Nicotine protects cultured striatal neurones against N-methyl-D-aspartate receptor-mediated neurotoxicity

Marin, Philippe; Maus, Marion; Desagher, Solange; Głowiński, J.; Prémont, Joël

doi:10.1097/00001756-199410000-00035

Cited by 102 publications

(52 citation statements)

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“…5). This range is similar to the nicotine concentration, from 1 to 100 M, found to be neuroprotective in studies with neuronal cultures (Akaike et al, 1994;Marin et al, 1994;Kihara et al, 1998Kihara et al, , 2001DajasBailador et al, 2000). Minana et al (1998) showed neuroprotection by 10 nM nicotine against glutamate and 10 M against NMDA.…”

Section: Discussionsupporting

confidence: 72%

“…Although nicotine and other nAChR agonists were shown to be neuroprotective in a variety of experimental systems, they were never studied in acute slices. Nicotine was found to be neuroprotective in neuronal cultures against glutamate, NMDA, and some of its analogs (Akaike et al, 1994;Marin et al, 1994). Nicotinic neuroprotective activity was reported to be dependent on active ␣7 nAChRs and Ca 2ϩ (Dajas-Bailador et al, 2000;Kihara et al, 2001).…”

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confidence: 99%

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Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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Although in neuronal cultures nicotine was reported to prevent early and delayed excitotoxic death, no studies with nicotinic drugs have been done with acute hippocampal slices. We investigated the effect of nicotine and methyllycaconitine (MLA) on the toxicity of N-methyl-D-aspartate (NMDA) in the CA1 area of hippocampal slices. The excitotoxic effect of NMDA was assessed as decreased recovery of the capability to produce synaptically evoked population spikes (PSs). Application of nicotine or MLA before NMDA application increased the recovery of PSs. This electrophysiological recovery was used as a measure of the early neuroprotective events. The neuroprotection conferred by both nicotine and MLA was inhibited by dihydro-␤-erythroidine, showing mediation of neuroprotection by ␣4␤2 neuronal nicotinic receptors (nAChRs). Because nicotine activates ␣4␤2 and other nAChR subtypes, whereas 10 nM MLA inhibits the ␣7 subtype, we propose the involvement of a neuronal circuitry-dependent mechanism for nicotinic neuroprotection. The effect of nicotine downstream from the receptors was investigated using inhibitors of cell signaling. The results suggest that the effect of nicotine is mediated by tyrosine receptor kinases, 1,2-phosphatidylinositol-3 kinase, and the mitogen-activated extracellular signal-regulated kinases. Although nicotine neuroprotection is Ca 2ϩ -dependent, neither L-type Ca 2ϩ channels nor calmodulin-dependent protein kinase is involved in the effect of nicotine. In summary, these results suggest that in acute slices nicotinic protection is initiated either by direct activation of ␣4␤2 or indirectly by inhibition of ␣7 followed by signal transduction involving tyrosine kinases, phospholipid-dependent kinases, and mitogen-activated kinases.

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Section: Discussionsupporting

confidence: 72%

mentioning

confidence: 99%

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Ferchmin

Pérez²,

Eterović³

et al. 2003

J Pharmacol Exp Ther

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“…Thus, it is not yet known whether this spatial learning deficit is attributable to a ␤2 receptor involvement in the task, increased neurodegeneration, or both. Nicotine has been shown to protect primary cells in culture from cell death induced by excitotoxic amino acids (Borlongan et al 1995;Marin et al 1994) and it has been suggested that there is an inverse correlation between smoking and the incidence of Alzheimer's disease (van Duijn and Hofman 1991). These data, taken together, may suggest a neuroprotective function for nAChRs with high affinity for nicotine.…”

Section: Nicotine Learning and Memory And Neurodegenerative Disordersmentioning

confidence: 99%

Nicotinic Receptors in the Brain Links between Molecular Biology and Behavior

Picciotto

Caldarone

King

et al. 2000

Neuropsychopharmacology

318

181

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The physiological effects of nicotine are mediated through binding to, and activation of, nicotinic acetylcholine receptors (nAChRs). These nAChRs are pentamers made up of subunits that have distinct, but overlapping expression patterns in subsets of neurons. Molecular cloning and in situ hybridization have been used to identify the expression patterns of different nAChR subunits. Parallel pharmacological studies have characterized the various behavioral actions of nicotine in the whole animal, but it has been difficult to correlate particular subunit compositions of nAChRs with these nicotine-elicited behaviors. This review will attempt to integrate what is known about the molecular, anatomical, and pharmacological properties of nAChR subunits with behavioral data, and summarize current opinions about which nAChR subtypes are responsible for particular behaviors.

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“…In vitro, nicotine can protect primary cultures of striatal neurons against NMDA neurotoxicity (Marin et al, 1994). In vivo, chronic nicotine treatment can rescue dopaminergic cell bodies in substantia nigra (Janson and Moller, 1993) and nerve terminals in striatum (Fuxe et al, 1990) from mechanical lesion, restore glucose utilization in lesioned areas (Owman et al, 1989), counteract lesion-induced dopamine receptor up-regulation (Janson et al, 1994), and increase dopamine turnover rate (Fuxe et al, 1990).…”

Section: Neuronal Nachrs and Neuroprotectionmentioning

confidence: 99%

Nicotinic receptors in aging and dementia

2002

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Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia. Nicotine and nicotinic agonists have been shown to improve cognitive function in aged or impaired subjects. Smoking has also been shown in some epidemiological studies to be protective against the development of neurodegenerative diseases. This is supported by animal studies that have shown nicotine to be neuroprotective both in vivo and in vitro. Treatment with nicotinic agonists may therefore be useful in both slowing the progression of neurodegenerative illnesses, and improving function in patients with the disease. While increased nicotinic function has been shown to be beneficial, loss of cholinergic markers is often seen in patients with dementia, suggesting that decreased cholinergic function could contribute to both the cognitive deficits, and perhaps the neuronal degeneration, associated with dementia. In this article we will review the literature on each of these areas. We will also present hypotheses that might address the mechanisms underlying the ability of nAChR function to protect against neurodegeneration or improve cognition, two potentially distinct actions of nicotine.

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Nicotine protects cultured striatal neurones against N-methyl-D-aspartate receptor-mediated neurotoxicity

Cited by 102 publications

References 0 publications

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Nicotinic Receptors Differentially RegulateN-Methyl-d-aspartate Damage in Acute Hippocampal Slices

Nicotinic Receptors in the Brain Links between Molecular Biology and Behavior

Nicotinic receptors in aging and dementia

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