後端島腦皮層在大鼠神經痛模式中扮演之角色

Abstract

神經痛是臨床上難以根治的一種神經疾病。它會造成中樞神經系統神統神經 可塑性永久的變化。島腦皮質是大腦中可接受不同種類感覺訊息傳入的部位，許 多研究顯示後端島腦能接收體感覺訊息，尤其是疼痛相關訊息的處理。然而，後 端島腦對於神經痛的形成與維持的貢獻仍然不清楚。本實驗將後端島腦進行永久 性破壞，觀察破壞後對神經痛模式大鼠行為指標的影響。結果顯示，破壞後端島 腦可以使得神經痛造成的機械性觸感痛有緩慢少許的回覆；冷覺反應也在破壞後 端島腦後有短暫減緩的情形。神經痛之前先破壞後端島腦則造成機械性觸感痛發 展較輕微；自發性疼痛沒有明顯差別，而冷覺觸感痛有加速發展的現象。神經追 蹤劑的研究結果發現，後端島腦會投射至視丘的後端三角核，而此核區主要接受 來自於脊髓的痛覺訊息。本實驗發現到後端島腦可能參與了神經痛在機械性觸感 痛的長期維持。此外，不同的神經痛症狀可能由不同大腦核區處理。

Neuropathic pain is an intractable disease in daily life and clinical research. It can result in long-term changes in central nervous system. Insular cortex is a brain region participated in processing of different sensory modalities. Evidences have also shown that posterior insular cortex may be related to somatosensory perception especially in nociception. However, the role for how PIC contributes to the initiation or maintenance of neuropathic pain is less understood. In the present study, permanent lesion by NMDA excitotoxicity in PIC was used to assess the response to pain. Results showed that after PIC lesion in neuropathic rats, the mechanical threshold recovered gradually. The spontaneous paw lifting showed no improve, and withdrawal response to cold were transiently diminished. PIC pre-lesion resulted in less decreased mechanical threshold, and transient decrement of spontaneous paw lifting. However, there were faster development of cold allodynia. Tracer study revealed that PIC had a strong connection to posterior triangular thalamic nucleus and periaqueductal gray. These data suggested the partial role of PIC to maintain mechanical allodynia in neuropathic pain. Moreover, spontaneous pain, mechanical allodynia and cold allodynia of neuropathic pain might be differentially processed in the forebrain.