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In vivo activity-dependent plasticity at cortico-striatal connections: evidence for physiological long-term potentiation.
Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):7036-40. doi: 10.1073/pnas.94.13.7036.
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Bidirectional activity-dependent plasticity at corticostriatal synapses.
J Neurosci. 2005 Dec 7;25(49):11279-87. doi: 10.1523/JNEUROSCI.4476-05.2005.
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Long-term synaptic depression in the striatum: physiological and pharmacological characterization.
J Neurosci. 1992 Nov;12(11):4224-33. doi: 10.1523/JNEUROSCI.12-11-04224.1992.
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Dopamine receptor activation is required for corticostriatal spike-timing-dependent plasticity.
J Neurosci. 2008 Mar 5;28(10):2435-46. doi: 10.1523/JNEUROSCI.4402-07.2008.
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Altered function of glutamatergic cortico-striatal synapses causes output pathway abnormalities in a chronic model of parkinsonism.
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Bi-directional changes in synaptic plasticity induced at corticostriatal synapses in vitro.
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Cell-specific spike-timing-dependent plasticity in GABAergic and cholinergic interneurons in corticostriatal rat brain slices.
J Physiol. 2008 Jan 1;586(1):265-82. doi: 10.1113/jphysiol.2007.144501. Epub 2007 Nov 1.
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Spike-dependent intrinsic plasticity increases firing probability in rat striatal neurons in vivo.
J Physiol. 2003 Aug 1;550(Pt 3):947-59. doi: 10.1113/jphysiol.2003.043125. Epub 2003 Jul 4.

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Dynamic regulation of corticostriatal glutamatergic synaptic expression during reversal learning in male mice.
Neurobiol Learn Mem. 2024 Feb;208:107892. doi: 10.1016/j.nlm.2024.107892. Epub 2024 Jan 17.
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Spike-Timing-Dependent Plasticity Mediated by Dopamine and its Role in Parkinson's Disease Pathophysiology.
Front Netw Physiol. 2022 Mar 4;2:817524. doi: 10.3389/fnetp.2022.817524. eCollection 2022.
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Compensatory Relearning Following Stroke: Cellular and Plasticity Mechanisms in Rodents.
Front Neurosci. 2019 Jan 31;12:1023. doi: 10.3389/fnins.2018.01023. eCollection 2018.
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The effects of electrical stimulation of the peripheral vestibular system on neurochemical release in the rat striatum.
PLoS One. 2018 Oct 29;13(10):e0205869. doi: 10.1371/journal.pone.0205869. eCollection 2018.
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The α2δ-1-NMDA receptor coupling is essential for corticostriatal long-term potentiation and is involved in learning and memory.
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A competitive model for striatal action selection.
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Building action repertoires: memory and learning functions of the basal ganglia.
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The corticostriatal projection: from synaptic plasticity to dysfunctions of the basal ganglia.
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Depression of excitatory synaptic input in rat striatal neurons.
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A synaptic model of memory: long-term potentiation in the hippocampus.
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