1. The effect of vitamin B12 on synaptic plasticity of hippocampus in Alzheimer's disease model rats
- Author
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Nikmahzar Emsehgol, Elyasi Leila, and Jahanshahi Mehrdad
- Subjects
medicine.medical_specialty ,General Neuroscience ,Neurexin ,Hippocampus ,Inflammation ,Neuroligin ,General Medicine ,Biology ,Hippocampal formation ,Endocrinology ,Internal medicine ,Synaptic plasticity ,medicine ,Vitamin B12 ,medicine.symptom ,Postsynaptic density - Abstract
BACKGROUND Hippocampus cells, responsible for learning and memory, are disturbed in Alzheimer's disease (AD), resulting in production of several inflammatory markers, such as neurexin 1 -neuroligin, cyclooxygenase-2 (COX-2), and caspase-3 proteins, used in measurement of AD's severity and development. Vitamin B12, which plays a role in brain functioning, has anti-inflammatory properties and its impairment is associated with apoptosis in Alzheimer's disease. This study aimed to investigate the effect of vitamin B12 on restoration of Synaptic Plasticity on scopolamine-induced AD in rats. METHODS To simulate AD, Rats, except the control group were i.p. injected with 3 mg/kg scopolamine. Before scopolamine the pretreatment group vitamin B12 (0.5, 2, and 4 mg/kg) was injected every day for the next 14 days. After 24 h, sectioning the rats' brains, the concentration of postsynaptic density protein 95 (PSD-95), neurexin 1-neurolgin, COX-2, and caspase-3 proteins in hippocampus were measured using immunoblotting. RESULTS B12 significantly enhanced molecular balance. PSD-95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX-2 and activated caspase-3 were enhanced in the hippocampus of scopolamine-injected subjects. Their alterations were decreased after B12 administration. CONCLUSIONS Vitamin B12 protected scopolamine-injected rats and inhibited hippocampal inflammation and apoptosis and preserved pre- and post-synaptic proteins and possibly synaptic integrity in hippocampus route.
- Published
- 2021