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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.

|August 5, 2015

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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.

Keywords:

epileptogenesis gene expression ictogenesis mouse model seizure voltage-gated calcium channel

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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.