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In the dendrites the labeling covers on average the proximal 30% of the total dendritic length. On high potassium depolarization, the labeling of BDNF and TrkB mRNA extends on average to 68% of the dendritic length. This increase does not depend on new RNA synthesis, is inhibited by the Na<jats:sup>+<\/jats:sup>channel blocker tetrodotoxin, and involves the activation of glutamate receptors. Extracellular Ca<jats:sup>2+<\/jats:sup>, partly flowing through L-type Ca<jats:sup>2+<\/jats:sup>channels, is absolutely required for this process to occur. At the protein level, a brief stimulation of hippocampal neurons with 10 m<jats:sc>m<\/jats:sc>KCl leads to a marked increase of BDNF and TrkB immunofluorescence density in the distal portion of dendrites, which also occurs, even if at lower levels, when transport is inhibited by nocodazole. The protein synthesis inhibitor cycloheximide abolishes this increase. The activity-dependent modulation of mRNA targeting and protein accumulation in the dendrites may provide a mechanism for achieving a selective local regulation of the activity of neurotrophins and their receptors, close to their sites of action.<\/jats:p>","DOI":"10.1523\/jneurosci.17-24-09492.1997","type":"journal-article","created":{"date-parts":[[2018,4,3]],"date-time":"2018-04-03T13:35:32Z","timestamp":1522762532000},"page":"9492-9505","source":"Crossref","is-referenced-by-count":283,"title":["Activity-Dependent Dendritic Targeting of BDNF and TrkB mRNAs in Hippocampal 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