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Pentylenetetrazole-Induced Kindling Mouse Model
Published on: June 12, 2018
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Increased sensitivity to kindling in mice lacking TSP1.
D Mendus1, E K Rankin-Gee2, M Mustapha3
1The Department of Neurology, School of Medicine, Stanford University, Stanford, CA 94305, USA; The Department of Otolaryngology - Head and Neck Surgery, School of Medicine, Stanford University, Stanford, CA 94305, USA.
Neuroscience
|August 5, 2015
Summary
Thrombospondin 1 (TSP1) deficiency increases seizure susceptibility in a mouse epilepsy model. TSP1 may regulate seizure risk by affecting calcium channel subunit levels.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Epilepsy development involves neuronal hyperexcitability.
- Thrombospondins (TSPs) modulate synaptogenesis via calcium channel binding.
- The role of TSPs in epilepsy pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the involvement of TSP1 and TSP2 in epilepsy development.
- To explore the relationship between TSPs, calcium channel subunits, and seizure susceptibility.
Main Methods:
- Utilized a pentylenetetrazole (PTZ) kindling model in mice lacking TSP1 and/or TSP2.
- Analyzed mRNA and protein levels of calcium channel subunits (CACNA2D1, CACNA2D2).
- Assessed seizure susceptibility and TGF-β signaling.
Main Results:
- TSP1 knockout (KO) mice showed increased PTZ kindling sensitivity.
- TSP1/2 KO mice exhibited similar PTZ sensitivity as TSP1 KO mice.
- Decreased CACNA2D2 mRNA and α2δ-1/2 protein levels were observed in TSP1 KO and TSP1/2 KO mice.
Conclusions:
- TSP1 deficiency enhances seizure susceptibility, potentially by reducing CACNA2D2 levels.
- TSP1 may act as a modifier of epilepsy risk through its regulation of calcium channel subunits.
