In rodents, the barrel cortex is a specialized area within the somatosensory cortex that processes signals from the mystacial whiskers. We investigated the normal development of myelination in the barrel cortex of mice, as well as the effects of sensory deprivation on this pattern. Deprivation was achieved by trimming the whiskers on one side of the face every other day from birth. In control mice, myelin was not present until postnatal day 14 and did not show prominence until postnatal day 30; adult levels of myelination were reached by the end of the second postnatal month. Unbiased stereology was used to estimate axon density in the interbarrel septal region and barrel walls as well as the barrel centers. Myelin was significantly more concentrated in the interbarrel septa/barrel walls than in the barrel centers in both control and sensory-deprived conditions. Sensory deprivation did not impact the onset of myelination but resulted in a significant decrease in myelinated axons in the barrel region and decreased the amount of myelin ensheathing each axon. Visualization of the oligodendrocyte nuclear marker Olig2 revealed a similar pattern of myelin as seen using histochemistry, but with no significant changes in Olig2+ nuclei following sensory deprivation. Consistent with the anatomical results showing less myelination, local field potentials revealed slower rise times following trimming. Our results suggest that myelination develops relatively late and can be influenced by sensory experience.

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A number of hypotheses have been postulated over time to explain the clinical expression of schizophrenia. In this article, we discuss the neurodevelopmental (pre and perinatal), neuroanatomical (enlarged ventricles and reduced whole brain volume), neurochemical (dopamine, serotonin, norepinephrine), and neuropsychological (learning and memory, theory of mind) factors that are often correlated with schizophrenic presentations. While many of these factors are seen in many schizophrenic individuals, there is no one neurological marker seen consistently across patients. As a result, neurological evidence may help one understand the experience of schizophrenic individuals, but it is unable to explain fully the disorder's etiology.

Schizophrenia is an enigmatic diagnosis, and the etiology of the illness is not well understood. A large body of research has investigated the genetic factors underlying schizophrenia in hope of a genotype-based etiological explanation for the schizophrenic phenotype. This first article in a five-part series reviews and explores the current and historical genetic research on the diagnosis, and questions the assumption that genetic variables hold the explanatory key for unlocking the development of the disorder. The authors of this article posit that the Gestalt therapy treatment model is an effective treatment, given the disparate factors contributing to the clinical presentation.