ArticlePain2017
Neuropathic pain after chronic nerve constriction may not correlate with chloride dysregulation in mouse trigeminal nucleus caudalis neurons.
Article in Pain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Electrotherapy in the management of neuropathic corneal pain: narrative review.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- A glutamatergic brain neural circuit is critical for modulating trigeminal neuropathic pain.Pain · 2025Article
- The P2X7 Hypothesis of Central Post-Stroke Pain.International journal of molecular sciences · 2024Article
- Epigenetic combined with transcriptomic analysis of the m6A methylome after spared nerve injury-induced neuropathic pain in mice.Neural regeneration research · 2023Article
- Long March Toward Safe and Effective Analgesia by Enhancing Gene Expression ofFrontiers in molecular neuroscience · 2022Review
- Potential Molecular Targets for Treating Neuropathic Orofacial Pain Based on Current Findings in Animal Models.International journal of molecular sciences · 2021Review
- Mechanisms of Peripheral and Central Pain Sensitization: Focus on Ocular Pain.Frontiers in pharmacology · 2021Review
- An Amygdalo-Parabrachial Pathway Regulates Pain Perception and Chronic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Substance P and pain chronicity.Cell and tissue research · 2019Review
- αFrontiers in pharmacology · 2018Article
- The grimace scale reliably assesses chronic pain in a rodent model of trigeminal neuropathic pain.Neurobiology of pain (Cambridge, Mass.) · 2017Article
- Article
- In search of a rodent model of placebo analgesia in chronic orofacial neuropathic pain.Neurobiology of pain (Cambridge, Mass.)Article
- Amplified parabrachial nucleus activity in a rat model of trigeminal neuropathic pain.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Changes in chloride reversal potential in rat spinal cord neurons have previously been associated with persistent pain in nerve injury and inflammation models. These changes correlate with a decrease in the expression of the potassium chloride transporter, KCC2, and with increases in neuronal excitability. Here, we test the hypothesis that similar changes occur in mice with neuropathic pain induced by chronic constriction injury of the trigeminal infraorbital nerve (CCI-ION). This model allows us to distinguish an acute pain phase (3-5 days after injury) from a persistent pain phase (12-14 days after CCI-ION). Chronic constriction injury of the trigeminal infraorbital nerve induced significant decreases in mechanical pain thresholds in both the acute and persistent phases. To estimate GABAA reversal potentials in neurons from trigeminal nucleus caudalis, we obtained perforated patch recordings in vitro. GABAA reversal potential decreased by 8% during the acute phase in unidentified neurons, but not in GABAergic interneurons. However, at 12 to 14 days after CCI-ION, GABAA reversal potential recovered to normal values. Quantitative real-time polymerase chain reaction analysis revealed no significant changes, at either 3 to 5 days or 12 to 14 days after CCI-ION, in either KCC2 or NKCC1. These findings suggest that CCI-ION in mice results in transient and modest changes in chloride reversal potentials, and that these changes may not persist during the late phase. This suggests that, in the mouse model of CCI-ION, chloride dysregulation may not have a prominent role in the central mechanisms leading to the maintenance of chronic pain.
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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.