rTMS R7 58 ± 3%, P = 0.01; contralesional targets, 41 ± 15% vs. 65 ± 10%, P = 0.01) whereas it did not influence the detection of static targets (Static ipsilesional targets R7, 42 ± 5% vs. post-rTMS 48 ± 3%, P = 0.10; and contralesional post- rTMS R7, 38 ± 3% vs. post-rTMS 45 ± 12%, P = 0.56). These effects reverted to pre-rTMS values particularly for mid-central ipsilesional eccentricities (Moving 2: 45°, post-rTMS 50 ± 18% vs. rTMS R7 81 ± 19%, P = 0.24; 60°, 43 ± 19% vs. 67 ± 23%, P = 0.26; Fig. 8). Overall, the restoration of performance in Non-responders proved to be reversible once the rTMS regime ended,

which further supports the role of neurostimulation as being responsible for the maladaptive effects observed in this subset of animals. The intention of the experiment was to damage HDAC phosphorylation the homologue of the human posterior parietal cortex, known as pMS, and to later apply rTMS on the rostrally adjoining aMS cortex, which is known for its ability to adequately compensate lost function after lesion (see Fig. 1 for details on the anatomy). A comprehensive lesion analysis indicated that, for all animals, the majority of the injured cortical area was removed. Nonetheless, areas of incomplete GSI-IX cell line damage were found extending 1–3 mm rostrally in some subjects (n = 3 in Responders and n = 3 in

Non-responders), impinging into the aMS cortex (stereotaxic selleck chemicals levels A9–A11) or 1 mm caudally into the ventral posterior suprasylvian and the dorsal posterior suprasylvian regions (stereotaxic level P3; n = 2 in Responders and n = 3 in Non-responders). In addition, all 12 subjects showed very minor collateral damage to the pMS-adjacent visual areas such as primary visual area A19 and the splenial visual area, due to a minor but unpreventable diffusion of the neurotoxin. This spread appears to be consistent with other studies using the same methods (also see Rudolph & Pasternak, 1996; Huxlin et al.,

2008; Rushmore et al., 2010; Das et al., 2012; Supporting Information Figs S1 and S2). Quantification of injured area (mm2) showed no significant differences in the amount of lesion between groups, either for the medial (pMLS) or the lateral (pLLS) bank of the posterior parietal (pMS) cortex along the length of both pMS and aMS visual areas. Overall, the amount of spared tissue between Responders and Non-responders in both the injured pMS cortex (pMLS: 21 ± 8% vs. 14 ± 6%, P = 0.2; pLLS: 18 ± 6% vs. 15 ± 6%, P = 0.60) and the rTMS-stimulated aMS cortex (aMLS, 79 ± 7% vs. 58 ± 13%, P = 0.10 and aLLS, 79 ± 7% vs. 64 ± 13%, P = 0.10; data not shown in figure form) was not statistically different across groups. Responders and Non-responders also did not show significant differences in spared cortex at any specific coordinates across the rostral–caudal extent from pMS through aMS (medial bank, F4,32, P = 0.32; lateral bank, F4,32, P = 0.60).