Effects of repetitive transcranial magnetic stimulation on synaptic plasticity and apoptosis in vascular dementia rats

Behav Brain Res. 2015 Mar 15:281:149-55. doi: 10.1016/j.bbr.2014.12.037. Epub 2014 Dec 22.

Abstract

This study aims to determine whether low-frequency repetitive transcranial magnetic stimulation (rTMS) protects pyramidal cells from apoptosis and promotes hippocampal synaptic plasticity in a vascular dementia (VaD) rat model. Following establishment of a VaD rat model using two-vessel occlusion (2VO), learning and memory were evaluated via the Morris Water Maze (MWM), hippocampal CA1 neuron ultrastructure was examined via electron microscopy, and hippocampal synaptic plasticity was assessed by long-term potentiation (LTP). Western blot was used to detect the expression of N-methyl-d-aspartic acid receptor 1 (NMDAR1), Bcl-2, and Bax. Compared with VaD group, rats treated with low-frequency rTMS had reduced-escape latencies, increased swimming time in the target quadrant (P<0.05), and significantly less synaptic structure damage. LTP at hippocampal CA3-CA1 synapses was enhanced (P<0.05). Low-frequency rTMS significantly up-regulated NMDAR1 and Bcl-2 expression and down-regulated Bax expression. Low-frequency rTMS improves learning and memory, protects the synapse, and increases synaptic plasticity in VaD model rats. Increased Bcl-2 expression and reduced Bax expression may be a novel protective mechanism of low-frequency rTMS treatment for VaD.

Keywords: Apoptosis; Long-term potentiation; Morris water maze; Repetitive transcranial magnetic stimulation; Vascular dementia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Behavior, Animal
  • Dementia, Vascular / pathology
  • Dementia, Vascular / physiopathology
  • Dementia, Vascular / psychology
  • Dementia, Vascular / therapy*
  • Disease Models, Animal
  • Hippocampus / metabolism
  • Hippocampus / pathology*
  • Hippocampus / physiopathology
  • Long-Term Potentiation
  • Male
  • Maze Learning
  • Memory*
  • Neuronal Plasticity*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pyramidal Cells / metabolism
  • Pyramidal Cells / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Transcranial Magnetic Stimulation / methods*
  • Treatment Outcome
  • bcl-2-Associated X Protein / metabolism

Substances

  • NMDA receptor A1
  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, N-Methyl-D-Aspartate
  • bcl-2-Associated X Protein