ArticleJournal of neurophysiology2013
Regulation of dendritic calcium release in striatal spiny projection neurons.
Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
- Mechanistic explanation of neuroplasticity using equivalent circuits.Frontiers in computational neuroscience · 2026Article
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- Endoplasmic Reticulum Calcium Signaling in Hippocampal Neurons.Biomolecules · 2024Review
- CaCell reports · 2024Article
- Astragaloside IV protects brain cells from ischemia-reperfusion injury by inhibiting ryanodine receptor expression and reducing the expression of P-Src and P-GRK2.Scientific reports · 2024Article
- Distributed dopaminergic signaling in the basal ganglia and its relationship to motor disability in Parkinson's disease.Current opinion in neurobiology · 2023Review
- Making time and space for calcium control of neuron activity.Current opinion in neurobiology · 2023Review
- Pathway-specific alterations in striatal excitability and cholinergic modulation in a SAPAP3 mouse model of compulsive motor behavior.Cell reports · 2023Article
- A Pathogenic Missense Mutation in Kainate Receptors Elevates Dendritic Excitability and Synaptic Integration through Dysregulation of SK Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- CaBritish journal of pharmacology · 2023Review
- Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.Nature communications · 2023Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023Review
- A Conditioned Place Preference for Heroin Is Signaled by Increased Dopamine and Direct Pathway Activity and Decreased Indirect Pathway Activity in the Nucleus Accumbens.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Small Molecules as Modulators of Voltage-Gated Calcium Channels in Neurological Disorders: State of the Art and Perspectives.Molecules (Basel, Switzerland) · 2022Review
- Current Knowledge on the Background, Pathophysiology and Treatment of Levodopa-Induced Dyskinesia-Literature Review.Journal of clinical medicine · 2021Review
- Dopamine Oppositely Modulates State Transitions in Striosome and Matrix Direct Pathway Striatal Spiny Neurons.Neuron · 2020Article
- Local Postsynaptic Signaling on Slow Time Scales in Reciprocal Olfactory Bulb Granule Cell Spines Matches Asynchronous Release.Frontiers in synaptic neuroscience · 2020Article
- Thinking Outside the Box (and Arrow): Current Themes in Striatal Dysfunction in Movement Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Article
- Endoplasmic reticulum stress alters ryanodine receptor function in the murine pancreatic β cell.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The induction of corticostriatal long-term depression (LTD) in striatal spiny projection neurons (SPNs) requires coactivation of group I metabotropic glutamate receptors (mGluRs) and L-type Ca(2+) channels. This combination leads to the postsynaptic production of endocannabinoids that act presynaptically to reduce glutamate release. Although the necessity of coactivation is agreed upon, why it is necessary in physiologically meaningful settings is not. The studies described here attempt to answer this question by using two-photon laser scanning microscopy and patch-clamp electrophysiology to interrogate the dendritic synapses of SPNs in ex vivo brain slices from transgenic mice. These experiments revealed that postsynaptic action potentials induce robust ryanodine receptor (RYR)-dependent Ca(2+)-induced-Ca(2+) release (CICR) in SPN dendritic spines. Depolarization-induced opening of voltage-gated Ca(2+) channels was necessary for CICR. CICR was more robust in indirect pathway SPNs than in direct pathway SPNs, particularly in distal dendrites. Although it did not increase intracellular Ca(2+) concentration alone, group I mGluR activation enhanced CICR and slowed Ca(2+) clearance, extending the activity-evoked intraspine transient. The mGluR modulation of CICR was sensitive to antagonism of inositol trisphosphate receptors, RYRs, src kinase, and Cav1.3 L-type Ca(2+) channels. Uncaging glutamate at individual spines effectively activated mGluRs and facilitated CICR induced by back-propagating action potentials. Disrupting CICR by antagonizing RYRs prevented the induction of corticostriatal LTD with spike-timing protocols. In contrast, mGluRs had no effect on the induction of long-term potentiation. Taken together, these results make clearer how coactivation of mGluRs and L-type Ca(2+) channels promotes the induction of activity-dependent LTD in SPNs.
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Registered trials
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.