Repetitive microstimulation in rat primary somatosensory cortex (SI) strengthens the connection between homotopic sites in the opposite SI and leads to expression of previously ineffective input from the ipsilateral forelimb.
Repetitive microstimulation in rat primary somatosensory cortex (SI) strengthens the connection between homotopic sites in the opposite SI and leads to expression of previously ineffective input from the ipsilateral forelimb.
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大鼠初级体感皮层 (SI) 中的重复微刺激加强了相反 SI 中同伦位点之间的联系，并导致同侧前肢先前无效的输入表达。
DOI：
10.1016/j.brainres.2020.146694
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发表时间：
2020
期刊：
影响因子：
2.9
通讯作者：
Waters,RobertS
中科院分区：
文献类型：
--
作者：
DeCosta-Fortune,TinaM;Ramshur,JohnT;Li,ChengX;deJonghCurry,Amy;Pellicer-Morata,Violeta;Wang,Lie;Waters,RobertS
初级躯体感觉皮层(SI)接受对侧前肢的输入，投射到对侧SI的同位部位。由于SI中的同位部位通过一条胼胝体通路联系在一起，我们提出重复皮质内微刺激(ICMSr)SI前肢皮质V层神经元将增加对侧SI皮层的棘波放电，从而充分地加强了胼胝体通路，从而允许来自同侧前肢的正常无效刺激兴奋同侧SI细胞。通过机械和电刺激对侧前肢，定位一侧SI的前肢表示，在对侧SI中类似地确定同源位置，在两个同位位置测试同侧外周输入的存在，并使用ICMS在两个同位记录位置之间建立半球间连接。主要结果是：(1)SI内的每个同位前肢部位最初只接受来自对侧前肢的短潜伏期输入；(2)每个SI内V层的同位部位之间通过一条胼胝体通路相连；(3)ICMSr传递到一侧同位SI的V层时，对侧同位部位V层的诱发反应棘波放电普遍增加；(4)放电增加后往往伴随着来自同侧前肢的较长潜伏期的正常无效输入的表达；(5)这些较长的潜伏期反应与足以解释跨越腓总神经通路的延迟时间相一致；(6)刺激性放电的增加和由此产生的同侧外周输入也被体内细胞内记录所证实；(7)注射利多卡因或局部表面降温使SI的刺激部位失活，取消了同侧的反应，表明同侧的反应很可能是通过胼胝体通路传递的。这些结果表明，重复微刺激不仅可以扩大刺激电极附近区域的感受野，而且还可以改变对侧SI同位部位的感受野，使来自同侧前肢的无效输入表达出来。
The primary somatosensory cortex (SI) receives input from the contralateral forelimb and projects to homotopic sites in the opposite SI. Since homotopic sites in SI are linked by a callosal pathway, we proposed that repetitive intracortical microstimulation (ICMSr) of neurons in layer V of SI forelimb cortex would increase spike firing in the opposite SI cortex thereby strengthening the callosal pathway sufficiently to allow normally ineffective stimuli from the ipsilateral forelimb to excite cells in the ipsilateral SI. The forelimb representation in SI in one hemisphere was mapped using mechanical and electrical stimulation of the contralateral forelimb, a homotopic site was similarly identified in the opposite SI, the presence of ipsilateral peripheral input was tested in both homotopic sites, and ICMS was used to establish an interhemispheric connection between the two homotopic recording sites. The major findings are: (1) each homotopic forelimb site in SI initially received short latency input only from the contralateral forelimb; (2) homotopic sites in layer V in each SI were interconnected by a callosal pathway; (3) ICMSr delivered to layer V of the homotopic SI in one hemisphere generally increased evoked response spike firing in layer V in the opposite homotopic site; (4) increased spike firing was often followed by the expression of a longer latency normally ineffective input from the ipsilateral forelimb; (5) these longer latency ipsilateral responses are consistent with a delay time sufficient to account for travel across the callosal pathway; (6) increased spike firing and the resulting ipsilateral peripheral input were also corroborated using in-vivo intracellular recording; and (7) inactivation of the stimulating site in SI by lidocaine injection or local surface cooling abolished the ipsilateral response, suggesting that the ipsilateral response was very likely relayed across the callosal pathway. These results suggest that repetitive microstimulation can do more than expand receptive fields in the territory adjacent to the stimulating electrode but in addition can also alter receptive fields in homotopic sites in the opposite SI to bring about the expression of previously ineffective input from the ipsilateral forelimb.