Humoral Recognition-Behavioral Stress-Coping Glycolipids Produced By Mice Given Repeated Electroconvulsive Treatment
Abstract
Yutaka Masuda
Background: Stress-coping is a core event of mammalians. Depression symptoms are induced by the stress-coping failures. Repeated electroconvulsive treatment gives a strong stress to mammalians, however, the treatment has been used to improve depression symptoms. Mammalians have recognition-behavioral stress-coping neuronal modulesystem followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module. GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module. A sulfated Fucalpha1-2Gal-lipid protects the cholinergic module keeping the stress-coping memories from the ischemia-stress. I hypothesized mammalians given repeated electroconvulsive treatment would produce these glycolipids, and would increase the stress-coping ability.
Materials and Methods: I examined the glycolipid productions of mice given repeated electroconvulsive treatment under general-anesthesia.
Results: I found mice only given the general-anesthesia produced sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1- 3GalNAc-lipid, and mice given the repeated electroconvulsive treatment under general-anesthesia further produced sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1-3GalNAc-lipid, and increased sulfated Fucalpha1-2Gal-lipid production.
Conclusion: Depression symptoms are closely related to serotonergic and adrenergic module activities. I understood repeated electroconvulsive treatment would improve depression symptoms via the sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1-3GalNAc-lipid productions.