This finding was substantiated when

This finding was substantiated when selenoprotein biosynthesis was inactivated selectively inneurons, through the conditional inactivation of tRNA[Ser]Sec [17]. Specifically, parvalbumin(PV)-expressing neurons, a subset of GABAergic interneurons, were completely lacking inthe somatosensory cortex and hippocampus of CamK-Cre; Trspfl/fl mice, while the principalneurons and calretinin (CR) expressing interneurons were apparently less affected or only affected later [17]. Interestingly, cortical PV+ interneurons express Lrp8, the Sepp receptor[18]. The critical selenoprotein in the brain is GPx4, since lack of PV+ GABA ergicinterneurons was also observed in mice deficient in neuronal GPx4 [7, 17]. Similarly, in arelated mouse model, which targeted Gpx4 in cerebellar neurons, Purkinje cells degenerated along parasagittal stripes, and cerebellar hypoplasia was associated with reducedproliferation of granule cells and increased apoptosis [19]. Remarkably, Purkinje cells arePV+ and use the GABA as their neurotransmitter.