OD-plasticity of WT and PSD‐93 KO mice during late critical period

Similar to WT and PSD-93 KO mice in the mid CP without MD, control animals in the late CP showed contralateral dominance with stronger visual cortical activation after contra eye stimulation than after visual stimulation of the ipsi eye. Representative 2-dimensional ocular dominance maps in the left V1 of both genotypes showed warm, red colors indicating contralateral dominance and all control mice exhibited positive ocular dominance indices (Figure 60).

Figure 60: Representative examples of ocular dominance maps and indices in WT and PSD-93 KO mice without MD obtained with optical imaging of intrinsic signals in vivo during the late critical period. Optical imaging maps of contralateral and ipsilateral cortical responses to visual stimulation of either eye with a horizontal moving bar (elevation) of 20° are displayed from (A, B) two WT mice and (C, D) two PSD-93 KO mice without MD,

Results

reflectance x 10^-4), color-coded phase maps of retinotopy (bottom rows), histograms of the OD-scores (top right of panels) and color-coded OD-maps (right bottom including the average ODI value) are illustrated. In control mice of both genotypes, the activity patches evoked by stimulation on the contralateral (contra) eye were always darker than those evoked by ipsilateral (ipsi) eye stimulation. The average ODI was always positive and warm, red colors prevailed in the 2-dimensional OD-map, indicating contralateral dominance.

After 4 days of monocular deprivation, WT mice showed weakened cortical activity after visual stimulation of the contra eye, whereas ipsi eye stimulation activated the visual cortex stronger, hence showing OD-plasticity. The representative 2-dimensional ocular dominance maps in the left V1 of WT mice showed cold, blue colors, indicating ipsilateral dominance (Figure 61 A, B). The histograms were shifted to the left and all mice exhibited negative ocular dominance indices. In contrast, this was not the case in PSD-93 KO mice. Here, 4 days of MD did not induce OD-plasticity and the cortical activation after visual stimulation of the contra eye remained higher than after visual stimulation of the ipsi eye. Additionally, the 2- dimensional OD-maps showed warm, red colors indicating contralateral dominance and all mice showed positive ocular dominance indices (Figure 61 C, D).

Results

Figure 61: Representative examples of ocular dominance maps and indices of WT and PSD-93 KO mice after 4 days of MD obtained with optical imaging of intrinsic signals in vivo during the late-critical period. Optical imaging maps of contralateral and ipsilateral cortical responses to visual stimulation of either eye with a horizontal moving bar (elevation) of 20° are displayed from (A, B) two WT mice and (C, D) two PSD-93 KO mice after 4 days of MD, respectively. Grayscale coded response magnitude maps (top rows, expressed as fractional change in reflectance x 10^-4) with black circles indicating monocular deprivation of the eye and white circles indicating that the respective eye remained open. Color-coded phase maps of retinotopy (bottom rows), histograms of the OD-scores (top right of panels) and color-coded OD-maps (right bottom including the average ODI value), are illustrated. After 4 days of MD in WT mice, there was an OD-shift towards zero. Activity patches evoked by stimulation of the contralateral eye were equally strong to that after ipsi eye stimulation and the histogram shifted to the left. The average ODI was negative and cold, blue colors prevailed in the 2-dimensional OD-map, indicating ipsilateral dominance and hence ocular dominance plasticity. In contrast to that, in PSD-93 KO mice, the activity patches evoked by stimulation of the contra eye after 4 days of MD were still darker than those evoked by ipsi eye stimulation. The average ODI was always positive and warm, red colors prevailed in the 2-dimensional OD-map, indicating contralateral dominance and no ocular dominance plasticity.

Results

Quantification of the data revealed that already in the late CP (P 28 - 35), OD-plasticity was completely abolished in PSD-93 KO mice (ODI no MD: 0.32 ± 0.02; n = 5; after 4 d MD: 0.28 ± 0.02; n = 6; p = 0.17; t-test), whereas it persists in WT mice after 4 days of MD (ODI no MD:

0.37 ± 0.03; n = 5; after 4 d MD: -0.01 ± 0.02; n = 7; p < 0.001; t-test) (Figure 62 A). The OD- shift in WT mice was similar to that of mice in the mid CP and also mediated by reduced contralateral eye responses (contra no MD: 1.85 ± 0.14; n = 5; after 4 d MD: 1.15 ± 0.18; n = 7; p < 0.05; t-test), whereas ipsilateral eye responses remained unchanged (ipsi no MD: 0.81

± 0.08; n = 5; after 4 d MD: 1.04 ± 0.14; n = 7; p = 0.23; t-test) (Figure 62 B).

These results already suggest that there is an earlier closure of the CP for OD-plasticity around P 28 when PSD-93 is lacking.

Results

Figure 62: Ocular dominance indices and average response magnitudes of WT (n = 5) and PSD -93 KO mice without MD (n = 5) and after four days of MD (WT, n = 7 / KO, n = 6) during the late-critical period. (A) A positive ODI indicates dominance of the contralateral eye, a negative ODI indicates ipsilateral dominance.

Unicolored circles represent ODI values of individual animals without MD, half-filled circles represent individual animals after 4 days of MD; means are marked by thick horizontal lines and the standard deviation is illustrated with small horizontal lines. WT (gray) and PSD-93 KO mice (red) without MD showed ocular dominance of the contralateral eye and similar ODI values (t-test, p = 0.17). Four days of monocular deprivation in WT mice induced a significant OD-shift towards the open eye (t-test, p < 0.001), which was significantly different from values of PSD-93 KO mice which did not show ocular dominance plasticity after MD (t-test, p < 0.001). (B) Average cortical responses expressed as a change in reflectance x 10^-4 by stimulation of the contralateral (C) or ipsilateral (I) eye in WT (gray) and PSD-93 KO mice (red) without MD and after four days of MD. In all control animals without MD, cortical activation after visual stimulation of the contralateral eye was significantly higher than after ipsilateral eye stimulation (WT: p < 0.01; KO: p < 0.001; paired t-test), reflecting the dominance of the contralateral eye in

Results

mice. In WT mice after four days of MD, response strength of the two eyes were no longer significantly different since the deprived eye responses were significantly reduced compared to controls (WT: p < 0.05; t-test). In contrast to that, cortical responses did not change in PSD-93 KO mice after MD and remained higher after contralateral eye stimulation in comparison to cortical activation after ipsilateral eye stimulation (p < 0.01;

paired t-test). Number of tested animals from Leon Hosang (n = 11) and Sophia Stodieck (n = 12).