ArticlePain2018
NALCN channels enhance the intrinsic excitability of spinal projection neurons.
Article in Pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanisms and Cell Type-Dependence of Non-Hebbian Long-Term Potentiation at Primary Afferent Synapses in the Mouse Spinal Superficial Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- Article
- A Viral Labelling Study of Spinal Trigeminal Nucleus Caudalis Projection Neurons Targeting the Parabrachial Nucleus.Journal of neurochemistry · 2025Article
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Article
- Noise or signal? Spontaneous activity of dorsal horn neurons: patterns and function in health and disease.Pflugers Archiv : European journal of physiology · 2024Review
- Contributions of the Sodium Leak Channel NALCN to Pacemaking of Medial Ventral Tegmental Area and Substantia Nigra Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Sodium Leak Channel in Glutamatergic Neurons of the Lateral Parabrachial Nucleus Modulates Inflammatory Pain in Mice.International journal of molecular sciences · 2023Article
- Role of sodium leak channel (NALCN) in sensation and pain: an overview.Frontiers in pharmacology · 2023Review
- D1/D5 Dopamine Receptors and mGluR5 Jointly Enable Non-Hebbian Long-Term Potentiation at Sensory Synapses onto Lamina I Spinoparabrachial Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ.The Journal of physiology · 2021Article
- Elevated Expression and Activity of Sodium Leak Channel Contributes to Neuronal Sensitization of Inflammatory Pain in Rats.Frontiers in molecular neuroscience · 2021Article
- A Leptin-Mediated Neural Mechanism Linking Breathing to Metabolism.Cell reports · 2020Article
- Volatile Anesthetics Activate a Leak Sodium Conductance in Retrotrapezoid Nucleus Neurons to Maintain Breathing during Anesthesia in Mice.Anesthesiology · 2020Article
- Intellectual disability-associated UNC80 mutations reveal inter-subunit interaction and dendritic function of the NALCN channel complex.Nature communications · 2020Article
- Article
- Methylation determines the extracellular calcium sensitivity of the leak channel NALCN in hippocampal dentate granule cells.Experimental & molecular medicine · 2019Article
- Functional expression of CLIFAHDD and IHPRF pathogenic variants of the NALCN channel in neuronal cells reveals both gain- and loss-of-function properties.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal projection neurons convey nociceptive signals to multiple brain regions including the parabrachial (PB) nucleus, which contributes to the emotional valence of pain perception. Despite the clear importance of projection neurons to pain processing, our understanding of the factors that shape their intrinsic membrane excitability remains limited. Here, we investigate a potential role for the Na leak channel NALCN in regulating the activity of spino-PB neurons in the developing rodent. Pharmacological reduction of NALCN current (INALCN), or the genetic deletion of NALCN channels, significantly reduced the intrinsic excitability of lamina I spino-PB neurons. In addition, substance P (SP) activated INALCN in ascending projection neurons through downstream Src kinase signaling, and the knockout of NALCN prevented SP-evoked action potential discharge in this neuronal population. These results identify, for the first time, NALCN as a strong regulator of neuronal activity within central pain circuits and also elucidate an additional ionic mechanism by which SP can modulate spinal nociceptive processing. Collectively, these findings indicate that the level of NALCN conductance within spino-PB neurons tightly governs ascending nociceptive transmission to the brain and thereby potentially influences pain perception.
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Registered trials
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.