"Calcium Channels, T-Type" - Books

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Select item 23871561.

Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition.

Noebels JL, Avoli M, Rogawski MA, et al., editors.

Bethesda (MD): National Center for Biotechnology Information (US); 2012.

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Select item 57048762.

Jasper's Basic Mechanisms of the Epilepsies. 5th edition.

Noebels JL, Avoli M, Rogawski MA, et al., editors.

New York: Oxford University Press; 2024.

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Select item 14152803.

Madame Curie Bioscience Database [Internet].

Austin (TX): Landes Bioscience; 2000-2013.

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Select item 44036684.

StatPearls [Internet].

Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

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Select item 23580525.

Probe Reports from the NIH Molecular Libraries Program [Internet].

Bethesda (MD): National Center for Biotechnology Information (US); 2010-.

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Select item 14051746.

The Epilepsies: Seizures, Syndromes and Management.

Panayiotopoulos CP.

Oxfordshire (UK): Bladon Medical Publishing; 2005.

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Select item 18602427.

WormBook: The Online Review of C. elegans Biology [Internet].

Pasadena (CA): WormBook; 2005-2018.

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Select item 34012948.

Endotext [Internet].

Feingold KR, Ahmed SF, Anawalt B, et al., editors.

South Dartmouth (MA): MDText.com, Inc.; 2000-.

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Select item 46267149.

Calcium Entry Channels in Non-Excitable Cells.

Kozak JA, Putney JW Jr, editors.

Boca Raton (FL): CRC Press/Taylor & Francis; 2018.

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Select item 480224610.

Nicotinic Acetylcholine Receptor Signaling in Neuroprotection [Internet].

Akaike A, Shimohama S, Misu Y, editors.

Singapore: Springer; 2018.

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Select item 255555411.

Translational Pain Research: From Mouse to Man.

Kruger L, Light AR, editors.

Boca Raton (FL): CRC Press/Taylor & Francis; 2010.

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Select item 254519612.

The Endothelium: Part 1: Multiple Functions of the Endothelial Cells—Focus on Endothelium-Derived Vasoactive Mediators.

Félétou M.

San Rafael (CA): Morgan & Claypool Life Sciences; 2011.

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Select item 188138213.

Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

Siegel GJ, Agranoff BW, Albers RW, et al., editors.

Philadelphia: Lippincott-Raven; 1999.

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Select item 567214414.

Cannabidiol (Epidiolex): Therapeutic area: Lennox-Gastaut syndrome: CADTH Reimbursement Review [Internet].

Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2024 Aug.

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Select item 455477415.

Magnesium in the Central Nervous System [Internet].

Vink R, Nechifor M, editors.

Adelaide (AU): University of Adelaide Press; 2011.

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Select item 556422616.

Cenobamate (Xcopri): CADTH Reimbursement Review: Therapeutic area: Epilepsy, partial onset seizures [Internet].

Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2023 Nov.

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Select item 553046817.

Cardiovascular Signaling in Health and Disease [Internet].

Parinandi NL, Hund TJ, editors.

Cham (CH): Springer; 2022.

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Select item 280561418.

Effectiveness and Safety of Antiepileptic Medications in Patients With Epilepsy [Internet].

Talati R, Scholle JM, Phung OJ, et al.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2011 Dec. (Comparative Effectiveness Reviews, No. 40.)

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Select item 265918219.

Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews [Internet].

York (UK): Centre for Reviews and Dissemination (UK); 1995-.

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Select item 449207020.

Neurobiology of TRP Channels.

Emir TLR, editor.

Boca Raton (FL): CRC Press/Taylor & Francis; 2017.

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Figure 3T-type calcium channels and absence epilepsy

(a-b) In the GAERS rodent model of absence epilepsy an arginine to proline missense mutation at position 1584 (R1584P) correlates with the expression of seizure activity. Mating GAERS with a non-epileptic strain (NEC) through two generations produces offspring that have no copies (wt/wt), one copy (wt/m) or two copies (m/m) of the R1584P mutation in an otherwise similar genetic background. Animals with two copies of the mutation spend increased time in seizure activity and experience more seizures than animals with no copies of the R1584P mutation. The missense GAERS mutation does not affect either the duration or morphology of individual seizures. (c) The WAG/Rij model of absence epilepsy displays increased expression of the Ca_V3.1 T-type calcium channel in thalamic centrolateral (CL) and lateral geniculate (LGN) neurons and of the Ca_V3.3 T-type in CL and RTN neurons. (d) In mice with a genetically enhanced expression of Ca_V3.1 channels (Tg1 and Tg2) larger T-type currents are observed in lateral dorsal (LDN) and ventrobasal (VB) thalamic neurons and the mice display spontaneous bilateral spike-wave discharges in EEG recordings.

Voltage-Gated Calcium Channels in Epilepsy.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.
Figure 22–2.

Ca_V3.1 and Ca_V3.3 are the dominant T-type calcium channel subunits expressed in TC relay nuclei and in the nRT. A. Sagittal section of mouse brain indicating location of the nRT and TC relay nuclei (labels are not drawn to scale). All images obtained from the Allen Brain Atlas (https://mouse.brain-map.org/search/index). B and C. Top: In-situ hybridization of mRNA probes against the α1 subunit of high-voltage activated P/Q and R-type calcium channels. Bottom: Fluorescent expression in magnified region (red box) to highlight the relative expression in nRT and TC relay nuclei. Staining intensity should not be compared across subunits, which were performed as different experiments; however, regional heterogeneity of subunit expression can be appreciated in each section. D–F. Same as in B and C, but for three α1 subunits types of low-voltage activated T-type calcium channels. Note the selective expression of Cacna1i (encoding the Ca_V3.3 T-type subunit) in the nRT, and lack of expression of Cacna1g (encoding the Ca_V3.1 T-type subunit) in the nRT. All images (A–F) obtained from the Allen Brain Atlas, as described in Lein et al. (2007).

Convergence of Thalamic Mechanisms in Genetic Epilepsies.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies. 5th edition. New York: Oxford University Press; 2024.
Figure 1Voltage-gated calcium channels

(a) Schematic illustrating the topography of the high voltage-activated calcium channel complex showing the main pore-forming α₁ subunit and ancillary subunits. The α₁ and δ subunits are integral membrane proteins, the β subunit is intracellular and binds directly to the α_1, while the α₂ subunit is thought to be largely extracellular. (b) Schematic diagram showing structure of the calcium channel α₁ subunit with its four domain structure. (c) The left panel shows the phylogenic relationship between the ten known calcium channel α₁ subunits. Ca_V1 subunits form the L-type subfamily, Ca_V2 channels the P/Q-type, N-type and R-type, and the Ca_V3 subunits form the low voltage-activated T-type calcium channels. The right panel shows representative traces of calcium currents recorded from reticular thalamic neurons in response to depolarization of the membrane potential. The upper trace shows a slow inactivating high voltage-activated current and the lower trace shows the fast inactivating low voltage-activated current.

Voltage-Gated Calcium Channels in Epilepsy.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.
Figure 21–3.

Pathophysiology of absence epilepsy. Monogenic mutations leading to absence epilepsy fit into a general scheme with entry points in decreasing fast feed-forward inhibition, increasing tonic inhibition and de-inactivation of T-type calcium channels. ¹Celli et al, Neuropharmacology 2020; ²Marks et al, Brain Behav Res 2019; Henbid et al, Exp Neuro 2017; Marks et al, Neuroscience 2016; Marks et al, Neurobio Dis 2016; Tringham et al, Sci Trans Med, 2012; ³Jafarian et al, Brain Res 2021; ⁴Leclercq et al, J Pharmacol Exp Ther 2020 (Padsenovil); Duveau et al, CNS Neurosci Ther 2019 (PF-06372865); ⁵Maheshwari et al, Epilepsia 2016; ⁶Krook-Magnuson et al, J Neurophys. 2008.

Cortical and Thalamic PV+ Interneuron Dysfunction in the Pathogenesis of Absence Epilepsy.

Noebels JL, Avoli M, Rogawski MA, et al., editors. Jasper's Basic Mechanisms of the Epilepsies. 5th edition. New York: Oxford University Press; 2024.