Effects of inflammatory pain in rats on synaptic plasticity in anterior cingulate cortex time and space


Effect of inflammatory pain in rats on synaptic plasticity of anterior cingulate cortex time and space in multi-electrode array recording system
Spatial and temporal plasticity of synaptic organization in anterior cingulate cortex following peripheral inflammatory pain:multi-electrode array recordings in rats
 
Yun-Fei Lu, Yan Wang, Ying He, Fu-Kang Zhang, Ting He, Rui-Rui Wang, Xue-Feng Chen, Fei Yang, Ke-Rui Gong, Jun Chen
Neurosci Bull May, 2013. http:// DOI: 10.1007/s12264-013-1344-9
 
To investigate whether inflammatory pain has a certain effect on synaptic tissue in the cortex, we used Japanese MED64 (AlphaMed, Osaka) planar multi-electrode array (MEA) technology and 2-dimensional current source density (2D-CSD) imaging technology to Rat anterior cingulate cortex (ACC) sections were studied. Deep electrical stimulation was performed using MED64 electrodes to induce synaptic activity between different layers of ACC. We analyzed the localized field potential (LFP) of untested rats and the pharmacological properties of current sink diffusion calculated by 2-dimensional current source density analysis. In addition, changes in induced long-term potentiation (LTP) and LTP amplitude were also evaluated. We found that in untested rats, the current trap was originally produced on layer 6 (layer VI) and then spread to layer 5 (layer V) and eventually to layer 2/3 (layer II-III). The spatial characteristics of the current trap diffusion are consistent with the spatial characteristics of the depolarization position change from the deep layer (V-VI layer) to the surface layer (II-III), and the II-III layer is also the signal input terminal of the inner cortex and the outer cortex. point. When the plantar venom was injected into the foot to induce inflammation in the rats (2 hours long), the spatial distribution of synaptic tissue in the ACC was significantly changed, showing an enlarged current trap distribution compared with the experimental and physiological saline-free rats. The left-shifted stimulus response curve. These changes are more pronounced in the shallow (II-III) than in the deep. In terms of speed, the induction rate of LTP caused by inflammatory pain increased significantly in the II-III layer. However, there is no significant increase in the magnitude of the LTP. In summary, inflammatory pain produces significant synaptic plasticity position and rate changes in ACC, which may result in changes and modulation of synaptic transmission.
Med64 planar multi-electrode array recording system
 
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