Social experience modulates ocular dominance plasticity differentially in adult male and female mice.

Environmental factors have long been known to regulate brain plasticity. We investigated the potential influence of social experience on ocular dominance plasticity. Fully adult female or male mice were monocularly deprived for four days and kept a) either alone or in pairs of the same sex and b) either in a small cage or a large, featureless arena. While mice kept alone did not show ocular dominance plasticity, no matter whether in a cage or in an arena, paired female mice in both environmental conditions displayed a shift of ocular dominance towards the open eye. Paired male mice, in contrast, showed no plasticity in the cage, but a very strong ocular dominance shift in the arena. This effect was not due to increased locomotion, since the covered distance was similar in single and paired male mice in the arena, and furnishing cages with a running wheel did not enable ocular dominance plasticity in cage-housed mice. Confirming recent results in rats, the plasticity-enhancing effect of the social environment was shown to be mediated by serotonin. Our results demonstrate that social experience has a strong effect on cortical plasticity that is sex-dependent. This has potential consequences both for animal research and for human education and rehabilitation.

Temporally coherent visual stimuli boost ocular dominance plasticity.

Does cortical plasticity depend on the temporal coherence of visual stimuli? We addressed this question by studying ocular dominance (OD) plasticity in mice that were stimulated by moving square wave gratings for 6 h/d during a period of monocular deprivation (MD). It turned out that 4 d of deprivation were sufficient to induce a saturated shift in plasticity in adult (older than postnatal day 100) mice. Seeking to determine the shortest effective period of stimulation, we further showed that even 2 d of deprivation and stimulation shifted OD at any age. This shift was achieved by a decline in deprived-eye input that was saturated within 2 d and did not change during 7 d of MD. However, after 2 weeks of MD, cortical activity induced by both eyes increased again and this increase did not depend on continued stimulation, suggesting a homeostatic mechanism. Starting stimulation 4 d before MD did not mask OD plasticity, showing that the effect is not merely due to the "stimulus-dependent response potentiation" described recently (Frenkel et al., 2006). These results are the first to demonstrate the influence of stimulus quality on cortical plasticity and that cortical responses can be changed within very short periods of time (merely 2 d).