Acute rosmarinic acid treatment enhances long-term potentiation, BDNF and GluR-2 protein expression, and cell survival rate against scopolamine challenge in rat organotypic hippocampal slice cultures
| Autor: | Seok Lee, SangSeong Kim, Ga-Young Choi, S.-H. Lee, Eun-Sang Hwang, Hyun Bum Kim, Ji Ho Park |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Long-Term Potentiation Biophysics Pharmacology Biology Biochemistry Neuroprotection Depsides Hippocampus Antioxidants Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Organ Culture Techniques medicine Animals Propidium iodide Receptors AMPA Molecular Biology Neuronal Plasticity Cell Death Rosmarinic acid Brain-Derived Neurotrophic Factor Niflumic acid Long-term potentiation Cell Biology Rats 030104 developmental biology Neuroprotective Agents chemistry Cinnamates Excitatory postsynaptic potential CNQX Cholinergic 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Biochemical and biophysical research communications. 475(1) |
| ISSN: | 1090-2104 |
| Popis: | Background Rosmarinic acid (RA) is a polyphenolic ester of caffeic acid and is commonly found in the Nepetoideae subfamily of flowering mint plants. Because RA has previously exhibited antioxidant, neuroprotective, and antidepressant-like effects, we evaluated its influences on cellular functions in neuronal cultures. Objective To elucidate possible mechanisms of RA, we investigated the influences of acute RA administration on long-term potentiation (LTP), plasticity-related protein expression, and scopolamine-induced cell death in organotypic hippocampal slice cultures. Methods LTP analysis in organotypic hippocampal slice cultures (OHSCs) was carried out with various ion channel blockers, such as AP5 (10 μM), CNQX (10 μM), niflumic acid (100 μM), and scopolamine (300 μM) in response to RA (1, 10 or 100 μg/mL) treatment. Protein expression and cell death assays in the presence of scopolamine were examined to observe the effects of RA. For LTP analysis, baseline field excitatory postsynaptic potentials (fEPSPs) were recorded in CA1 by a 60-channel multielectrode array (MEA) every min for 40 min before 15 min of high-frequency stimulation (HFS) to the Schaffer collaterals and commissural pathways, followed by a successive 50 min of recording. For protein expression measurements, anti-BDNF and anti-GluR2 antibodies were used for Western blotting assays in whole-hippocampal tissue homogenate. Finally, for cell death assays, OHSCs were exposed to a culture medium containing propidium iodide (PI) for 24 or 48 h, followed by the assessment of cell death by fluorescent image analysis of PI uptake. Results and discussion: Our results indicate that RA treatment enhances fEPSPs following HFS in CA1 synapses at 1 and 10 μg/ml RA, an effect that was inhibited by CNQX and NFA but not by AP5. RA treatment also increases the expression of BDNF and GluR-2 proteins and prevents cell death of scopolamine-exposed OHSCs. Our results suggest the possibility that rosmarinic acid can enhance neural plasticity by modulating glutamatergic signaling pathways, as well as providing neuroprotection with reduced cholinergic activity. |
| Databáze: | OpenAIRE |
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