ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
A Ca(2+) threshold for induction of spike-timing-dependent depression in the mouse striatum.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
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- Asymmetric Voltage Attenuation in Dendrites Can Enable Hierarchical Heterosynaptic Plasticity.eNeuro · 2023Article
- Glutamate spillover drives robust all-or-none dendritic plateau potentials-anFrontiers in cellular neuroscience · 2023Article
- Synaptic Plasticity Is Predicted by Spatiotemporal Firing Rate Patterns and Robust to In Vivo-like Variability.Biomolecules · 2022Article
- 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
- A silent eligibility trace enables dopamine-dependent synaptic plasticity for reinforcement learning in the mouse striatum.The European journal of neuroscience · 2019Article
- Molecular mechanisms underlying striatal synaptic plasticity: relevance to chronic alcohol consumption and seeking.The European journal of neuroscience · 2019Article
- Cholinergic modulation of striatal microcircuits.The European journal of neuroscience · 2019Review
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- Reinforcement determines the timing dependence of corticostriatal synaptic plasticity in vivo.Nature communications · 2017Article
- Calcium dynamics predict direction of synaptic plasticity in striatal spiny projection neurons.The European journal of neuroscience · 2017Article
- The Sodium Channel β4 Auxiliary Subunit Selectively Controls Long-Term Depression in Core Nucleus Accumbens Medium Spiny Neurons.Frontiers in cellular neuroscience · 2017Article
- M4 Muscarinic Receptor Signaling Ameliorates Striatal Plasticity Deficits in Models of L-DOPA-Induced Dyskinesia.Neuron · 2015Article
- Calcium: amplitude, duration, or location?The Biological bulletin · 2015Review
- The origin of glutamatergic synaptic inputs controls synaptic plasticity and its modulation by alcohol in mice nucleus accumbens.Frontiers in synaptic neuroscience · 2015Article
- Depression biased non-Hebbian spike-timing-dependent synaptic plasticity in the rat subiculum.The Journal of physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The striatum is the principal input nucleus of the basal ganglia, receiving glutamatergic afferents from the cerebral cortex. There is much interest in mechanisms of synaptic plasticity in the corticostriatal synapses. We used two-photon microscopy and whole-cell recording to measure changes in intracellular calcium concentration ([Ca(2+)](i)) associated with spike-time-dependent plasticity in mouse striatum. Uncaging glutamate adjacent to a dendritic spine caused a postsynaptic potential at the soma and a rise in spine [Ca(2+)](i). Action potentials elicited at the soma raised both dendrite and spine [Ca(2+)](i). Pairing protocols in which glutamate uncaging preceded action potentials by 10 ms (pre-post protocol) produced supralinear increases in spine [Ca(2+)](i) compared with the sum of increases seen with uncaging and action potentials alone, or timing protocols in which the uncaging followed the action potentials (post-pre protocols). The supralinear component of the increases in [Ca(2+)](i) were eliminated by the voltage-sensitive calcium channel blocker nimodipine. In the adjacent parent dendrites, the increases in [Ca(2+)](i) were neither supralinear nor sensitive to the relative pre-post timing. In parallel experiments, we investigated the effects of these pairing protocols on spike-timing-dependent synaptic plasticity. Long-term depression (t-LTD) of corticostriatal inputs was induced by pre-post but not post-pre protocols. Intracellular calcium chelators and calcium antagonists blocked pre-post t-LTD, confirming that elevated calcium entering via voltage-sensitive calcium channels is necessary for t-LTD. These findings confirm a spine [Ca(2+)](i) threshold for induction of t-LTD in the corticostriatal pathway, mediated by the supralinear increase in [Ca(2+)](i) associated with pre-post induction protocols.
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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.