ArticleThe Journal of clinical investigation2011
Modulation of subthalamic T-type Ca(2+) channels remedies locomotor deficits in a rat model of Parkinson disease.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Cerebellar neural populations orchestrate dopamine reward signaling with single-trial precision.Nature communications · 2026Article
- Cinnarizine, a Calcium Channel Blocker, Partially Prevents the Striatal Dopamine Decline and Loss of Nigral Dopamine Neurons in the Lactacystin-Induced Rat Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- Automated gait analysis indicates efficacy of T-type calcium channel inhibition for mitigation of disrupted calcium signalling in an SCA5 mouse model.Scientific reports · 2025Article
- Motor cortex stimulation ameliorates parkinsonian locomotor deficits: effectual and mechanistic differences from subthalamic modulation.NPJ Parkinson's disease · 2025Article
- Neural signatures of indirect pathway activity during subthalamic stimulation in Parkinson's disease.Nature communications · 2024Article
- Neuronal and synaptic adaptations underlying the benefits of deep brain stimulation for Parkinson's disease.Translational neurodegeneration · 2023Review
- T-type calcium channels as therapeutic targets in essential tremor and Parkinson's disease.Annals of clinical and translational neurology · 2023Review
- Review
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Efonidipine Inhibits JNK and NF-κB Pathway to Attenuate Inflammation and Cell Migration Induced by Lipopolysaccharide in Microglial Cells.Biomolecules & therapeutics · 2022Article
- Deep brain stimulation rectifies the noisy cortex and irresponsive subthalamus to improve parkinsonian locomotor activities.NPJ Parkinson's disease · 2022Article
- Small Molecules as Modulators of Voltage-Gated Calcium Channels in Neurological Disorders: State of the Art and Perspectives.Molecules (Basel, Switzerland) · 2022Review
- An electrophysiological perspective on Parkinson's disease: symptomatic pathogenesis and therapeutic approaches.Journal of biomedical science · 2021Review
- Sex Differences in Electrophysiological Properties of Mouse Medial Preoptic Area Neurons Revealed by In Vitro Whole-cell Recordings.Neuroscience bulletin · 2021Article
- Neural Burst Firing and Its Roles in Mental and Neurological Disorders.Frontiers in cellular neuroscience · 2021Article
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Zonisamide can ameliorate the voltage-dependence alteration of the T-type calcium channel CaMolecular brain · 2020Article
- Article
- Voltage-Gated Calcium Channels and α-Synuclein: Implications in Parkinson's Disease.Frontiers in molecular neuroscience · 2019Review
- Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits.The Journal of clinical investigation · 2018Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increase in neuronal burst activities in the subthalamic nucleus (STN) is a well-documented electrophysiological feature of Parkinson disease (PD). However, the causal relationship between subthalamic bursts and PD symptoms and the ionic mechanisms underlying the bursts remain to be established. Here, we have shown that T-type Ca(2+) channels are necessary for subthalamic burst firing and that pharmacological blockade of T-type Ca(2+) channels reduces motor deficits in a rat model of PD. Ni(2+), mibefradil, NNC 55-0396, and efonidipine, which inhibited T-type Ca(2+) currents in acutely dissociated STN neurons, but not Cd(2+) and nifedipine, which preferentially inhibited L-type or the other non–T-type Ca(2+) currents, effectively diminished burst activity in STN slices. Topical administration of inhibitors of T-type Ca(2+) channels decreased in vivo STN burst activity and dramatically reduced the locomotor deficits in a rat model of PD. Cd(2+) and nifedipine showed no such electrophysiological and behavioral effects. While low-frequency deep brain stimulation (DBS) has been considered ineffective in PD, we found that lengthening the duration of the low-frequency depolarizing pulse effectively improved behavioral measures of locomotion in the rat model of PD, presumably by decreasing the availability of T-type Ca(2+) channels. We therefore conclude that modulation of subthalamic T-type Ca(2+) currents and consequent burst discharges may provide new strategies for the treatment of PD.
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