ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023
Modulation of SK Channels via Calcium Buffering Tunes Intrinsic Excitability of Parvalbumin Interneurons in Neuropathic Pain: A Computational and Experimental Investigation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 20 citations in OpenAlex.
- Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain.Nature communications · 2026Article
- Parvalbumin interneurons in Alzheimer's disease: Physiological insights and pathophysiological mechanisms.Journal of cell communication and signaling · 2026Review
- Rethinking parvalbumin: From passive marker to active modulator of hippocampal circuits.IBRO neuroscience reports · 2025Article
- In Search of Transcriptomic Correlates of Neuronal Firing-Rate Adaptation across Subtypes, Regions and Species: A Patch-seq Analysis.bioRxiv : the preprint server for biology · 2025Article
- Thoracic Spinal Cord Contusion Impacts on Lumbar Enlargement: Molecular Insights.Molecular neurobiology · 2025Article
- Synergistic deficits in parvalbumin interneurons and dopamine signaling drive ACC dysfunction in chronic pain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Mechanisms for dysregulation of excitatory-inhibitory balance underlying allodynia in dorsal horn neural subcircuits.PLoS computational biology · 2025Article
- Biophysical modeling and experimental analysis of the dynamics of C. elegans body-wall muscle cells.PLoS computational biology · 2025Article
- 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
- ElecFeX is a user-friendly toolbox for efficient feature extraction from single-cell electrophysiological recordings.Cell reports methods · 2024Article
- Sortilin-Mediated Inhibition of TREK1/2 Channels in Primary Sensory Neurons Promotes Prediabetic Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Sialyltransferase Mutations Alter the Expression of Calcium-Binding Interneurons in Mice Neocortex, Hippocampus and Striatum.International journal of molecular sciences · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Parvalbumin-expressing interneurons (PVINs) play a crucial role within the dorsal horn of the spinal cord by preventing touch inputs from activating pain circuits. In both male and female mice, nerve injury decreases PVINs' output via mechanisms that are not fully understood. In this study, we show that PVINs from nerve-injured male mice change their firing pattern from tonic to adaptive. To examine the ionic mechanisms responsible for this decreased output, we used a reparametrized Hodgkin-Huxley type model of PVINs, which predicted (1) the firing pattern transition is because of an increased contribution of small conductance calcium-activated potassium (SK) channels, enabled by (2) impairment in intracellular calcium buffering systems. Analyzing the dynamics of the Hodgkin-Huxley type model further demonstrated that a generalized Hopf bifurcation differentiates the two types of state transitions observed in the transient firing of PVINs. Importantly, this predicted mechanism holds true when we embed the PVIN model within the neuronal circuit model of the spinal dorsal horn. To experimentally validate this hypothesized mechanism, we used pharmacological modulators of SK channels and demonstrated that (1) tonic firing PVINs from naive male mice become adaptive when exposed to an SK channel activator, and (2) adapting PVINs from nerve-injured male mice return to tonic firing on SK channel blockade. Our work provides important insights into the cellular mechanism underlying the decreased output of PVINs in the spinal dorsal horn after nerve injury and highlights potential pharmacological targets for new and effective treatment approaches to neuropathic pain.
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