ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Cholinergic suppression of KCNQ channel currents enhances excitability of striatal medium spiny neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 236 citations in OpenAlex.
- Cholinergic interneuron control of GABAergic circuits targeting spiny projection neurons is disrupted in parkinsonian models.bioRxiv : the preprint server for biology · 2026Article
- Cannabidiol dose modulates behavioral response to acute and repeated administration of Δ9-Tetrahydrocannabinol by strain and sex.bioRxiv : the preprint server for biology · 2026Article
- Postnatal reduction of eIF4E overexpression in D1-SPNs ameliorates KCNQ channel dysfunction, hyperexcitability and ASD-like behaviours.Cellular and molecular life sciences : CMLS · 2026Article
- An anatomical hotspot for striatal dopamine-acetylcholine interactions during reward and movement.bioRxiv : the preprint server for biology · 2026Article
- Striatal cholinergic interneurons exhibit compartment-specific anatomical and functional organization in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dual cholinergic mechanisms for sculpting striatal dopamine in vivo.bioRxiv : the preprint server for biology · 2025Article
- Cannabidiol Reduces D1 and D2 Medium Spiny Neuron Excitability in the Nucleus Accumbens Core.bioRxiv : the preprint server for biology · 2025Article
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.Science advances · 2025Article
- Distinct spatially organized striatum-wide acetylcholine dynamics for the learning and extinction of Pavlovian associations.Nature communications · 2025Article
- Does Dysregulation Of The Indirect Pathway Contribute To The Pathophysiology Of Catatonia Through Neurotransmitter Imbalance?Clinical neuropsychiatry · 2025Article
- Repetitive Levodopa Treatment Drives Cell Type-Specific Striatal Adaptations Associated With Progressive Dyskinesia in Parkinsonian Mice.bioRxiv : the preprint server for biology · 2025Article
- Neuroligin 1 Regulates Autistic-Like Repetitive Behavior through Modulating the Activity of Striatal D2 Receptor-Expressing Medium Spiny Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.bioRxiv : the preprint server for biology · 2025Article
- Quantitative Systems Pharmacology Development and Application in Neuroscience.Handbook of experimental pharmacology · 2025Review
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- Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens.Cellular and molecular life sciences : CMLS · 2024Article
- Early deficits in an in vitro striatal microcircuit model carrying the Parkinson's GBA-N370S mutation.NPJ Parkinson's disease · 2024Article
- Regional heterogeneity in the membrane properties of mouse striatal neurons.Frontiers in cellular neuroscience · 2024Article
- Distributed dopaminergic signaling in the basal ganglia and its relationship to motor disability in Parkinson's disease.Current opinion in neurobiology · 2023Review
65 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In response to glutamatergic synaptic drive, striatal medium spiny neurons in vivo transition to a depolarized "up state" near spike threshold. In the up state, medium spiny neurons either depolarize enough to spike or remain below spike threshold and are silent before returning to the hyperpolarized "down state." Previous work has suggested that subthreshold K+ channel currents were responsible for this dichotomous behavior, but the channels giving rise to the current and the factors determining its engagement have been a mystery. To move toward resolution of these questions, perforated-patch recordings from medium spiny neurons in tissue slices were performed. K+ channels with pharmacological and kinetic features of KCNQ channels potently regulated spiking at up-state potentials. Single-cell reverse transcriptase-PCR confirmed the expression of KCNQ2, KCNQ3, and KCNQ5 mRNAs in medium spiny neurons. KCNQ channel currents in these cells were potently reduced by M1 muscarinic receptors, because the effects of carbachol were blocked by M1 receptor antagonists and lost in neurons lacking M1 receptors. Reversal of the modulation was blocked by a phosphoinositol 4-kinase inhibitor, indicating a requirement for phosphotidylinositol 4,5-bisphosphate resynthesis for recovery. Inhibition of protein kinase C reduced the efficacy of the muscarinic modulation. Finally, acceleration of cholinergic interneuron spiking with 4-aminopyridine mimicked the effects of exogenous agonist application. Together, these results show that KCNQ channels are potent regulators of the excitability of medium spiny neurons at up-state potentials, and they are modulated by intrastriatal cholinergic interneurons, providing a mechanistic explanation for variability in spiking during up states seen in vivo.
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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.