title: ÐÐ»Ð¸ÑÐ½Ð¸Ðµ Ð±ÐµÐ»ÐºÐ° Bcl-2 Ð½Ð° ÑÐ¸Ð½Ð°Ð¿ÑÐ¸ÑÐµÑÐºÑÑ Ð¿Ð»Ð°ÑÑÐ¸ÑÐ½Ð¾ÑÑÑ Ð² Ð³Ð¸Ð¿Ð¿Ð¾ÐºÐ°Ð¼Ð¿Ðµ Ð¼ÑÑÐµÐ¹ Ñ Ð¼Ð¾Ð´ÐµÐ»ÑÑ Ð±Ð¾Ð»ÐµÐ·Ð½Ð¸ ÐÐ»ÑÑÐ³ÐµÐ¹Ð¼ÐµÑÐ°
title: Ð²ÑÐ¿ÑÑÐºÐ½Ð°Ñ ÐºÐ²Ð°Ð»Ð¸ÑÐ¸ÐºÐ°ÑÐ¸Ð¾Ð½Ð½Ð°Ñ ÑÐ°Ð±Ð¾ÑÐ° Ð±Ð°ÐºÐ°Ð»Ð°Ð²ÑÐ°
titleType: Subtitle
title: Effect of Bcl-2 protein on synaptic plasticity in the hippocampus of mice with Alzheimers disease model
Creators: name: ÐÐ¸Ð½Ð¾ÐºÑÑÐ¾Ð², ÐÐ³Ð¾Ñ
Publisher: name: Ð¡Ð°Ð½ÐºÑ-ÐÐµÑÐµÑÐ±ÑÑÐ³ÑÐºÐ¸Ð¹ Ð¿Ð¾Ð»Ð¸ÑÐµÑÐ½Ð¸ÑÐµÑÐºÐ¸Ð¹ ÑÐ½Ð¸Ð²ÐµÑÑÐ¸ÑÐµÑ ÐÐµÑÑÐ° ÐÐµÐ»Ð¸ÐºÐ¾Ð³Ð¾
Year: 2023
Subjects: Ð±Ð¾Ð»ÐµÐ·Ð½Ñ ÐÐ»ÑÑÐ³ÐµÐ¹Ð¼ÐµÑÐ°
Ð±ÐµÐ»Ð¾Ðº Bcl-2
Ð´Ð¾Ð»Ð³Ð¾Ð²ÑÐµÐ¼ÐµÐ½Ð½Ð°Ñ Ð¿Ð¾ÑÐµÐ½ÑÐ¸Ð°ÑÐ¸Ñ
ÐºÐ¾Ð³Ð½Ð¸ÑÐ¸Ð²Ð½ÑÐµ Ð½Ð°ÑÑÑÐµÐ½Ð¸Ñ
Ð½ÐµÐ¹ÑÐ¾Ð½Ð°Ð»ÑÐ½Ð°Ñ Ð°ÐºÑÐ¸Ð²Ð½Ð¾ÑÑÑ
Alzheimers disease
Bcl-2 protein
long-term potentiation
cognitive impairment
neuronal activity

description: Ð Ð´Ð°Ð½Ð½Ð¾Ð¹ ÑÐ°Ð±Ð¾ÑÐµ Ð¸ÑÑÐ»ÐµÐ´Ð¾Ð²Ð°Ð½Ð¾ Ð²Ð»Ð¸ÑÐ½Ð¸Ðµ Ð¸Ð½Ð³Ð¸Ð±Ð¸ÑÐ¾ÑÐ° ÐºÐ°Ð»ÑÑÐ¸ÐµÐ²ÑÑ ÐºÐ°Ð½Ð°Ð»Ð¾Ð² Ð±ÐµÐ»ÐºÐ° Bcl-2 Ð½Ð° Ð¸Ð·Ð¼ÐµÐ½ÐµÐ½Ð¸Ðµ Ð´Ð¾Ð»Ð³Ð¾Ð²ÑÐµÐ¼ÐµÐ½Ð½Ð¾Ð¹ Ð¿Ð¾ÑÐµÐ½ÑÐ¸Ð°ÑÐ¸Ð¸ (ÐÐÐ). ÐÑÑÑÐµÑÑÐ²Ð»ÑÐ»Ð°ÑÑ ÑÐµÐ³Ð¸ÑÑÑÐ°ÑÐ¸Ñ Ð¿Ð¾Ð»ÐµÐ²ÑÑ Ð²Ð¾Ð·Ð±ÑÐ¶Ð´Ð°ÑÑÐ¸Ñ Ð¿Ð¾ÑÑÑÐ¸Ð½Ð°Ð¿ÑÐ¸ÑÐµÑÐºÐ¸Ñ Ð¿Ð¾ÑÐµÐ½ÑÐ¸Ð°Ð»Ð¾Ð² (Ð¿ÐÐÐ¡Ð) Ð¿Ð¾Ð»Ñ CA1 Ð³Ð¸Ð¿Ð¿Ð¾ÐºÐ°Ð¼Ð¿Ð° Ð² Ð¿ÐµÑÐµÐ¶Ð¸Ð²Ð°ÑÑÐ¸Ñ ÑÑÐµÐ·Ð°Ñ Ñ Ð¼ÑÑÐµÐ¹ Ð´Ð¸ÐºÐ¾Ð³Ð¾ ÑÐ¸Ð¿Ð° (WT) Ð¸ Ð¼ÑÑÐµÐ¹ Ñ Ð¼Ð¾Ð´ÐµÐ»ÑÑ Ð±Ð¾Ð»ÐµÐ·Ð½Ð¸ ÐÐ»ÑÑÐ³ÐµÐ¹Ð¼ÐµÑÐ° (5xFAD) Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ². Ð ÐµÐ³Ð¸ÑÑÑÐ°ÑÐ¸Ñ Ð¿ÑÐ¾Ð²Ð¾Ð´Ð¸Ð»Ð°ÑÑ ÑÐµÑÐµÐ· 4 Ð¼ÐµÑÑÑÐ° Ð¿Ð¾ÑÐ»Ðµ Ð²Ð²ÐµÐ´ÐµÐ½Ð¸Ñ Ð°Ð´ÐµÐ½Ð¾Ð°ÑÑÐ¾ÑÐ¸Ð¸ÑÐ¾Ð²Ð°Ð½Ð½ÑÑ Ð²Ð¸ÑÑÑÐ¾Ð² (ÐºÐ¾Ð½ÑÑÐ¾Ð»ÑÐ½ÑÐ¹ AAV2/7âmCherry, AAV2/7â3xFLAGâBcl-2-P2AâmCherry, AAV2/7â3xFLAGâ Bcl-2K17DâP2AâmCherry). ÐÐ¾ÑÐ»Ðµ Ð±ÑÐ»Ð° Ð¿ÑÐ¾Ð²ÐµÐ´ÐµÐ½Ð° Ð¾ÑÐµÐ½ÐºÐ° ÑÐ¸Ð½Ð°Ð¿ÑÐ¸ÑÐµÑÐºÐ¾Ð¹ Ð¿Ð»Ð°ÑÑÐ¸ÑÐ½Ð¾ÑÑÐ¸ Ð² Ð¿ÐµÑÐµÐ¶Ð¸Ð²Ð°ÑÑÐ¸Ñ ÑÑÐµÐ·Ð°Ñ Ð³Ð¸Ð¿Ð¿Ð¾ÐºÐ°Ð¼Ð¿Ð° Ð¼ÑÑÐµÐ¹ ÐºÐ¾Ð½ÑÑÐ¾Ð»ÑÐ½ÑÑ Ð¸ ÑÐºÑÐ¿ÐµÑÐ¸Ð¼ÐµÐ½ÑÐ°Ð»ÑÐ½ÑÑ Ð³ÑÑÐ¿Ð¿ Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ² Ð´Ð¾ Ð¸ Ð¿Ð¾ÑÐ»Ðµ Ð²Ð¾Ð·Ð´ÐµÐ¹ÑÑÐ²Ð¸Ñ Bcl-2 Ð¸ ÐµÐ³Ð¾ Ð¼ÑÑÐ°Ð½ÑÐ½Ð¾Ð¹ ÑÐ¾ÑÐ¼Ñ Bcl-2K17D. ÐÑÐ»Ð¾ Ð²ÑÑÑÐ½ÐµÐ½Ð¾, ÑÑÐ¾ Ð² Ð³ÑÑÐ¿Ð¿Ðµ Ð¼ÑÑÐµÐ¹ Ñ Ð¼Ð¾Ð´ÐµÐ»ÑÑ ÐÐ (5xFAD) Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ² ÐÐÐ Ð¾ÑÐ»Ð°Ð±Ð»ÐµÐ½Ð° Ð¿Ð¾ ÑÑÐ°Ð²Ð½ÐµÐ½Ð¸Ñ Ñ Ð¼ÑÑÐ°Ð¼Ð¸ Ð´Ð¸ÐºÐ¾Ð³Ð¾ ÑÐ¸Ð¿Ð° (WT), ÑÑÐ¾ ÑÐ¾Ð³Ð»Ð°ÑÑÐµÑÑÑ Ñ Ð»Ð¸ÑÐµÑÐ°ÑÑÑÐ½ÑÐ¼Ð¸ Ð´Ð°Ð½Ð½ÑÐ¼Ð¸.Â  Ð£ Ð¼ÑÑÐµÐ¹ Ð´Ð¸ÐºÐ¾Ð³Ð¾ ÑÐ¸Ð¿Ð° (WT) Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ² Ð¾ÑÐ»Ð°Ð±Ð»ÐµÐ½Ð¸Ðµ ÑÐ¾ÑÐ¼Ð¸ÑÐ¾Ð²Ð°Ð½Ð¸Ñ ÐÐÐ Ð²ÑÐ·ÑÐ²Ð°ÐµÑ Ð¼ÑÑÐ°Ð½ÑÐ½Ð°Ñ ÑÐ¾ÑÐ¼Ð° Ð±ÐµÐ»ÐºÐ° Bcl-2K17D. Ð£ Ð¼ÑÑÐµÐ¹ Ñ Ð¼Ð¾Ð´ÐµÐ»ÑÑ ÐÐ (5xFAD) Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ² Ð±ÐµÐ»Ð¾Ðº Bcl-2 Ð²Ð»Ð¸ÑÐµÑ Ð½Ð° ÑÐ¸Ð½Ð°Ð¿ÑÐ¸ÑÐµÑÐºÑÑ Ð¿Ð»Ð°ÑÑÐ¸ÑÐ½Ð¾ÑÑÑ Ð² Ð¿Ð¾Ð»Ðµ CA1 Ð³Ð¸Ð¿Ð¿Ð¾ÐºÐ°Ð¼Ð¿Ð°, ÑÑÐ¾ Ð¿ÑÐ¾ÑÐ²Ð»ÑÐµÑÑÑ Ð² ÑÐ²ÐµÐ»Ð¸ÑÐµÐ½Ð¸Ð¸ ÐÐÐ Ð¿Ð¾ ÑÑÐ°Ð²Ð½ÐµÐ½Ð¸Ñ Ñ ÐºÐ¾Ð½ÑÑÐ¾Ð»ÑÐ½Ð¾Ð¹ Ð³ÑÑÐ¿Ð¿Ð¾Ð¹ Ð¸ ÐµÐµ Ð²Ð¾ÑÑÑÐ°Ð½Ð¾Ð²Ð»ÐµÐ½Ð¸Ð¸ Ð´Ð¾ ÑÐ¸Ð·Ð¸Ð¾Ð»Ð¾Ð³Ð¸ÑÐµÑÐºÐ¾Ð¹ Ð½Ð¾ÑÐ¼Ñ (WT). ÐÑÐ¸ ÑÑÐ¾Ð¼ Ð±ÐµÐ»Ð¾Ðº Bcl-2 Ð¸ ÐµÐ³Ð¾ Ð¼ÑÑÐ°Ð½ÑÐ½Ð°Ñ ÑÐ¾ÑÐ¼Ð° Bcl-2K17D Ð½Ðµ Ð¾ÐºÐ°Ð·ÑÐ²Ð°ÑÑ Ð²Ð»Ð¸ÑÐ½Ð¸Ðµ Ð½Ð° Ð¿Ð¾ÑÑÑÐµÑÐ°Ð½Ð¸ÑÐµÑÐºÑÑ Ð¿Ð¾ÑÐµÐ½ÑÐ¸Ð°ÑÐ¸Ñ Ñ Ð¼ÑÑÐµÐ¹ Ð´Ð¸ÐºÐ¾Ð³Ð¾Â  ÑÐ¸Ð¿Ð° (WT) Ð¸ Ñ Ð¼Ð¾Ð´ÐµÐ»ÑÑ ÐÐ (5xFAD) Ð² Ð²Ð¾Ð·ÑÐ°ÑÑÐµ 6 Ð¼ÐµÑÑÑÐµÐ².
description: In this work we investigated the effect of the calcium channel inhibitor protein Bcl-2 on changes in long-term potentiality (LTP). Field excitatory postsynaptic potentials (FEPs) of the CA1 field of the hippocampus were recorded in the surviving slices in wild-type mice (WT) and mice with Alzheimers disease model (5xFAD) at 6 months of age. Registration was performed 4 months after injection of adeno-associated viruses (control AAV2/7-mCherry, AAV2/7-3xFLAG-Bcl-2-P2A-mCherry, AAV2/7-3xFLAG- Bcl-2K17D-P2A-mCherry). After that, synaptic plasticity was evaluated in the surviving hippocampal slices of control and experimental mice at 6 months of age before and after exposure to Bcl-2 and its mutant form. It was found that in the control group of AD model mice (5xFAD) at 6 months of age, LTP was attenuated compared with wild-type (WT) mice, which is consistent with the literature data.Â  In wild-type (WT) mice at 6 months of age, a mutant form of protein Bcl-2K17D causes attenuation of LTP formation. In AD model (5xFAD) mice at 6 months of age, the Bcl-2 protein affects synaptic plasticity in the CA1 field of the hippocampus, which is manifested by an increase in LTP compared with the control group and its restoration to physiological norm (WT). At the same time, Bcl-2 protein and its mutant form Bcl-2K17D have no effect on posttetanic potentiality in wild-type (WT) and AD model (5xFAD) mice at 6 months of age.