomes to mediate the release of these cytokines and involves both P2X7 receptors and a7 nAChRs (Deutschman and Tracey, 2014).…”
Section: G A7 Nicotinic Acetylcholine Receptors and The Immune Connementioning
confidence: 99%
“…One approach to evaluate a role for nicotine is to investigate its neuroprotective properties against nigrostriatal damage in parkinsonian animal models (Belluardo et al, 2000;O'Neill et al, 2002;Quik et al, 2007b;Picciotto and Zoli, 2008;Bencherif, 2009). A frequently used rat model involves unilateral administration of 6-hydroxydopamine into the striatum, SN pars compacta, or medial forebrain bundle or hemisection of the nigrostriatal dopaminergic pathway (Figs.…”
Section: B Nicotine Neuroprotection In Parkinsonian Animal Modelsmentioning
confidence: 99%
“…nAChRs are implicated in neuroprotection mechanisms against acute cell distress (Bencherif, ) induced by excitotoxicity, namely a process of over‐activation of glutamate receptors considered as a paradigm of neurodegeneration (Choi, , ). Nicotine‐mediated neuroprotection has been reported in vitro (Garrido, King‐Pospisil, Son, Hennig, & Toborek, ), in vivo (Xue, Liu, Zhang, & Gao, ) and in epidemiological studies (Quik, Perez, & Bordia, ), suggesting potential strategies to contrast neuronal death.…”
Section: Introductionmentioning
confidence: 99%