Search results for "1-methyl-4"
showing 10 items of 34 documents
CCDC 704265: Experimental Crystal Structure Determination
2009
Related Article: A.Prades, M.Viciano, M.Sanau, E.Peris|2008|Organometallics|27|4254|doi:10.1021/om800377m
CCDC 1525503: Experimental Crystal Structure Determination
2017
Related Article: Ngong Kodiah Beyeh, Hyun Hwa Jo, Igor Kolesnichenko, Fangfang Pan, Elina Kalenius, Eric V. Anslyn, Robin H. A. Ras, Kari Rissanen|2017|J.Org.Chem.|82|5198|doi:10.1021/acs.joc.7b00449
CCDC 1484545: Experimental Crystal Structure Determination
2016
Related Article: Ugur Kaya, Suruchi Mahajan, Jan-Hendrik Schöbel, Arto Valkonen, Kari Rissanen and Dieter Enders|2016|Synthesis|48|4091|doi:10.1055/s-0035-1562473
Both Short- and Long-Acting D-1/D-2 Dopamine Agonists Induce Less Dyskinesia than l-DOPA in the MPTP-Lesioned Common Marmoset (Callithrix jacchus)
2002
Abstract The current concept of dyskinesia is that pulsatile stimulation of D-1 or D-2 receptors by l -DOPA or short-acting dopamine agonists is more likely to induce dyskinesia compared to long-acting drugs producing more continuous receptor stimulation. We now investigate the ability of two mixed D-1/D-2 agonists, namely pergolide (long-acting) and apomorphine (short-acting), to induce dyskinesia in drug-naive MPTP-lesioned primates, compared to l -DOPA. Adult common marmosets ( Callithrix jacchus ) were lesioned with MPTP (2 mg/kg/day sc for 5 days) and subsequently treated with equieffective antiparkinsonian doses of l -DOPA, apomorphine, or pergolide for 28 days. l -DOPA, apomorphine, …
Downregulation of PMCA2 increases the vulnerability of midbrain neurons to mitochondrial complex I inhibition
2013
Parkinson's disease is an age-associated disorder characterized by selective degeneration of dopaminergic neurons. The molecular mechanisms underlying the selective vulnerability of this subset of neurons are, however, not fully understood. Employing SH-SY5Y neuroblastoma cells and primary mesencephalic neurons, we here demonstrate a significant increase in cytosolic calcium after inhibition of mitochondrial complex I by means of MPP(+), which is a well-established environmental toxin-based in vitro model of Parkinson's disease. This increase in calcium is correlated with a downregulation of the neuron-specific plasma membrane Ca(2+)-ATPase isoform 2 (PMCA2). Interestingly, two other import…
Alterations in striatal neuropeptide mRNA produced by repeated administration of L-DOPA, ropinirole or bromocriptine correlate with dyskinesia induct…
2002
Chronic administration of L-DOPA to MPTP-treated common marmosets induces marked dyskinesia while repeated administration of equivalent antiparkisonian doses of ropinirole and bromocriptine produces only mild involuntary movements. The occurrence of dyskinesia has been associated with an altered balance between the direct and indirect striatal output pathways. Using in situ hybridisation histochemistry, we now compare the effects of these drug treatments on striatal preproenkephalin-A (PPE-A) and adenosine A(2a) receptor mRNA expression as markers of the indirect pathway and striatal preprotachykinin (PPT) mRNA and preproenkephalin-B (PPE-B, prodynorphin) mRNA expression as markers of the d…
7-nitroindazole protects striatal dopaminergic neurons against MPP+-induced degeneration: an in vivo microdialysis study.
2007
The neuropathological hallmark of Parkinson's disease (PD) is the selective degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNc). In this study, using a microdialysis technique, we investigated whether an inhibitor of neuronal nitric oxide synthase (nNOS), 7-nitrindazole (7-NI), could protect against DAergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) in freely moving rats. Experiments were performed over 2 days in three groups of rats: (a) nonlesioned, (b) MPP(+)-lesioned, and (c) 7-NI pretreated MPP(+)-lesioned rats. On day 1, control rats were perfused with an artificial CSF, while 1 mM MPP(+) was infuse…
Transgenic expression and activation of PGC-1α protect dopaminergic neurons in the MPTP mouse model of Parkinson’s disease
2011
Mitochondrial dysfunction and oxidative stress occur in Parkinson’s disease (PD), but little is known about the molecular mechanisms controlling these events. Peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) is a transcriptional coactivator that is a master regulator of oxidative stress and mitochondrial metabolism. We show here that transgenic mice overexpressing PGC-1α in dopaminergic neurons are resistant against cell degeneration induced by the neurotoxin MPTP. The increase in neuronal viability was accompanied by elevated levels of mitochondrial antioxidants SOD2 and Trx2 in the substantia nigra of transgenic mice. PGC-1α overexpression also protected against MP…
Distinct effects of atypical 1,4-dihydropyridines on 1-methyl-4-phenylpyridinium-induced toxicity.
2006
Our previous data obtained from in vivo experiments demonstrated high neuroprotective effects of three novel atypical neuronal non-calcium antagonistic 1,4-dihydropyridine (DHP) derivatives cerebrocrast, glutapyrone and tauropyrone. The present studies were carried out in vitro to clarify, at least in part, their mechanism of action in primary culture of cerebellar granule cells by use of 1-methyl-4-phenylpyridinium (MPP+) as a neurotoxic agent which causes dramatic oxidative stress. Cerebrocrast (highly lipophilic, with a classical two-ring structure) dose-dependently (0.01-10.0 microM, EC50 = 13 nM) reduced MPP+-induced cell death. At the same time, the calcium antagonist nimodipine (refe…
Caki-1 cells as a model system for the interaction of renally secreted drugs with OCT3.
2008
<i>Background/Aims:</i> Organic cation transporters (OCT) in the proximal tubules (PTs) participate in the renal secretion of several therapeutic agents. The exact role of OCT3 in renal secretion remains undetermined, partially due to the lack of an appropriate in vitro model system. The current work introduces the PT representative cell line, Caki-1, as a model system for studying the involvement of OCT3 in renal secretion. <i>Methods:</i> Caki-1 cells were characterized for OCT3 expression via real-time RT-PCR and immunocytochemical staining techniques. Uptake kinetics of OCT3 in Caki-1 cells was determined using prototypical substrates and inhibitors. Inhibition o…