ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Differential regulation of action potential- and metabotropic glutamate receptor-induced Ca2+ signals by inositol 1,4,5-trisphosphate in dopaminergic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
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- Transient Activation of GABAB Receptors Suppresses SK Channel Currents in Substantia Nigra Pars Compacta Dopaminergic Neurons.PloS one · 2016Article
- Cocaine Decreases Metabotropic Glutamate Receptor mGluR1 Currents in Dopamine Neurons by Activating mGluR5.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Somatodendritic dopamine release: recent mechanistic insights.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Tonic firing rate controls dendritic Ca2+ signaling and synaptic gain in substantia nigra dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Cocaine increases dopaminergic neuron and motor activity via midbrain α1 adrenergic signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Synaptic changes induced by melanocortin signalling.Nature reviews. Neuroscience · 2014Review
- Food restriction increases glutamate receptor-mediated burst firing of dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- New insights on neurobiological mechanisms underlying alcohol addiction.Neuropharmacology · 2013Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ca2+ signals associated with action potentials (APs) and metabotropic glutamate receptor (mGluR) activation exert distinct influences on neuronal activity and synaptic plasticity. However, it is not clear how these two types of Ca2+ signals are differentially regulated by neurotransmitter inputs in a single neuron. We investigated this issue in dopaminergic neurons of the ventral midbrain using brain slices. Intracellular Ca2+ was assessed by measuring Ca2+-sensitive K+ currents or imaging the fluorescence of Ca2+ indicator dyes. Tonic activation of metabotropic neurotransmitter receptors (mGluRs, alpha1 adrenergic receptors, and muscarinic acetylcholine receptors), attained by superfusion of agonists or weak, sustained (approximately 1 s) synaptic stimulation, augmented AP-induced Ca2+ transients. In contrast, Ca2+ signals elicited by strong, transient (50-200 ms) activation of mGluRs with aspartate iontophoresis were suppressed by superfusion of agonists. These opposing effects on Ca2+ signals were both mediated by an increase in intracellular inositol 1,4,5-trisphosphate (IP3) levels, because they were blocked by heparin, an IP3 receptor antagonist, and reproduced by photolytic application of IP3. Evoking APs repetitively at low frequency (2 Hz) caused inactivation of IP3 receptors and abolished IP3 facilitation of single AP-induced Ca2+ signals, whereas facilitation of Ca2+ signals triggered by bursts of APs (five at 20 Hz) was attenuated by less than half. We further obtained evidence suggesting that the psychostimulant amphetamine may augment burst-induced Ca2+ signals via both depression of basal firing and production of IP3. We propose that intracellular IP3 tone provides a mechanism to selectively amplify burst-induced Ca2+ signals in dopaminergic neurons.
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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.