Neurodegenerative and morphogenic changes in a mouse model of temporal lobe epilepsy do not depend on the expression of the calcium-binding proteins parvalbumin, calbindin, or calretinin

Calcium-binding proteins may not play a critical role in the neurochemical phenotype or excitability of the hippocampus in a kainate model of epilepsy.

• Single- and double-knockout mice lacking parvalbumin, calretinin, and calbindin D-28k showed no differences in hippocampal structure compared to wild-type mice.
• These mutant mice were not more susceptible to acute excitotoxicity from kainate or to long-term effects of recurrent seizures.
• Neurochemical alterations, such as the increase of neuropeptide Y in granule cells, were similar across all genotypes.
• Morphological changes, including the enlargement and dispersion of dentate gyrus granule cells, occurred similarly in both mutant and wild-type mice.
• The calcium-binding proteins investigated do not appear to influence gene expression changes in granule cells following seizures.

AI simplified