The present study was aimed to investigate the ability of free radical scavenger(hydroxyl radical scavenger, dimethyl sulfoxide, DMSO) to change the release of 5-hydroxytryptamine(5-HT)from the hypoxia-sensitive rat hippocampal slices.
The hippocampus was obtained from the rat brain and sliced 400µm thickness with the manual chopper. After 30min's preincubation in the normal buffer, the slices were incubated for 20min in a buffer containing[3H]-5-HT(0.1µM, 74µCi/8ml) for uptake, and washed. To measure the release of [3H]-5-HT into the buffer, the incubation medium was drained off and refilled every ten minutes through sequence of 14 tubes. Induction of hypoxia(gassing it with 95% N2, 5% CO2) was done in 6th and 7th tube, and DMSO was added 10 minutes prior to these manipulations. The radioactivities in each buffer and the tissue were counted using liquid scintillation counter and the results were expressed as a percentage of the total radioactivities.
When slices were exposed to hypoxia for 20min, [3H]-5-HT release was decreased and a rebound release of [3H]-5-HT was observed on the post-hypoxic period. Administration of DMSO(10mM) increased the spontaneous release of [3H]-5-HT in the control group. And DMSO also prevented hypoxia-induced decrease of [3H]-5-HT release. But the rebound release of [3H]-5-HT during post-hypoxic period was not affected by DMSO.
In addition to the hydroxyl radical scavenging effect, DMSO has direct stimulation effect on the firing of 5-HT neuron.
, Mi Sun Jo, Yeon Joo Jung, Kyung Eun Lee Alzheimer's disease(AD) is primarily characterized by neurofibrillary tangles, senile plaques, and neurodegeneration. The major component of senile plaques is the beta-amyloid peptide(A β), Which is considered to have a causal role in AD. However, the biological activities of Aβ in AD has not been clearly defined. In this study we have investigated the effects of Aβ 25-35 fragment to neurons using organotypic hippocampal slice culture system which maintained intact hippocampal synaptic circuit and anatomy. Hippocampal slice culture is prepared from rat postnatal 10-old days and after 14 days culture, slices were treated with 10uM Aβ 25-35 fragment. Neuronal death was measured with propidium iodide(PI) uptake and NeuN, neuronal marker, staining. After treatment of Aβ 25-35 fragment for 3days or 7days on hippocampal slice culture, we observed the increased PI uptake and the decreased number of NeuN-stained neuron in CA1 region of hippocampal pyramidal layer or dentate gyrus. These results suggested that Aβ 25-35 fragment exerts the neurotoxicity in hippocampal slice culture.
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