Stroke is a leading cause of death and disability in industrialized countries. Although surviving patients exhibit a certain degree of restoration of function attributable to brain plasticity, the majority of
stroke survivors has to struggle with persisting deficits. In order to potentiate post-
stroke recovery, several rehabilitation
therapies have been undertaken and many experimental studies have reported that
brain-derived neurotrophic factor (
BDNF) is central to many facets of neuroplastic processes. However, although
BDNF role in brain plasticity is well characterized through strategies that manipulate its content, the involvement of this
neurotrophin in spontaneous post-
stroke recovery remains to be clarified. Besides, while the neuroplastic role of
BDNF is restricted to its mature form, most studies investigating the proper effect of
ischemia on post-
stroke BDNF metabolism focused on
mRNA or total
protein expressions. In addition, these studies are mainly performed in brain regions collected either at or around the lesion site. Therefore, the objective of the present study was to investigate in both hemispheres, the long-term expression (up to one month) of both pro- and mature
BDNF forms in rats subjected to photothrombotic
ischemia. These assessments were performed in the cortex and in the hippocampus, two regions known to subserve functional recovery after
stroke and were coupled to the study of
synaptophysin expression, a marker of synaptogenesis. Our study reports that
stroke induces an early and transient increase (4h) in mature
BDNF expression in the cortex of both hemispheres that was associated with a delayed rise (30d) in
synaptophysin levels ipsilateraly. In both hippocampal territories, the pattern of mature
BDNF expression shows a more delayed increase (from 8 to 30d), which coincides with the evolution of
synaptophysin expression. Interestingly, in these hippocampal territories,
pro-BDNF levels evolve differently suggesting a differential gene regulation between the two hemispheres. While highlighting the complexity of changes in
BDNF metabolism after
stroke, our data suggest that
BDNF involvement in spontaneous post-
stroke plasticity is region-dependent.