ArticlePflugers Archiv : European journal of physiology2007
Nonselective cation channels are essential for maintaining intracellular Ca2+ levels and spontaneous firing activity in the midbrain dopamine neurons.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 43 citations in OpenAlex.
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- Mechanism of Pacemaker Activity in Zebrafish DC2/4 Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Modulation of Dopaminergic Neuronal Excitability by Zinc through the Regulation of Calcium-related Channels.Experimental neurobiology · 2019Article
- SKF-96365 strongly inhibits voltage-gated sodium current in rat ventricular myocytes.Pflugers Archiv : European journal of physiology · 2015Article
- Balance between the proximal dendritic compartment and the soma determines spontaneous firing rate in midbrain dopamine neurons.The Journal of physiology · 2014Article
- Calcium-activated non-selective cation currents are involved in generation of tonic and bursting activity in dopamine neurons of the substantia nigra pars compacta.The Journal of physiology · 2011Article
- The transient receptor potential channel antagonist SKF96365 is a potent blocker of low-voltage-activated T-type calcium channels.British journal of pharmacology · 2010Article
- Cellular mechanisms underlying burst firing in substantia nigra dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Robust pacemaking in substantia nigra dopaminergic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
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6 authors at 2 institutions in 1 country.
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Abstract
Intracellular Ca2+ and Ca2+-permeable ion channels are important in regulating the firing activity and pattern of midbrain dopamine neurons, but the role of Ca2+-permeable nonselective cation channels (NSCCs) on spontaneous firing activity is unclear. Therefore, we investigated how Ca2+-permeable NSCCs modulate spontaneous firing activity and cytosolic Ca2+ concentration ([Ca2+]c) in acutely isolated midbrain dopamine neurons of the rat. Applications of voltage-dependent Ca2+ channels antagonists failed to abolish spontaneous firing activity completely, but they decreased firing rate and [Ca2+]c. However, a blockade of NSCCs by 2-APB or SKF96365 more potently suppressed spontaneous firings with a depolarization of membrane potential and strong decreases in basal [Ca2+]c levels. The depolarization of membrane potentials was attenuated by intracellular dialysis with 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). NSCCs blockers inhibited oscillatory potentials and decreased basal [Ca2+]c in the presence of tetrodotoxin. Apamin, a small-conductance Ca2+-activated K+ channel inhibitor, depolarized membrane potentials and enhanced firing rates. From these data, we conclude that NSCCs not only make up the tonic Ca2+ entry pathways to uphold basal [Ca2+]c levels but also contribute to generation of spontaneous firings, thereby regulating spontaneous firing activities of the midbrain dopamine neurons.
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