Effects of transcranial magneto-acoustical stimulation on beta oscillations in neural circuits of healthy and Parkinson’s disease rats

doi:10.12307/2024.302

Abstract

Abstract: BACKGROUND: Transcranial magneto-acoustical electrical stimulation (TMAES) is a non-invasive, high-precision neurofocused stimulation method based on magneto-acoustic coupling electrical effect, which can regulate the rhythmic oscillation of nerve activity, thereby affecting the brain’s movement, cognition and other functions.
OBJECTIVE: To explore the effect of TMAES on beta oscillations in the neural circuits of healthy rats and Parkinson’s rats.
METHODS: (1) Animal experiments: Twenty-four Wistar rats were randomly divided into four groups (n=6 per group). The rats in the normal control group received no intervention, while those in the normal stimulation group received TMAES (the average spatial peak pulse intensity: 13.33 W/cm2, fundamental frequency: 0.4 MHz, the number of fundamental wave cycles: 1000, and pulse frequency: 200 Hz). The model control group and model stimulation group were established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. After successful modeling, the rats in the model control group received sham TMAES stimulation in the prefrontal cortex, and those in the model stimulation group received TMAES in the prefrontal cortex, and the duration of stimulation was 2.0 minutes per day. After an interval of 8-10 minutes, the local field potential signals of rats were collected during the execution of T-maze test and the correct rate of behavior was recorded at the same time to compare and analyze the time-frequency distribution of local field potential signals and behavioral differences among the groups. The stimulation experiment and T-maze test were stopped when the correct rate of rats was higher than 80% for 3 consecutive days. (2) Modeling and simulation experiments: The cortical-basal ganglion circuit model under TMAES was established, and the ultrasonic emission period (5, 10, 20 ms), ultrasonic emission duty cycle (30%, 50%, 90%) and induced current density (20, 50, 100 μA/cm2) were changed respectively to compare the power spectral density values of beta oscillations in healthy rats and Parkinson’s rats under different stimulation parameters.
RESULTS AND CONCLUSION: (1) Animal experiments: The spatial learning ability of the rats in the normal control group was stronger than that of the model control group (P < 0.001), the spatial learning ability of the rats in the normal stimulation group was stronger than that of the normal control group (P < 0.05), and the spatial learning ability of the rats in the model stimulation group was stronger than that of the model control group (P < 0.01). The distribution of beta oscillation energy in the normal control group was more concentrated, and the beta oscillation signal energy was reduced in the normal stimulation group compared with the normal control group. The beta oscillation energy was widely distributed and the energy value was significantly higher in the model control group and the model stimulation group than the normal control and normal stimulation groups. Moreover, the beta oscillation signal energy in the model stimulation group was significantly lower than that in the model control group. (2) Modeling and simulation experiments: the peak power spectral density of the beta band of healthy rats without stimulation (30 dB) was significantly lower than that of Parkinson’s rats (55 dB). The power spectral density value generally decreased after stimulation. The peak power spectral density in the beta band was positively correlated with the ultrasonic emission period and negatively correlated with the induced current density. In addition, the peak power spectral density value was the lowest when the duty cycle of ultrasonic emission was 50%. These findings indicate that TMAES suppresses beta oscillations in healthy and Parkinson's disease rats, thereby improving motor function and decision-making cognitive function in rats.

Key words: transcranial magneto-acoustical electrical stimulation, cortical-basal ganglion circuit, beta oscillation, Parkinson’s disease, local field potential, T maze, neuromodulation

CLC Number:

Zhang Shuai, You Shengnan, Du Wenjing, Wang Lei, Xu Guizhi. Effects of transcranial magneto-acoustical stimulation on beta oscillations in neural circuits of healthy and Parkinson’s disease rats[J]. Chinese Journal of Tissue Engineering Research, 2024, 28(16): 2519-2526.

Figures/Tables 7

施加经颅磁声电刺激后，普遍存在功率谱密度值下降的现象，如图8A所示，当超声发射占空比为50%、感应电流密度为100 μA/cm2时，调节超声发射周期为5，10，20 ms时发现，正常刺激组发射周期为5 ms时的功率谱密度值最低、20 ms时的功率谱密度值最高，但低于正常对照组。说明对健康大鼠施加经颅磁声电刺激降低了beta频段的功率谱密度值，且功率谱密度值随着超声发射周期的增加而增大。调节超声发射周期改变了神经元放电节律，推测与超声发射周期和神经元动作电位的发放率呈正比关系有关[6]，发射周期的增大导致神经元动作电位发放率的增大，进而出现更多较高频的beta节律振荡。如图8B所示，当超声发射周期为10 ms、感应电流密度为100 μA/cm2时，调节正常刺激组超声发射的占空比为30%，50%，90%时发现，当占空比为50%时，功率谱密度值最低且波动最小，占空比为30%和90%时的功率谱密度幅值均高于50%，但低于正常对照组。由此看出，当占空比接近50%时，经颅磁声电刺激抑制beta振荡的效果最好，这可能与占空比可影响经颅磁声电刺激的去同步效果有关，神经系统对调制波的占空比具有选择性，系统的同步状态分布在占空比为10%-30%和80%-90%之间，去同步状态集中于40%-70%[42]，在去同步状态中beta频段振幅降低，导致功率谱密度值低于其他占空比。如图8C所示，当超声发射周期为10 ms、占空比为50%时，改变正常刺激组感应电流密度为20，50，100 μA/cm2时发现，感应电流密度为100 μA/cm2时功率谱密度值最低，当感应电流密度为50 μA/cm2时，功率谱密度值有所提高，但低于正常对照组，当感应电流密度进一步降低为20 μA/cm2时功率谱密度值进一步提高。说明改变经颅磁声电刺激的感应电流密度可调节beta频段的功率谱密度值，二者之间呈现负相关，推测是因为感应电流密度的提高增大了皮质神经元的突触输入，皮质基底神经节直接通路与间接通路共同发挥作用，抑制了大鼠皮质-基底神经节环路中的beta振荡。 2.2.2 帕金森病大鼠仿真实验结果如图9所示，过度的beta振荡是帕金森病的主要特征，由于帕金森病大鼠黑质纹状体内多巴胺显著减少，导致直接通路中含有D1受体的纹状体神经元的兴奋性降低、间接通路中含有D2类受体的纹状体神经元的抑制性降低，进一步导致纹状体对苍白球内侧部的抑制削弱，使得健康状态的平衡被打破，进而促进帕金森病疾病的表现，使beta频段功率谱密度值主要在10-52 dB范围内波动，明显高于健康大鼠。"

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