Speakers
Description
Neuronal plasticity is a fundamental process in brain development. Understanding the mechanisms involved in it is crucial for finding solutions to neurodevelopmental disorders. To study plasticity in vivo, we used ocular dominance plasticity (ODP) in mouse primary visual cortex (V1) induced by monocular deprivation (MD). In standard-cage raised adult mice, 4 days of MD are not sufficient to induce an OD-shift, and contralateral eye input continues to dominate V1-activity. However, juvenile ODP can be restored by e.g. knock-down of PSD-95 which increases the numbers of AMPA-silent synapses in adult V1. The present study investigates the role of subanesthetic ketamine in restoring juvenile ODP in the binocular region of adult mouse V1 beyond the critical period for ODP. To image plasticity, we used intrinsic signal optical imaging. Adult standard cage mice (P58-P91) were treated with ketamine or saline before and during MD.
Our data show that adult ketamine-treated standard-cage raised mice display ODP after only 4d of MD: The ocular dominance index (ODI), which quantifies V1-activation through the ipsi- and contralateral eye, was reduced compared to before MD (0.25 to 0.06±0.049, p= 0.0052, one way ANOVA), and both eyes activated V1 equally. This ODI reduction was mediated by a decrease in contralateral eye-induced V1 activation (2.8 before MD to 1.8±0.347 after, p= 0.007, 2 way ANOVA), indicating the presence of juvenile ODP. In saline-treated mice, however, V1 remained dominated by the contralateral eye, indicative of absent ODP. Thus, subanesthetic ketamine restores juvenile ODP in adult mice.
