Bifemelane Protects Cultured Cortical Neurons Against N-Methyl-D-aspartate Receptor-Mediated Glutamate Cytotoxicity

Akaike, Akinori; Maeda, Takehiko; Kume, Toshiaki; Kaneko, Satoshi

doi:10.1254/jjp.76.313

Cited by 7 publications

(7 citation statements)

References 12 publications

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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: 73%

“…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: 73%

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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“…121 Taken together experimental and clinical data largely indicate a neuroprotective/trophic role of nAChR modulation involving mainly ␣4, ␤2-and ␣7-nAChR subtypes. 120,[122][123][124][125][126][127][128] While it is clear that some level of nAChR activation is required for these neuroprotective/trophic effects to occur, it is also clear that overstimulation of certain nAChR subunits, such as ␣7 can lead to cytotoxicity. 129,130 In fact, many of the neuroprotective nAChR ligands, including nicotine, have been characterized as partial agonists allowing for only a percentage of the current that would be achieved by full ACh-induced nAChR activation.…”

Section: Limitationsmentioning

confidence: 99%

Nicotinic acetylcholine receptors as targets for antidepressants

et al. 2002

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While the monoamine deficiency hypothesis of depression is still most commonly used to explain the actions of antidepressant drugs, a growing body of evidence has accumulated that is not adequately explained by the hypothesis. This article draws attention to contributions from another apparently common pharmacological property of antidepressant medications-the inhibition of nicotinic acetylcholine receptors (nAChR). Evidence is presented suggesting the hypercholinergic neurotransmission, which is associated with depressed mood states, may be mediated through excessive neuronal nicotinic receptor activation and that the therapeutic actions of many antidepressants may be, in part, mediated through inhibition of these receptors. In support of this hypothesis, preliminary evidence is presented suggesting that the potent, centrally acting nAChR antagonist, mecamylamine, which is devoid of monoamine reuptake inhibition, may reduce symptoms of depression and mood instability in patients with comorbid depression and bipolar disorder. If this hypothesis is supported by further preclinical and clinical research, nicotinic acetylcholine receptor antagonists may represent a novel class of therapeutic agents for treating mood disorders.

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“…Nicotine protects against the degeneration of dopamine neurons in animal models of Parkinson's disease or after high doses of METH (Maggio et al, 1998;Costa et al, 2001;Ryan et al, 2001;Parain et al, 2003) through its ability to modulate NMDA receptor function (Rao et al, 1997) and protect against NMDA-mediated excitotoxicity that may occur due to increases in striatal glutamate after METH (Nash and Yamamoto, 1992). In fact, in vitro studies suggest that ␣7 nicotinic receptor modulation is protective against NMDA-mediated excitotoxicity to PC12 cells and hippocampal cultures (Akaike et al, 1994;Carlson et al, 1998;Prendergast et al, 2001). Conversely, the protective effect of nicotine is absent in ␣7 NAchR knockout mice (Gahring et al, 2003).…”

Section: Lobeline Effects On Methamphetamine Toxicity 165mentioning

confidence: 99%

Lobeline Attenuates Methamphetamine-Induced Changes in Vesicular Monoamine Transporter 2 Immunoreactivity and Monoamine Depletions in the Striatum

Eyerman¹,

Yamamoto²

2004

J Pharmacol Exp Ther

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L-Lobeline is an alkaloid that inhibits the behavioral effects of methamphetamine (METH) in rats. No studies have examined the effects of lobeline on the acute and long-term neurochemical changes produced by neurotoxic doses of METH. The effects of lobeline on METH-induced dopamine release, alterations in vesicular monoamine transporter 2 (VMAT-2) distribution, and long-term depletions of dopamine and serotonin (5-HT) content in the rat striatum were examined. METH increased body temperature and dopamine release, decreased VMAT-2 immunoreactivity at 1 and 24 h after METH, and decreased dopamine and 5-hydroxytryptamine (5-HT) content in striatum when examined 7 days later. Prevention of METH-induced hyperthermia attenuated the decrease in VMAT-2 as well as dopamine and 5-HT content. Lobeline pretreatment did not affect METH-induced dopamine release but attenuated the decreases in VMAT-2 after METH and the long-term decreases in striatal dopamine and 5-HT content. These effects of lobeline were due partly to the attenuation of METH-induced hyperthermia. The maintenance of hyperthermia during lobeline ϩ METH exposure restored the effects of METH on decreases in VMAT-2 as well as dopamine and 5-HT content. To examine the effects of lobeline independent of its effects on METHinduced hyperthermia, lobeline was administered after METH when body temperature returned to normal. Lobeline treatment at 5 and 7 h after METH attenuated the METH-induced decreases in synaptosomal, membrane-associated, and vesicular VMAT-2 24 h after METH, as well as the METH-induced decreases in dopamine and 5-HT content 7 days later. Therefore, lobeline has both temperature-dependent and -independent neuroprotective effects against METH toxicity.Methamphetamine (METH, ice, crystal) is an amphetamine derivative whose use has increased exponentially in the United States. METH is a significant health concern because of its abuse liability and potential neurotoxic effects, which include long-term monoamine depletions, degradation of both dopamine and serotonin (5-HT) striatal terminals in rodents and primates (Wagner et al., 1980;Gibb et al., 1987;Ricaurte and McCann, 1992), decreases in tyrosine hydroxylase activity (Gibb and Kogan, 1979), and loss of dopamine and serotonin transporters (Wagner et al., 1980). Despite these observed changes, the mechanisms underlying the toxic effects of METH remain to be elucidated.METH also affects the vesicular monoamine transporter 2 (VMAT-2), the protein that regulates the sequestration of monoamines into vesicles for subsequent release. Repeated administrations of high doses of METH cause a loss of VMAT protein on the vesicular membrane 1 h after a repeated high-dose regimen of METH (Riddle et al., 2002) and a decrease in VMAT-2 function 1 and 24 h after the last METH administration (Brown et al., 2000). Although the transient effects of METH on VMAT-2 function have been examined, it is unknown if the distribution of VMAT-2 protein is altered 24 h after METH and how this relates to the long-term effe...

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Bifemelane Protects Cultured Cortical Neurons Against N-Methyl-D-aspartate Receptor-Mediated Glutamate Cytotoxicity

Cited by 7 publications

References 12 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 acetylcholine receptors as targets for antidepressants

Lobeline Attenuates Methamphetamine-Induced Changes in Vesicular Monoamine Transporter 2 Immunoreactivity and Monoamine Depletions in the Striatum

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