ArticleNeuroscience2014
Altered expression of the voltage-gated calcium channel subunit α₂δ-1: a comparison between two experimental models of epilepsy and a sensory nerve ligation model of neuropathic pain.
Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 26 citations in OpenAlex.
- Pregabalin Depresses Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission by Modulating Glun2a-Containing Nmda Receptors in Mice In Vitro.International journal of molecular sciences · 2026Article
- Salidroside Attenuates Epilepsy and Cognitive Dysfunction in Rats by Downregulating Complement C3-C3aR Pathway-Mediated Activation of Microglia and Astrocytes.Neurochemical research · 2025Article
- Evaluation ofACS chemical neuroscience · 2023Article
- Development of a PET radioligand for α2δ-1 subunit of calcium channels for imaging neuropathic pain.European journal of medicinal chemistry · 2022Article
- Response of Voltage-Gated Sodium and Calcium Channels Subtypes on Dehydroepiandrosterone Treatment in Iron-Induced Epilepsy.Cellular and molecular neurobiology · 2021Article
- Pregabalin Treatment does not Affect Amyloid Pathology in 5XFAD Mice.Current Alzheimer research · 2021Article
- Different functions of two putative Drosophila αScientific reports · 2020Article
- Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Calcium Channel Subunit α2δ4 Is Regulated by Early Growth Response 1 and Facilitates Epileptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The αCell reports · 2018Article
- Voltage-gated calcium channel αF1000Research · 2018Review
- Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction.OBM neurobiology · 2018Article
- Estrogen deficiency is associated with hippocampal morphological remodeling of early postmenopausal mice.Oncotarget · 2017Article
- Single-cell RNA-seq reveals distinct injury responses in different types of DRG sensory neurons.Scientific reports · 2016Article
- Dorsal root ganglion transcriptome analysis following peripheral nerve injury in mice.Molecular pain · 2016Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Mechanisms and Mediators That Drive Arthritis Pain.Current osteoporosis reports · 2015Review
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6 authors at 2 institutions in 1 country.
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Abstract
The auxiliary α2δ-1 subunit of voltage-gated calcium channels is up-regulated in dorsal root ganglion neurons following peripheral somatosensory nerve damage, in several animal models of neuropathic pain. The α2δ-1 protein has a mainly presynaptic localization, where it is associated with the calcium channels involved in neurotransmitter release. Relevant to the present study, α2δ-1 has been shown to be the therapeutic target of the gabapentinoid drugs in their alleviation of neuropathic pain. These drugs are also used in the treatment of certain epilepsies. In this study we therefore examined whether the level or distribution of α2δ-1 was altered in the hippocampus following experimental induction of epileptic seizures in rats, using both the kainic acid model of human temporal lobe epilepsy, in which status epilepticus is induced, and the tetanus toxin model in which status epilepticus is not involved. The main finding of this study is that we did not identify somatic overexpression of α2δ-1 in hippocampal neurons in either of the epilepsy models, unlike the upregulation of α2δ-1 that occurs following peripheral nerve damage to both somatosensory and motor neurons. However, we did observe local reorganization of α2δ-1 immunostaining in the hippocampus only in the kainic acid model, where it was associated with areas of neuronal cell loss, as indicated by absence of NeuN immunostaining, dendritic loss, as identified by areas where microtubule-associated protein-2 immunostaining was missing, and reactive gliosis, determined by regions of strong OX42 staining.
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