[Induction of neuron morphological resistance to beta-amyloid].
The effect of training adaptive vestibular stimulations on goldfish Mauthner neurons (MN) function and three-dimensional morphology was studied in experimental amyloidosis caused by application of aggregated beta-amyloid protein (Abeta25-35). It was found that as compared with control, adapted (trained) MN gained significant resistance to Abeta25-35. Taking into consideration the key role of dopamine in MN adaptation to sensory stimulations, its effect on the development of model amyloidosis was studied. It was shown that the application of dopamine onto MN as well as the increase of its concentration in brain by means of L-dopa protected MN structure and function against pathogenic influence of Abeta25-35. Using electron microscopy it was shown that dopamine protective action on neurons was due to its ability to dissociate polymer amyloid molecules into short inactive fragments.
N A
NA
Kokanova
G Z
GZ
Mikhaĭlova
R Sh
RSh
Shtanchaev
N R
NR
Tiras
D A
DA
Moshkov
D000222:Adaptation, Physiological; D016229:Amyloid beta-Peptides / Q000008:administration & dosage / Q000378:metabolism* / Q000648:ultrastructure; D000686:Amyloidosis / Q000139:chemically induced / Q000473:pathology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D006054:Goldfish / Q000378:metabolism* / Q000502:physiology; D007980:Levodopa / Q000008:administration & dosage; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D010446:Peptide Fragments / Q000008:administration & dosage / Q000378:metabolism* / Q000648:ultrastructure; D011108:Polymers / Q000378:metabolism; D014722:Vestibule, Labyrinth / Q000502:physiology
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D011108:Polymers; C074636:amyloid beta-protein (25-35); D007980:Levodopa; D004298:Dopamine