On 2013 Dec 28, Tsuyoshi Miyakawa commented:

Reduction in the number of parvalbumin positive cells is one of the most consistently observed phenomena in the post-mortem brains of the patients with schizophrenia. This excellent paper provides the evidence supporting the idea that the reduction reflects the immaturity of the type of the cells (fast-spiking GABAergic interneurons (FS neurons)), instead of the reduction of the number of the types of the cells. The reduction of perineuronal net, a maturation marker of the neurons, in the postmortem brains of schizophrenia patients (Pantazopoulos H, 2010) is also in line with this idea. This may not be trivial, since, if it is the case, an approach to get them normally mature could be a potential therapeutic strategy. These important findings raise another question. Is such pseudo-immature status of the type of neurons due to maturation failure or de-maturation of the neurons? There are some evidence that FS neurons may undergo de-maturation by some experimental manipulations, such as chronic fluoxetine treatment (Karpova NN, 2011; Ohira K, 2013) and environmental enrichment (Donato F, 2013). Let me also point out that reduction of parvalbumin is associated with pseudo-immaturity of granule cells in the dentate gyrus in adulthood in the mice lacking a transcription factor, schnurri-2 (also known as MHC enhancer binding protein 2 or human immunodeficiency virus type I enhancer binding protein 2 (HIVEP2)) (Takao K, 2013). We consider schnurri-2 KO mice as an animal model of schizophrenia and, in these mice, pseudo-immaturity of granule cells seem to be due to de-maturation (Supplementary Figure 9 in Takao K, 2013). Considering these findings, it is quite possible that the pseudo-immaturity of FS neurons could also be due to de-maturation (, though it is still quite speculative).

On 2013 Dec 28, Tsuyoshi Miyakawa commented:

Reduction in the number of parvalbumin positive cells is one of the most consistently observed phenomena in the post-mortem brains of the patients with schizophrenia. This excellent paper provides the evidence supporting the idea that the reduction reflects the immaturity of the type of the cells (fast-spiking GABAergic interneurons (FS neurons)), instead of the reduction of the number of the types of the cells. The reduction of perineuronal net, a maturation marker of the neurons, in the postmortem brains of schizophrenia patients (Pantazopoulos H, 2010) is also in line with this idea. This may not be trivial, since, if it is the case, an approach to get them normally mature could be a potential therapeutic strategy. These important findings raise another question. Is such pseudo-immature status of the type of neurons due to maturation failure or de-maturation of the neurons? There are some evidence that FS neurons may undergo de-maturation by some experimental manipulations, such as chronic fluoxetine treatment (Karpova NN, 2011; Ohira K, 2013) and environmental enrichment (Donato F, 2013). Let me also point out that reduction of parvalbumin is associated with pseudo-immaturity of granule cells in the dentate gyrus in adulthood in the mice lacking a transcription factor, schnurri-2 (also known as MHC enhancer binding protein 2 or human immunodeficiency virus type I enhancer binding protein 2 (HIVEP2)) (Takao K, 2013). We consider schnurri-2 KO mice as an animal model of schizophrenia and, in these mice, pseudo-immaturity of granule cells seem to be due to de-maturation (Supplementary Figure 9 in Takao K, 2013). Considering these findings, it is quite possible that the pseudo-immaturity of FS neurons could also be due to de-maturation (, though it is still quite speculative).