BDNF stimulation of protein synthesis in cortical …
Brain-derived neurotrophic factor - Wikipedia
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BDNF is a vital neurotrophic factor in the brain
At CA1 synapses, does newly synthesized BDNF come from pre- or postsynaptic neurons? When the Schaffer-collateral pathway is stimulated with HFS, an increase in BDNF mRNA was only observed in postsynaptic CA1, but not in presynaptic CA3, neurons (). This finding indicates that L-LTP requires postsynaptic BDNF mRNA synthesis. In addition, the activity-dependent up-regulation of postsynaptic BDNF gene expression requires an increase in intracellular Ca2+ concentration through NMDA receptors or L-type Ca2+ channels activated during HFS (; ; ; ; ; ). This is inconsistent with a presynaptic Ca2+ influx, since it is restricted to presynaptic terminals and is mediated primarily through N- or P/Q type Ca2+ channels. Moreover, pairing of a weak presynaptic tetanus with repetitive somatic action potentials in CA1 neurons was sufficient to induce transcription of genes, including BDNF, as well as L-LTP (; ). Taken together, the existing data support the notion that while activity-dependent secretion of BDNF from presynaptic sites may be necessary for E-LTP, the long-term maintenance of L-LTP requires sustained supply of BDNF through activity-dependent transcription and translation in the postsynaptic neurons ().
There is no dispute that L-LTP requires a sustained increase in endogenous BDNF for its long-lasting maintenance. An interesting and yet unresolved issue is whether the endogenous BDNF is derived pre- or postsynaptically. Early work suggests that E-LTP at the Schaffer collateral-CA1 synapses requires BDNF derived from presynaptic CA3 neurons, but not postsynaptic CA1 neurons (). The initial surge of BDNF may be due to the secretion of preexisting BDNF-containing vesicles from presynaptic terminals of CA3 neurons, induced by high frequency stimulation (HFS). This may be important for the induction of E-LTP. Due to the low expression level of BDNF in neurons, however, the existing BDNF would eventually be exhausted. Thus, for the long-term maintenance of L-LTP, a sustained supply of BDNF may come primarily from new protein synthesis triggered by repeated strong synaptic stimulation. This idea is supported by the findings that BDNF mRNA levels in the hippocampus are significantly increased 1-3 hours after the L-LTP-inducing tetanic stimulation (; ; ; ). Moreover, the slow kinetics of BDNF transcription may also serve as a potential mechanism that translates acute high-frequency synaptic activity to long-lasting alteration of synaptic physiology and morphology ().
Signaling pathways underlying the pathophysiology …
Expression of a local reporter with the long, but not the short, Bdnf 3' UTR was increased in the distal dendrites of hippocampal neurons stimulated either by KCl depolarization or PMA-mediated PKC activation. This result is in agreement with a previous finding that chemical LTP induction through TEA treatment can selectively increase dendritic expression of a local translation reporter with the long, but not the short, Bdnf 3' UTR . Pre-treatment of cultures with an inhibitor of PKC completely abolished the increased dendritic translation after PMA treatment, as expected if PMA is acting through PKC, and was able to reduce, but not block, the increased reporter synthesis after KCl stimulation, suggesting that depolarization can trigger PKC-dependent and—independent pathways to increase translation of mRNAs with the long Bdnf 3' UTR. Dendritic reporter translation could be modulated either by a change in the pool of dendritic reporter mRNAs or by a direct effect on the rate of translation of pre-existing dendritic mRNAs. While we found that 3 hours of PMA treatment was able to increase reporter mRNA levels in dendrites, the 1 hour treatment used in reporter assay experiments did not result in any significant difference, suggesting the PKC activity-dependent increase in reporter expression is due to a mechanism operating to increase the translation of pre-existing local mRNAs.
The physiological relevance of these results is highlighted by the similar subcellular distributions of Bdnf mRNAs and HuD, with both found either in translationally repressed mRNP complexes or associated with polysomes, sites of active translation [,]. Activation of PKC results in the nucleocytoplasmic shuttling of Hu proteins, their threonine phosphorylation, and increased association of the cytoskeleton and polysomes , establishing a pathway whereby neuronal activity could lead to HuD-mediated increase in BDNF synthesis.
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Revista Brasileira de Psiquiatria Print version ISSN 1516-4446 Rev
Brain-derived neurotrophic factor, also known as BDNF, is a protein that, in humans, is encoded by the BDNF gene
Zinc is an essential mineral involved in regulating many enzymes
Signaling pathways underlying the pathophysiology and treatment of depression: novel mechanisms for rapid-acting agents
It is an antioxidant and immune-boosting supplement
18/11/2017 · Biology 202, Spring 2005 Second Web Papers On Serendip
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In situ hybridization of cultured neurons was performed as described  with modifications. Antisense and sense RNA probes were synthesized from linearized plasmids using T3 and T7 RNA polymerases (Promega, Madison, WI, USA) and DIG-labeled ribonucleotides. Probe concentrations were 500 ng/ml for Bdnf mRNA and 100 ng/ml for GFP mRNA. For combined FISH and ICC, rabbit polyclonal antibody to GFP (Clontech) was included at a 1:2,000 dilution after the hybridization step. Coverslips were washed four times for 10 min in TNT buffer (100 mM Tris-Cl, pH7.5, 150 mM NaCl, and 0.05% Tween 20), and were incubated with secondary antibody as described above for ICC and washed again with TNT buffer. Then, in situ signals were amplified with the TSA Plus Fluorescein System (PerkinElmer) according to the manufacturer's instructions. The coverslips were mounted onto slides with gelvatol and examined by fluorescence or confocal microscopy. In situ hybridization images from the antisense probe and its sense control probe were taken with the same settings. Green fluorescence from GFP in transfected neurons was not detectable after the hybridization and wash steps.
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Based on the investigations of BDNF regulation of L-LTP, there are several hypotheses that remain to be tested behaviorally. One of these is that BDNF-TrkB signaling may serve as a PRP-synaptic tag pair (). As discussed above, synaptic tagging allows for synapse specificity of plasticity and, under appropriate conditions, can generate heterosynaptic L-LTP if weak stimulation, sufficient to produce a synaptic tag, can capture PRPs induced by stimulation of an independent pathway. Evidence for “behavioral tagging” was recently reported in a study designed to test whether novelty exposure before or after weak training could provide the PRPs necessary to convert STM to LTM (). Weak inhibitory avoidance conditioning (IA) normally results in a STM memory detectable at 15 minutes, but not 1 or 24 hrs, after training. The same training produces LTM if coupled with novelty exposure. This effect was dependent on protein synthesis as infusion of anisomycin, a protein synthesis inhibitor, immediately after the pretraining exposure to novelty blocked the formation of LTM (). Because BDNF has been suggested to be a critical PRP, it would be interesting to test the sufficiency of this protein to induce LTM by replacing novelty exposure with a transient increase in BDNF expression. Likewise, the role of TrkB in synaptic tagging could be evaluated with a temporally restricted disruption of the receptor at the time of the weak training.
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All images were analyzed using NIH ImageJ software. Background was subtracted using a “rolling ball” algorithm. Dendritic processes were straightened and binned into 50 μm sections for ICC or 20 μm sections for combined FISH and ICC. The mean fluorescence for each bin was calculated as the mean of the brightest pixel of each line transecting the dendrite crosswise, emphasizing puncta representing areas of local synthesis. A minimum of 30 dendrites for each of 3 separate experiments were analyzed for each condition. Co-localization experiments were analyzed by an intensity correlation coefficient-based (ICCB) method using the JACoP plugin () for ImageJ. Confocal images of Bdnf mRNA FISH and HuD ICC were thresholded to include most of the dendritic process, and Pearson's and Manders' coefficients were calculated.
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