beta-Amyloid Neurotoxicity on Basal Forebrain Cholinergic Neuron Cultures / 대한해부학회지

beta-amyloid[Abeta] peptide consisting of 40 of 42 amino acids peptide is the principal constituent of senile plaques in Alzheimer`s disease. Recently, it has been demonstrated that this peptide and its constituent fragments are toxic to neuron. Basal forebrain cholinergic neurons are preferentially damaged early in the course of Alzheimer`s disease, and the degree of cholinergic decrement correlates well with the severity of dementia. Taking into consideration of toxic properties of Abeta and the selective vulnerability of the cholinergic system, possible effects of beta-amyloid on the cultured basal forebrain cholinergic neurons were tested. Our result showed tha Abeta1-40 induced marked neurodegenerative changes including loss of cell body and dystrophic neurites in the basal forebrain neuronal cultures at 20micrometer. Immunocytochemical study showed that Abeta1-40 causes apparent loss of choline acetyltransferase[ChAT] immunoreactivity and acetycholine esterase[AchE] positive neuritic intergrity in large basal forebrain cholinegic neurons. However, the number of ChAT immunoreactive neurons was not significantly decreased as compared to other neurons in mixed culture system. These results suggest that the basal forebrain neurons are not particularly vulnearable to Abeta and that preferential injury to basal forebrain cholinergic neurons in Alzheimer`s disease may be caused by some other medchanism.

c-kit and Ligand Expression in the Mouse Hippocampus after Kainate-induced Seizure / 대한해부학회지

In the present study, we have etamined the role of c-kit and KL ligand in the mouse brain after kainate-induced seizure. To investigate whether c-kit receptor and KL ligand might involved in kainate-induced apoptosis, the expression patterns of c-kit and KL mRNA and localization of immunoreactivity for c-Kit, SCF and Bcl-2 protein were examined by in situ hybridization technique and immunohistochemical method, respectively, in the mouse hippocampus after kainate treatment. This report is the first demonstration for the role of c-kit receptor and KL ligand in the kainate-induced apoptosis. Our conclusion is based on : 1] c-kit and KL mRNA expressions were increased in CA3 region of the hippocampus in 1h after kainate treatment, 2] immunoreactivities for c-Kit protein and SCF were detected higher level in the CA1 and CA3 sectors in 24h after kainate treatment, 3] expression level for Bcl-2 protein was increased in the CA3 region of the hippocampus 24h after kainate treatment. These results suggest that bcl-2 could promote cell survival of injured neurons in CA3 after kainate-induced seizure. And increased translations of c-kit receptor and KL ligand after kainate injection in this area susgest that c-kit receptor and KL ligand could have a role in the kainate-induced apoptosis.