Effects of iptakalim on rotenone-induced cytotoxicity and dopamine release from PC12 cells
Section snippets
Acknowledgements
These studies were supported in part by grants of National Natural Science Foundation of China (No. 39970846) and the state key project of new drug research and development (No. 969010101) of National Ministry of Science and Technology of China.
References (20)
- et al.
Molecular pathways involved in the neurotoxicity of 6-OHDA
Prog. Neurobiol.
(2001) - et al.
Implication of dopamine transporter system on 1-methyl-4-phenylpyridinium and rotenone effect in striatal synaptosomes
Eur. J. Pharmacol.
(1995) - et al.
Mitochondrial toxin inhibition of [(3)H]dopamine uptake into rat striatal synaptosomes
Biochem. Pharmacol.
(2002) - et al.
Complex I inhibitor effect on the nigral and striatal release of dopamine in the presence and absence of nomifensine
Eur. J. Pharmacol.
(1995) - et al.
Chronic systemic pesticide exposure reproduces features of Parkinson’s disease
Nat. Neurosci.
(2000) - et al.
Anoxia-induced dopamine release from rat striatal slices: involvement of reverse transport mechanism
J. Neurochem.
(1999) - et al.
The cytotoxicity of dopamine may be an artefact of cell culture
J. Neurochem.
(2002) - et al.
Neuroprotective and neurorestorative strategies for Parkinson’s disease
Nat. Neurosci.
(2002) Opening mitochondrial K(ATP) in the heart—what happens, and what does not happen
Basic Res. Cardiol.
(2000)- et al.
Expression of dopamine transporter at the tips of growing neurites of PC12 cells
J. Histochem. Cytochem.
(1996)
Cited by (33)
Dexmedetomidine attenuates the induction and reverses the progress of 6-hydroxydopamine- induced parkinsonism; involvement of K<inf>ATP</inf> channels, alpha 2 adrenoceptors and anti-inflammatory mechanisms
2019, Toxicology and Applied PharmacologyCitation Excerpt :KATP channels are mostly close under physiological condition but are activated by a decrease in ATP/ADP ratio and stabilize the membrane potential and mitochondrial matrix volume (Liss and Roeper, 2001). Emerging evidences indicate that opening and activation of KATP channels provides neuronal cells protection against neurotoxins (Liss and Roeper, 2001; Nagy et al., 2004; Yang et al., 2004; Wang et al., 2005). KATP channels also mediate neuroprotective activity of several compounds including atrial natriuretic peptide (López-Morales et al., 2018), Sildenafil (Son et al., 2018), hydrogen sulfide (Sarookhani et al., 2018) and melatonin (Waseem et al., 2016).
Mitochondrial ATP-sensitive potassium channel regulates mitochondrial dynamics to participate in neurodegeneration of Parkinson's disease
2018, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :These findings were exactly the opposite of previous hypotheses and several studies. Some studies have shown that the opening of KATP or mitoKATP has protective effects on rotenone induced neurotoxicity [32,33]. First, we assumed that the difference in the effect of diazoxide on rotenone-induced dopamine neurodegeneration may be related to the use of different cell lines.
Etiology and Progression of Parkinson's Disease: Cross-Talk Between Environmental Factors and Genetic Vulnerability
2016, Handbook of Behavioral NeuroscienceCitation Excerpt :In addition, Lewy bodies are seemingly absent from nigral dopamine cells in humans, who became parkinsonian by injecting MPTP (Langston et al., 1999). There are limited reports of α-synuclein-positive aggregates in the chronic MPTP mouse model, but only in mice that had lost more than 70% of their dopamine neurons after treatment (Meredith et al., 2004, 2002a; Yang et al., 2004). However, the aggregates are granular and do not resemble Lewy bodies (Fig. 40.2).
ABCC9/SUR2 in the brain: Implications for hippocampal sclerosis of aging and a potential therapeutic target
2015, Ageing Research ReviewsCitation Excerpt :Iptakalim has been shown to exert effects that hint at the potential for clinical benefits. The drug is neuroprotective in experimental models of stroke and Parkinson’s disease (Hu et al., 2005; Wang et al., 2005a,b,c, 2004, 2005, 2006; Yang et al., 2004, 2005, 2009; Zhang et al., 2011; Zhou et al., 2007). Other experimental results reported for iptakalim in mammals include beneficial neurochemical effects that may help to combat depression or psychoses (Lu et al., 2014; Volf et al., 2012).
Iptakalim protects against hypoxic brain injury through multiple pathways associated with ATP-sensitive potassium channels
2008, NeuroscienceCitation Excerpt :Deprived of oxygen, as under the HH-induced circumstances or during stroke, all cells of a mammalian organism die eventually, but neurons of the CNS are considered to be especially vulnerable compared with other cells (Johansen et al., 1987; Schlander et al., 1987). Previous studies from our laboratory as well as those from our coworkers (Wang et al., 2004; Yang et al., 2004), using different animal models of stroke or cell culture, have shown that Ipt provides significant neuroprotection through KATP channel activation, not only in promoting behavioral recovery but also in protecting neurons against necrosis and apoptosis. Using a rat model for HH brain injury as described in this report, we reconfirmed the neuroprotective effects of Ipt and also found that its neuroprotective effects are exerted not only through the activation of plasma KATP channels expressed in neurons but also through those mitochondrialATP channels in glial cells (astrocytes and microglial cells), which comprise greater than 85% of the total population of brain cells.