Naspm - CAS 122306-11-0
Catalog number: 122306-11-0
Category: Inhibitor
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Molecular Formula:
C22H34N4O
Molecular Weight:
370.53
COA:
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Targets:
AMPAR
Description:
A poliamine amide as potent Spermidine uptake inhibitor.
Purity:
>98%
Synonyms:
1-Naphthylacetyl spermine
MSDS:
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InChIKey:
ZUINPPQIQARTKX-UHFFFAOYSA-N
InChI:
InChI=1S/C22H34N4O/c23-12-6-15-24-13-3-4-14-25-16-7-17-26-22(27)18-20-10-5-9-19-8-1-2-11-21(19)20/h1-2,5,8-11,24-25H,3-4,6-7,12-18,23H2,(H,26,27)
Canonical SMILES:
C1=CC=C2C(=C1)C=CC=C2CC(=O)NCCCNCCCCNCCCN
1.Rapid tumor necrosis factor alpha-induced exocytosis of glutamate receptor 2-lacking AMPA receptors to extrasynaptic plasma membrane potentiates excitotoxicity.
Leonoudakis D;Zhao P;Beattie EC J Neurosci. 2008 Feb 27;28(9):2119-30. doi: 10.1523/JNEUROSCI.5159-07.2008.
The postinjury inflammatory response in the CNS leads to neuronal excitotoxicity. Our previous studies show that a major component of this response, the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), causes a rapid increase in AMPA glutamate receptors (AMPARs) on the plasma membrane of cultured hippocampal neurons. This may potentiate neuron death through an increased vulnerability to AMPAR-dependent excitotoxic stress. Here, we test this hypothesis with an in vitro lactose dehydrogenase death assay and examine in detail the AMPAR surface delivery time course, receptor subtype, and synaptic and extrasynaptic distribution after TNFalpha exposure. These data demonstrate that surface levels of glutamate receptor 2 (GluR2)-lacking Ca2+-permeable AMPARs peak at 15 min after TNFalpha treatment, and the majority are directed to extrasynaptic sites. TNFalpha also induces an increase in GluR2-containing surface AMPARs but with a slower time course. We propose that this activity contributes to excitotoxic neuron death because TNFalpha potentiation of kainate excitotoxicity is blocked by a Ca2+-permeable AMPAR antagonist [NASPM (1-naphthyl acetyl spermine)] and a specific phosphoinositide 3 kinase (PI3 kinase) inhibitor (LY294,002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one]) previously shown to block the TNFalpha-induced increase in AMPAR surface delivery.
2.Methoxychlor and fenvalerate induce neuronal death by reducing GluR2 expression.
Umeda K;Kotake Y;Miyara M;Ishida K;Sanoh S;Ohta S J Toxicol Sci. 2016 Apr;41(2):255-64. doi: 10.2131/jts.41.255.
GluR2, an α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunit, plays important roles in neuronal survival. We previously showed that exposure of cultured rat cortical neurons to several chemicals decreases GluR2 protein expression, leading to neuronal toxicity. Methoxychlor, the bis-p-methoxy derivative of dichlorodiphenyltrichloroethane, and fenvalerate, a synthetic pyrethroid chemical, have been used commercially as agricultural pesticides in several countries. In this study, we investigated the effects of long-term methoxychlor and fenvalerate exposure on neuronal glutamate receptors. Treatment of cultured rat cortical neurons with 1 or 10 µM methoxychlor and fenvalerate for 9 days selectively decreased GluR2 protein expression; the expression of other AMPA receptor subunits GluR1, GluR3, and GluR4 did not change under the same conditions. Importantly, the decreases in GluR2 protein expression were also observed on the cell surface membrane where AMPA receptors typically function. In addition, both chemicals decreased neuronal viability, which was blocked by pretreatment with 1-naphtylacetylspermine, an antagonist of GluR2-lacking AMPA receptors, and MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist.
3.Group I mGluR-dependent depotentiation in the lateral amygdala does not require the removal of calcium-permeable AMPA receptors.
Park K;Song S;Hong I;Song B;Kim J;Park S;Lee J;Song S;An B;Kim J;Lee CJ;Shin KS;Choi S;Lee S Front Behav Neurosci. 2014 Aug 8;8:269. doi: 10.3389/fnbeh.2014.00269. eCollection 2014.
There is conflicting evidence regarding whether calcium-permeable receptors are removed during group I mGluR-mediated synaptic depression. In support of this hypothesis, AMPAR rectification, a correlative index of the synaptic expression of GluA2-lacking calcium-permeable AMPARs (CP-AMPARs), is known to decrease after the induction of several types of group I mGluR-mediated long-term depression (LTD), suggesting that a significant proportion of synaptic CP-AMPARs is removed during synaptic depression. We have previously demonstrated that fear conditioning-induced synaptic potentiation in the lateral amygdala is reversed by group 1 mGluR-mediated depotentiation. Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation. The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM. Importantly, the sensitivity to NASPM was not altered after induction of depotentiation. Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.
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Chemical Structure

CAS 122306-11-0 Naspm

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