In recent studies we have examined the potential role of one trophic growth factor, bFGF, in the processes of wound healing and functional recovery following experimental stroke. In studies of the endogenous expression of bFGF after focal cerebral infarction in rats, we found that bFGF gene expression was induced within 1 day and that bFGF protein levels were increased within 3 days in tissue surrounding focal infarcts. Increased bFGF expression was localized to reactive astroglia. Increased endogenous bFGF expression may contribute to neuronal survival and sprouting, glial proliferation, and new blood vessel growth (angiogenesis) in the poststroke brain. In studies of the exogenous administration of bFGF after infarction, we found that the early administration of bFGF reduces infarct size, whereas the later administration of bFGF, while not affecting infarct size, enhances functional recovery. The mechanism of this enhancement may include protection against the late retrograde death of distant neurons and/or the promotion of new neuronal sprouting and synapse formation. Basic FGF represents only one of many trophic growth factors and cytokines that are likely to act as important signaling molecules directing processes of tissue repair and functional reorganization following stroke. Our challenge in future studies is to understand the role of each of these factors singly, and in combination. One consequence of such studies should be the development of new molecular treatments to enhance recovery from stroke.