Localization and size of the cortical stroke.

<p>(A) Scheme of the average lesion location (red dotted circle/line) and size in the left motor cortex (M2) in respect to the primary visual cortex (V1) of a mouse brain. (B) Nissl-stained frontal section through a representative lesion, WM-white matter. Scale bar: 500μm.</p

A cortical lesion in M2 impairs OD-plasticity in the visual cortex of the lesioned hemisphere.

<p>Optically recorded activity maps of the contralateral (contra) and ipsilateral (ipsi) eye in the binocular region of mouse primary visual cortex (V1) in sham-treated control mice (A, B) and in mice with a PT-lesion in M2 of the recorded hemisphere (C, D). Activity maps without MD are illustrated in the left column (A, C), maps after MD in the right column (B, D). Gray-scale coded response-magnitude maps and their quantification (top), and color-coded phase and polar maps of retinotopy (middle, bottom) are illustrated. The magnitude of the optical responses is illustrated as fractional change in reflection x10^-4. For each experiment, the histogram of OD-scores (upper right), the OD-index (ODI), and the corresponding 2D OD-maps (ODI values are color-coded: red represents positive, blue negative values) are included. Note that without MD, activity patches evoked by stimulation of the contralateral eye were consistently darker than those after stimulation of the ipsilateral eye, 2D OD-maps display warm colors, and the average ODI is positive, indicating contralateral dominance (A, C). In contrast, MD for 7 days in control- (B) but <i>not</i> PT-animals (D) induced an OD-shift toward the open (ipsilateral) eye: the activity map of the ipsilateral eye was even darker than after contralateral (deprived) eye stimulation (black circle indicates MD eye), the histogram of OD-scores shifted to the left (blue arrow in B), the ODI was negative, and colder colors prevailed in the OD-map. In contrast, in PT-animals with MD (D), activity maps of the deprived (contra) eye remained darker than those of the open eye, the histogram of OD-scores and the average ODI were essentially unchanged and warm colors still prevailed in the OD-map.</p

The M2-lesion severely impaired improvements of visual capabilities of the open eye after MD.

<p>Spatial frequency selectivity of the optokinetic response of the open eye in cycles per degree (cyc/deg) plotted against days (A) and contrast sensitivity at 6 different spatial frequencies (B) in control and PT-mice without and with MD (+MD). In both, control and PT-mice, values of the nondeprived (open) eye increased compared to mice without MD. However, the increase in PT-mice was only about 50% of the improvement of control mice.</p

Quantification of the OD-indices and V1-activation.

<p>(A, B) Optically imaged OD-indices in sham-treated (control, blue) animals and after PT in M2 (red) without and with 7 days of MD of the right eye. Symbols represent ODI-values of individuals, means are marked by horizontal lines. (C, D) V1-activation elicited by stimulation of the contralateral (C) or ipsilateral (I) eye in control animals and after MD (black circle indicates MD eye). (A) In control mice, MD induced an OD-shift towards the open eye. In contrast, PT-mice did not show a significant OD-shift in the lesioned, left hemisphere. (B) In contrast, in the nonlesioned, right hemisphere, MD induced an OD-shift in PT-mice, as in control animals. (C, D) V1-activation after stimulation of the contra- and ipsilateral eye before and after MD in both control and PT-lesioned mice.</p

The experience-enabled enhancement of the optomotor reflex of the open eye after monocular deprivation (MD) was compromised in both PT-lesioned PSD-95 WT and PSD-95 KO mice.

<p>In contrast, enhancements of spatial vision were present in nonlesioned PSD-95 WT and PSD-95 KO mice. (A, B) Spatial frequency threshold of the optomotor response of the open eye in cycles per degree (cyc/deg) plotted against days after MD. After 7 days of MD, nonlesioned PSD-95 KO mice (A) as well as sham-treated control mice (B; data from Greifzu et al., 2011) showed a significant increase in the spatial frequency threshold of the optomotor reflex of the open eye. This experience-enabled increase was abolished by a PT in S1 (A, B). (C-F) Contrast sensitivity thresholds of the optomotor reflex of the open eye at 6 different spatial frequencies before (day 0) and 7 days after MD. For both nonlesioned PSD-95 KO (C) and PSD-95 WT mice (D), there was an increase in contrast sensitivity after 7 days of MD. After PT, this experience-enabled increase was absent in both groups (E, F).</p

Location of the photothrombotically induced cortical stroke lesion in a PSD-95 KO mouse in S1 (PT, red dashed line).

<p>(A) Top view of a representative mouse brain illustrating the lesion location in S1, on average 1 mm anterior to the anterior border of the primary visual cortex (V1, blue dashed line). (B) Nissl-stained frontal section through the lesion (same animal as in A). (C) Higher magnification composite image of the superficial vascular pattern of the brain and the superimposed optically recorded retinotopic map of the binocular part of V1 of a PSD-95 KO mouse in which the PT-lesion (L) was very close to V1; nevertheless, OD-plasticity was present in this animal (average ODI = 0.00). Scale bar all, 1 mm.</p

In adult PSD-95 KO mice, ocular dominance plasticity was preserved after a PT-stroke in S1.

<p>Optically recorded activity maps of the contralateral (contra) and ipsilateral (ipsi) eye in the binocular region of mouse primary visual cortex (V1) in PT-lesioned PSD-95 WT (A) and PSD-95 KO mice (B) after monocular deprivation (MD), and their quantification (C, D). Open and closed eyes indicated by a white or black circle. (A, B) Grayscale coded response magnitude maps of the contra- and ipsilateral eye (including average V1-activation of the illustrated example) and the histogram of OD-scores including the average OD-index (top row), color-coded polar maps of retinotopy and 2-dimensional OD-maps after MD (lower row) are illustrated. (A) In PSD-95 WT littermates, activity patches evoked by stimulation of the contralateral eye were darker than those of the ipsilateral eye, the average ODI was positive, and warm colors prevailed in the OD-maps, indicating contralateral dominance. In contrast, in PSD-95 KO mice, the contra- and ipsilateral eye activated V1 about equally strong, colder colors appeared in the OD-map, and the histogram of OD-scores shifted to the left (B). Scale bar: 1 mm. (C) Optically imaged OD-indices in PT-lesioned PSD-95 WT and PSD-95 KO mice (light red and red triangles). For comparison, ODIs of control (sham-treated) and PT-lesioned Bl6/J mice are illustrated (white and grey squares). Symbols represent ODI values of individuals, means are marked by horizontal lines. (D) V1-activation elicited by stimulation of the contralateral (C) or ipsilateral (I) eye in PSD-95 WT and PSD-95 KO mice after PT and MD. Note that V1-activtation after stimulation of the contra- and ipsilateral eye was not different in PSD-95 KO mice, indicating preserved juvenile-like OD-plasticity in V1 despite the S1-lesion.</p