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BDNF local translation in viable synaptosomes: implication in spine maturation.
Kusumika Gharami1, Sumantra Das1
1Neurobiology Department, Cell Biology & Physiology Division, CSIR-Indian Institute of Chemical Biology, 4 Raja S.C. Mullick Road, Jadavpur, Kolkata 700032, India.
Neurochemistry International
|March 18, 2014
Summary
Brain-derived neurotrophic factor (BDNF) can be translated in dendrites, a process dependent on glucose, calcium, and its receptor TrkB. This dendritic translation may contribute to spine maturation signaling.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Brain-derived neurotrophic factor (BDNF) plays crucial roles in neuronal function and survival.
- BDNF is encoded by distinct mRNA transcripts, including one with a long 3' untranslated region that localizes to dendrites.
- The translation and regulation of dendritic BDNF mRNA remain largely uncharacterized.
Purpose of the Study:
- To investigate the occurrence and regulation of BDNF translation in neuronal dendrites.
- To explore the potential role of dendritic BDNF translation in synaptic plasticity and spine maturation.
Main Methods:
- Utilized isolated synaptosomes to study translation independent of nuclear and other subcellular fractions.
- Stimulated synaptosomes with KCl (depolarization) or glutamate (excitation) to induce translation.
- Assessed BDNF translation and related signaling molecules using Western blotting.
Main Results:
- Depolarization and glutamate excitation induced BDNF translation in synaptosomes, similar to known dendritic mRNAs (CaMKllα, Homer, Arc).
- Synaptosomal BDNF translation was dependent on glucose concentration, TrkB receptor function, and intracellular calcium levels.
- KCl or glutamate treatment increased phospho-cofilin and phospho-PAK levels in synaptosomes, suggesting induction of spine maturation signaling.
Conclusions:
- BDNF translation occurs in dendrites and is regulated by neuronal activity, glucose, calcium, and TrkB signaling.
- Dendritic BDNF translation may be involved in initiating signaling pathways that lead to spine maturation and synaptic plasticity.

