ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Spontaneous opening of T-type Ca2+ channels contributes to the irregular firing of dopamine neurons in neonatal rats.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function.International journal of molecular sciences · 2022Review
- Methamphetamine increases dopamine release in the nucleus accumbens through calcium-dependent processes.Psychopharmacology · 2020Article
- αFrontiers in pharmacology · 2020Review
- Electrical Abnormalities in Dopaminergic Neurons of the Substantia Nigra in Mice With an Aromatic L-Amino Acid Decarboxylase Deficiency.Frontiers in cellular neuroscience · 2019Article
- Cooperative CRF and α1 Adrenergic Signaling in the VTA Promotes NMDA Plasticity and Drives Social Stress Enhancement of Cocaine Conditioning.Cell reports · 2018Article
- Article
- SK Channels Regulate Resting Properties and Signaling Reliability of a Developing Fast-Spiking Neuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.Scientific reports · 2015Article
- Article
- Aging decreases L-type calcium channel currents and pacemaker firing fidelity in substantia nigra dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Cell type-specific, presynaptic LTP of inhibitory synapses on fast-spiking GABAergic neurons in the mouse visual cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Physiological phenotype and vulnerability in Parkinson's disease.Cold Spring Harbor perspectives in medicine · 2012Review
- Protective Roles for Potassium SK/K(Ca)2 Channels in Microglia and Neurons.Frontiers in pharmacology · 2012Article
- Functional upregulation of Ca(2+)-activated K(+) channels in the development of substantia nigra dopamine neurons.PloS one · 2012Article
- The role of calcium and mitochondrial oxidant stress in the loss of substantia nigra pars compacta dopaminergic neurons in Parkinson's disease.Neuroscience · 2011Review
- The transient receptor potential channel antagonist SKF96365 is a potent blocker of low-voltage-activated T-type calcium channels.British journal of pharmacology · 2010Article
- Calcium homeostasis, selective vulnerability and Parkinson's disease.Trends in neurosciences · 2009Review
- Ca(2+) signaling by T-type Ca(2+) channels in neurons.Pflugers Archiv : European journal of physiology · 2009Review
- Metabotropic glutamate receptor type 5-dependent long-term potentiation of excitatory synapses on fast-spiking GABAergic neurons in mouse visual cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Nonselective cation channels are essential for maintaining intracellular Ca2+ levels and spontaneous firing activity in the midbrain dopamine neurons.Pflugers Archiv : European journal of physiology · 2007Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
During early postnatal development, midbrain dopamine (DA) neurons display anomalous firing patterns and amphetamine response. Spontaneous miniature hyperpolarizations (SMHs) are observed in DA neurons during the same period but not in adults. These hyperpolarizations have been shown to be dependent on the release of Ca2+ from internal stores and the subsequent activation of Ca2+-sensitive K+ channels. However, the triggering mechanism and the functional significance of SMHs remain poorly understood. To address these issues, using brain slices, we recorded spontaneous miniature outward currents (SMOCs) in DA neurons of neonatal rats. Two types of SMOCs were identified based on the peak amplitude. Both types were suppressed by intracellular dialysis of ruthenium red, a ryanodine receptor (RyR) antagonist, yet none of the known Ca2+-releasing messengers were involved. T-type Ca2+ channel blockers (Ni2+ and mibefradil) inhibited large-amplitude SMOCs without affecting the small-amplitude ones. The voltage dependence of SMOCs displayed a peak of approximately -50 mV, consistent with the involvement of low-threshold T-type Ca2+ channels. Blockade of SMOCs with cyclopiazonic acid or ryanodine converted the irregular firing of DA neurons in neonatal rats into an adult-like pacemaker pattern. This effect was reversed by the injection of artificial currents mimicking SMOCs. Finally, amphetamine inhibited SMOCs and transformed the irregular firing pattern into a more regular one. These data demonstrate that Ca2+ influx through T-type Ca2+ channels, followed by Ca2+-induced Ca2+ release via RyRs, contributes to the generation of SMOCs. We propose that SMOCs-SMHs may underlie the anomalous firing and amphetamine response of DA neurons during the postnatal developmental period.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.