Visual deprivation independent shift of ocular dominance induced by cross-modal plasticity
Fig 5
Exclusion of saturation of V1 responses evoked by contralateral eye stimulation.
(a) Representative V1 amplitude maps evoked by visual stimulation of the ipsi and contralateral eye and elicited by binocular stimulation of normal untreated mice (n = 4). (b) V1 responsiveness to ipsilateral eye stimulation was always weaker compared to V1 responsiveness to contralateral eye stimulation. However, V1 activity elicited by visual stimulation of the contralateral eye was significantly weaker than V1 activity evoked by binocular stimulation. Hence, V1 responses, measured with intrinsic signal imaging, are not saturated by the input through the contralateral eye. (c) V1 responses evoked by contralateral eye stimulation with a visual stimulus of 10% contrast at 0 and 3 days after WD (n = 4) remained unchanged. (d) However, there was a potentiation of V1 responses to the input through the ipsilateral eye between 0 and 3 days after WD. (e) Thus, the ODI significantly shifted towards zero. Hence, visual stimulation with a weaker visual stimulus reveals the same effect of WD on V1 activity like visual stimulation with a strong visual stimulus. Open circles represent measurements of individual animals. Closed circles represent the means of each group ± s.e.m.; *p<0.05, **p<0.01; Scale bar: 1 mm.