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We described previously a sequence of cortical activity changes after the unilateral stroke in the whiskers somatosensory representation – the barrel fi eld (BF). We aimed to check if this activity remodeling is linked to the restitution of the whiskers sensory function. To characterize poststroke defi cits and time related recovery we performed the gap-crossing test for a group of rats 3, 28 and 56 days after the photothrombotic stroke (DPS) in the BF. Rats learned to cross the gap between elevated platforms in darkness, using only sensory information from whiskers. We examined the minimum distances at which rats failed to cross (min) and the maximal distances (max) crossed by the rats in two scenarios at each time point: (1) with all their whiskers and (2) only with unilateral whiskers corresponding to the destroyed BF (contralateral to the stroke). Before the stroke there were no signifi cant differences in min and in max distances when rats used all versus unilateral whiskers. At 3DPS the max was lower when rats used whiskers with destroyed sensory representation. The fi rst fall was made by rats at shorter distances when they used just the impaired side whiskers. At 56DPS all the differences between crossing performance disappeared. At this time point, we previously found new activity foci in the spared somatosensory cortex of the injured hemisphere, specifi c for the whiskers stimulation – probably a new functional representation of the whiskers.
Filamentous inclusions of tau protein are hallmarks of tauopathies including Alzheimer’s disease. Here a rat model for tauopathies was developed using pore-forming halitoxin Poly-APS. Tau protein was delivered through the membrane into the neurons where it is metabolized. Rats were injected with recombinant human Tau441 only (controls), Tau+Poly-APS (double) and Tau+PolyAPS+Okadaic Acid (triple). Cognitive and neurodegenerative changes were examined with Morrris water maze behavioral test and immunohistochemistry, respectively. Acquisition of the spatial reference memory was unaffected by administration of Tau or Tau+Poly-APS. However, enhanced phosphorylation of exogenously delivered tau with the triple infusion impaired learning. Hippocampal tau was visualized using antibodies against Tau441 and phosphorylated Tau-S404. The higher intensity of Tau441 immunostaining in double and triple groups suggests that exogenous tau is sequestered from the infusion solution into the cells. With respect to phospho-tau izoform we observed different cellular compartmentalization of P-Tau-S404 in double and triple treated rats. In double treated rats P-TauS401 was distributed both in the cell bodies and neuronal fi bers, while in triple group presence of OA caused redistribution of phospho-tau staining from neuronal processes to the perikaryon. This is similar to age-dependent tau redistribution between cellular compartments and could be a result of hyperphosphorylation.
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