Effect of θ–γ neural oscillation stimulation in hippocampal CA3 area on spatial cognition ability in rats

θ-γ神经振荡刺激海马CA3区对大鼠空间认知能力的影响

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Abstract

Objective: To investigate the effects of θ–γ neural oscillation stimulation in hippocampal CA3 area on spatial cognition ability in rats. Methods: According to the results of Y maze shock avoidance training, the rats were divided into fast avoidance response group and general avoidance response group. Using endogenous θ–γ neural oscillations from the fast avoidance response rats to perform deep brain stimulation in vivo to the left and right hippocampal CA3 region of rats with general avoidance response, then the spatial cognition was tested by Y maze shock avoidance training. The variation of θ oscillation and low-γ neural oscillation phase-amplitude coupling (PAC) in CA3 area was analyzed by wavelet packet extraction technique. Western blotting was used to detect the expression of N-methyl-D-aspartate receptor 2B subunit (NR2B) and postsynaptic density(PSD)-95 in hippocampal tissues of rats to explore its molecular mechanism. Results: Compared with the general avoidance response rats, the days to reach the standard, the training number, the correct response time and the error reaction number in simulated stimulus avoidance response rats were significantly reduced, but the correct response rate was significantly increased (all P<0.01); the θ–γ neural oscillations PAC in the hippocampal CA3 region in the simulated stimulus avoidance response rats (3–5 Hz and 30–34, 38–42, 44–48 Hz; 5–7 Hz and 42–46, 44–48, 54–58 Hz) were significantly higher than that in the general avoidance response rats (all P<0.05). Meanwhile, the protein expressions of NR2B and PSD-95 in hippocampal tissues were significantly increased (both P<0.05) in simulated stimulus avoidance response rats. Conclusion: The spatial cognition of normal avoidance response rats can be significantly improved by endogenous θ–γ neural oscillation stimulation to hippocampal CA3 region, which may be caused by the enhancement of synaptic plasticity mediated by NR2B and PSD-95.

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