Autistic-like behaviour in the Parvalbumin knockout mouse

The EF-hand calcium-binding protein, parvalbumin (PV), is a cytosolic protein expressed in a subset of GABA-ergic interneurons of the cerebral cortex, Purkinje, stellate and basket cells of the cerebellum, fast-twitch skeletal muscle fibres and epithelial cells of the kidney distal nephron. It functions primarily as a mobile, slow acting calcium buffer and plays a principal role in intracellular calcium homeostasis. Studies on the PV knockout mouse (PV-/-) showed an outwardly normal phenotype and lifespan. However, skeletal muscle fibres showed a reduced relaxation rate and increased fatigue resistance, coupled to a ~50 % increase in mitochondrial volume [1]. This increase in mitochondria was also observed in the soma of Purkinje cells in PV-/mice [2]. The autism spectrum disorders (ASD) are human neurodevelopmental disorders, characterized primarily by impairments in social interaction / social communication and repetitive, restrictive behaviour. Autism is increasingly being seen as an impairment or imbalance of the GABA-ergic system and due to the selective expression pattern of PV, it was hypothesized that PV-deficiency would correlate with autistic-like behaviour.