Prospective Investigation of Video Game Use in Children and Subsequent Conduct Disorder and Depression Using Data from the Avon Longitudinal Study of Parents and Children.

There is increasing public and scientific concern regarding the long-term behavioural effects of video game use in children, but currently little consensus as to the nature of any such relationships. We investigated the relationship between video game use in children, degree of violence in games, and measures of depression and a 6-level banded measure of conduct disorder. Data from the Avon Longitudinal Study of Parents and Children were used. A 3-level measure of game use at age 8/9 years was developed, taking into account degree of violence based on game genre. Associations with conduct disorder and depression, measured at age 15, were investigated using ordinal logistic regression, adjusted for a number of potential confounders. Shoot-em-up games were associated with conduct disorder bands, and with a binary measure of conduct disorder, although the strength of evidence for these associations was weak. A sensitivity analysis comparing those who play competitive games to those who play shoot-em-ups found weak evidence supporting the hypothesis that it is violence rather than competitiveness that is associated with conduct disorder. However this analysis was underpowered, and we cannot rule out the possibility that increasing levels of competition in games may be just as likely to account for the observed associations as violent content. Overall game exposure as indicated by number of games in a household was not related to conduct disorder, nor was any association found between shoot-em-up video game use and depression.

Delayed expression of the Crx gene and photoreceptor development in the Chx10-deficient retina.

PURPOSE: The Chx10 homeobox gene is expressed in neural progenitor cells during retinal development. The absence of Chx10 causes microphthalmia in humans and in the mouse mutant ocular retardation. The purpose of this study was to examine how neuronal development is affected by absence of the Chx10 transcription factor in the mouse retina. METHODS: Expression of transcription factor genes, Crx, Pou4f2, and Pax6, that mark specific cell types as they begin to differentiate was analyzed by RNA in situ hybridization of retina from wild-type and Chx10-null ocular retardation mice (Chx10(or-J/or-J)). RT-PCR analysis was used to compare expression of these genes and putative targets of Crx regulation. Photoreceptor development was analyzed by using peanut agglutinin (PNA)-rhodamine and blue cone opsin antibody to label cones and rhodopsin antibody to label rods. RESULTS: The photoreceptor gene Crx, normally expressed during embryonic retinal development, was not detected in the embryonic mutant retina, but was expressed after birth. Expression of the targets of Crx regulation, rhodopsin, peripherin, rod phosphodiesterase beta (Pdeb), and arrestin, with the exception of interphotoreceptor retinoid binding protein (Irbp), was delayed in the Chx10(or-J/or-J) retina. Rhodopsin localization in rod outer segments was also delayed. By contrast, temporal and spatial expression of Pou4f2 and Pax6 in developing ganglion and amacrine cells and PNA and blue opsin in developing cone cells was relatively normal in the mutant. CONCLUSIONS: Delay of the normal temporal expression of genes essential for photoreceptor disc morphogenesis leads to failure of correct rod and cone outer segment formation in the Chx10(or-J/or-J) mutant retina. In addition, the absence of Chx10 appears to affect the development of late-born cells more than that of early-born cells, in that a low number of rods develops, whereas formation of ganglion, amacrine, and cone cells is relatively unaffected.