ArticleBrain research2010
Seizure susceptibility is associated with altered protein expression of voltage-gated calcium channel subunits in inferior colliculus neurons of the genetically epilepsy-prone rat.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Differential Expression of the β3 Subunit of Voltage-Gated CaMolecular neurobiology · 2023Article
- Activation of Calcium-Activated Chloride Channels Suppresses Inherited Seizure Susceptibility in Genetically Epilepsy-Prone Rats.Biomedicines · 2022Article
- Hyperexcitable superior colliculus and fatal brainstem spreading depolarization in a model of Sudden Unexpected Death in Epilepsy.Brain communications · 2022Article
- Rodent Brain Pathology, Audiogenic Epilepsy.Biomedicines · 2021Review
- Transcriptome of the Krushinsky-Molodkina Audiogenic Rat Strain and Identification of Possible Audiogenic Epilepsy-Associated Genes.Frontiers in molecular neuroscience · 2021Article
- Voltage-Dependent Calcium Channels, Calcium Binding Proteins, and Their Interaction in the Pathological Process of Epilepsy.International journal of molecular sciences · 2018Review
- Alcohol withdrawal upregulates mRNA encoding for CaAlcohol (Fayetteville, N.Y.) · 2018Article
- Genetically Epilepsy-Prone Rats Display Anxiety-Like Behaviors and Neuropsychiatric Comorbidities of Epilepsy.Frontiers in neurology · 2018Article
- CaEpilepsia · 2017Article
- Remote effects of short-term neonatal hyperthermia in Krushinsky-Molodkina rats prone to audiogenic seizures strain.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2017Article
- Abnormal alterations in the Ca²⁺/CaV1.2/calmodulin/caMKII signaling pathway in a tremor rat model and in cultured hippocampal neurons exposed to Mg²⁺-free solution.Molecular medicine reports · 2015Article
- Alcohol Withdrawal-Induced Seizure Susceptibility is Associated with an Upregulation of CaV1.3 Channels in the Rat Inferior Colliculus.The international journal of neuropsychopharmacology · 2015Article
- Postinhibitory rebound neurons and networks are disrupted in retrovirus-induced spongiform neurodegeneration.Journal of neurophysiology · 2014Article
- Rhythm and blues: animal models of epilepsy and depression comorbidity.Biochemical pharmacology · 2013Review
- Elucidating the mechanism of action of pregabalin: α(2)δ as a therapeutic target in anxiety.CNS drugs · 2012Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The inferior colliculus (IC) is the consensus site for seizure initiation in the genetically epilepsy-prone rat (GEPR). We have previously reported that the current density of high threshold voltage-activated (HVA) calcium (Ca(2+)) channels was markedly enhanced in IC neurons of the GEPR-3 (moderate seizure severity substrain of the GEPR). The present study examines whether subunit protein levels of HVA Ca(2+) channels are altered in IC neurons that exhibit enhanced Ca(2+) current density. Quantification shows that the levels of protein expression of the Ca(2+) channel pore-forming alpha1D (L-type) and alpha1E subunits (R-type) were significantly increased in IC neurons of seizure-naive GEPR-3s (SN-GEPR-3s) compared to control Sprague-Dawley (SD) rats. Significant increases and decreases in the levels of protein expression of Ca(2+) channel regulatory beta3 and alpha2delta subunits occurred in IC neurons of SN-GEPR-3s compared to control SD rats, respectively. No changes occurred in the protein expression of Ca(2+) channel pore-forming alpha1A (P/Q-type), alpha1B (N-type) and alpha1C (L-type) subunits in IC neurons of SN-GEPR-3s compared to control SD rats. A single seizure selectively enhanced protein expression of Ca(2+) channel alpha1A subunits in IC neurons of GEPR-3s. Thus, up-regulation of Ca(2+) channel alpha1D and alpha1E subunits may represent the molecular mechanisms for the enhanced current density of L- and R-type of HVA Ca(2+) channels in IC neurons of the GEPR, and may contribute to the genetic basis of their enhanced seizure susceptibility. The up-regulation of Ca(2+) channel alpha1A subunits induced by seizures may contribute to the increasing IC neuronal excitability that results from repetitive seizures in the GEPR.
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