ArticleThe Journal of physiology2013
Parvalbumin tunes spike-timing and efferent short-term plasticity in striatal fast spiking interneurons.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 93 citations in OpenAlex.
- Limited sucrose intake produces subregion-specific remodeling of perineuronal nets in the medial prefrontal cortex.Brain structure & function · 2026Article
- Prefrontal parvalbumin neurons as a target for enhancing cognition in non-pathological and 22q11.2 microdeletion syndrome mice.Molecular psychiatry · 2026Article
- Maternal Acrylamide Exposure Modulates Parvalbumin-Positive Interneurons in the Subiculum and Hippocampus of Rat Offspring.Biomolecules · 2026Article
- Loss of Thy1 in Cortico-Striatal Pathways Alters Response to Dopamine and Gabapentin.ASN neuro · 2026Article
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- Early synaptic dysfunction of striatal parvalbumin interneurons in a mouse model of Parkinson's disease.iScience · 2024Article
- Parvalbumin gates chronic pain through the modulation of firing patterns in inhibitory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sex differences in the distribution and density of regulatory interneurons in the striatum.bioRxiv : the preprint server for biology · 2024Article
- Sex differences in the distribution and density of regulatory interneurons in the striatum.Frontiers in cellular neuroscience · 2024Article
- Regional heterogeneity in the membrane properties of mouse striatal neurons.Frontiers in cellular neuroscience · 2024Article
- Modulation of SK Channels via Calcium Buffering Tunes Intrinsic Excitability of Parvalbumin Interneurons in Neuropathic Pain: A Computational and Experimental Investigation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Functional Autapses Form in Striatal Parvalbumin Interneurons but not Medium Spiny Projection Neurons.Neuroscience bulletin · 2023Article
- Bicuculline restores frequency-dependent hippocampal I/E ratio and circuit function in PGC-1ɑ null mice.Neuroscience research · 2022Article
- Tics: neurological disorders determined by a deficit in sensorimotor gating processes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Loss of KCC2 in GABAergic Neurons Causes Seizures and an Imbalance of Cortical Interneurons.Frontiers in molecular neuroscience · 2022Article
- PV-specific loss of the transcriptional coactivator PGC-1α slows down the evolution of epileptic activity in an acute ictogenic model.Journal of neurophysiology · 2022Article
- Estrogen-related Receptor Alpha (ERRα) is Required for PGC-1α-dependent Gene Expression in the Mouse Brain.Neuroscience · 2021Article
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- Operant conditioning deficits and modified local field potential activities in parvalbumin-deficient mice.Scientific reports · 2021Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Striatal fast spiking interneurons (FSIs) modulate output of the striatum by synchronizing medium-sized spiny neurons (MSNs). Recent studies have broadened our understanding of FSIs, showing that they are implicated in severe motor disorders such as parkinsonism, dystonia and Tourette syndrome. FSIs are the only striatal neurons to express the calcium-binding protein parvalbumin (PV). This selective expression of PV raises questions about the functional role of this Ca(2+) buffer in controlling FSI Ca(2+) dynamics and, consequently, FSI spiking mode and neurotransmission. To study the functional involvement of FSIs in striatal microcircuit activity and the role of PV in FSI function, we performed perforated patch recordings on enhanced green fluorescent protein-expressing FSIs in brain slices from control and PV-/- mice. Our results revealed that PV-/- FSIs fired more regularly and were more excitable than control FSIs by a mechanism in which Ca(2+) buffering is linked to spiking activity as a result of the activation of small conductance Ca(2+)-dependent K(+) channels. A modelling approach of striatal FSIs supports our experimental results. Furthermore, PV deletion modified frequency-specific short-term plasticity at inhibitory FSI to MSN synapses. Our results therefore reinforce the hypothesis that in FSIs, PV is crucial for fine-tuning of the temporal responses of the FSI network and for the orchestration of MSN populations. This, in turn, may play a direct role in the generation and pathology-related worsening of motor rhythms.
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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.