اثر ترمیمی پپتید غنی از پرولین هیپوتالاموس (PRP-1) روی فعالیت الکتریکی نورون‌های هیپوکامپ در بیماری آلزایمر ایجادشده به‌وسیله پپتیدهای بتا آمیلوئید (Aβ25-35) و (Aβ1-42) در موش‌های صحرایی

   Background & Aims: Alzheimer’s disease is the most common form of dementia which it destroyed memory and thinking skills slowly. There is no cure for the disease and it leads to death eventually. Proline rich peptide (PRP -1) is produced from neurosecretory cells of hypothalamus that has large spectrum of biological action on immune and nervous system . The Aβ1-42 is more effective in the development of Alzheimer’s disease than Aβ25-35. The purpose of this research is to study the effect of PRP-1 on the electrical activity of Hippocampus neurons in the Alzheimer’s disease induced by β amyloid proteins Aβ25-35 and Aβ1-42.  Materials & Methods: The present experimental study was carried out on 20 adult male wistar rat’s weighing 230±30gr and aged 3-4 months. At first, the rats were randomly divided into five groups (normal, Amyloids and Amyloids with PRP-1). In the control group without injection of β amyloid solutions and PRP-1, in the amyloid groups after injection of β amyloid solutions 3 m Lit and the amyloid with PRP-1 groups after injection of β amyloid solutions and treatment with PRP-1, experiment of electrophysiology with stimulus entorhinal cortex with frequency 50 and 100 HZ was performed and electrical activity of Hippocampus neurons on the base of tetanic potentiation and tetanic depression was recorded.  Results : The results of this research showed when administration of PRP-1 leads to approach of inhibitory and excitatory post stimulus early and late activity of hippocampus neurons to normal levels in Alzheimer’s disease produced by Аβ 25-35, but in the case of the Aβ 1-42 model the inhibitory post stimulus manifestations of activity didn’t reach the normal level.  Conclusion : During Aβ 25-35 and 1-42 intoxication, a possible GABA-ergic nature of the post stimulus depression was performed and the neurodegeneration was counteracted and the protective effect of PRP-1 was supported.    SOURCE: URMIA MED J 2014: 25(8): 717 ISSN: 1027-3727