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In this paper we report that BDNF is able to stimulate the release of glutamate not only in cerebrocortical nerve terminals, but also in cortical astrocytes. The process of glutamate release, in both nerve terminals and astrocytes, is dependent upon the extracellular and intracellular Ca2+ levels and involves exocytosis, since tetanus toxin treatment abolishes the release of glutamate from both preparations. Further, preincubation of nerve terminals or astrocytes with K252a (a tyrosine kinase inhibitor) inhibits BDNF-evoked glutamate release, suggesting the involvement of Trk B receptors in this process. In astrocytes, the level of BDNF-induced glutamate release is higher in immature than in more mature cells. The results suggest a new pathway of cross-talk between neurons and astrocytes, which may play a role in synaptic plasticity and neurotoxicity.