過度神經元刺激可促進腦神經可塑性，腦血循環與神經元活性息息相關。聲音刺激對幼鼠中樞聽覺神經系統之腦神經元及腦血管網絡之關係並不清楚。我們有興趣探討長期聲音刺激對聽覺中樞腦神經及血管結構之關係。我們利用幼鼠(出生第三週)為研究主要動物模式，給予低音頻刺激，在不同的音頻刺激時間觀察聽覺中樞腦神經元及相關腦區血管結構變化。首先我們利用功能性神經活性標幟(Fos)，標定幼鼠聽覺中腦(下丘)及耳蝸神經元在短時間對不同音頻的活性反應；實驗結果發現功能性神經活性標幟(Fos)表現於低音頻區而且表現的時間由十分鐘開始出現延至九十分鐘，表示短時間音頻刺激可誘發聽腦神經元活性變化。第二部份，我們觀察音頻刺激對聽覺中腦下丘及主要聽覺皮層的神經細胞之顯微結構(細胞核及細胞質)之影響；發現在音頻刺激後第五天後，聽覺中腦神經元之細胞質在低音頻區有增大現象，增長音頻刺激時間到第七天，聽覺神經元的增大現象由低音頻區擴大到高音頻區的趨勢。第三部份，我們探討音頻刺激的不同時間周期對聽覺中腦及主要聽覺皮層的血管結構之影響；發現音頻刺激後第三天，圍繞小血管旁的細胞數目表現量增加；音頻刺激後第七天，聽覺中腦及主要聽覺皮層的微血管密度增加，表示音頻刺激可能同時誘發聽覺神經元或血管的變化。最後我們探討音頻刺激對聽覺腦神經細胞及誘發血管重塑之相關機制，觀察細胞增生標幟(BrdU)神經膠細胞(GFAP)，促進血管新生因子(VEGF)之表現；發現音頻後第七天，已分化的細胞表現於聽覺中腦及聽覺皮層；進一步以雙重染色法確認分化細胞的來源，推測音頻刺激下可能同時誘發神經元或神經膠細胞分化；也發現音頻刺激後聽覺腦區的促進血管新生因子表現量增加的趨勢，推測音頻刺激可能誘發促進血管新生因子之表現進而促進血管新生。結果表示長期音頻刺激可誘發幼鼠聽覺中樞神經細胞與腦血管新生之相關性，實驗結果與文獻報導相關的刺激腦神經元活性可促進腦神經及腦血管可塑性吻合。

Over-activity of neurons leads to plastic changes in brain cells. Cerebral blood flow is also known to be tightly coupled to neural activities. Whether over-activity induced in a sensory system can drive both neural and vascular remodeling remain unclear. To answer this question, we used the auditory midbrain and cortex of young adult rats as a model, and investigated in 4 experiments the time course and details of sound exposure effects over a period of 2 weeks (immuno-histochemical study of Fos-expression, cyto-morphometrical study of neuronal size, morphometrical study of micro-vasculature, and cyto- and histo- chemical study with BrdU, GFAP and VEGF). Results from the first experiment revealed tonotopic Fos-expression in auditory neurons within hours after sound stimulation, with different subpopulations of neurons activated by sounds of different time-varying properties. Findings are consistent with an early onset of neural changes which could precede vascular remodeling. Results from the second experiment showed a marked sound-driven enlargement of neuronal size in a tonotopic manner on exposure day 5, and the effect spread to all frequency regions on day 7, but without affecting other non-auditory system. Results from the third experiment showed that sound-driven increases in the juxta-vascular cell density appeared first on day 3; whereas capillary density increased later (day 7). Findings suggested that vascular changes may occur concomitantly with, if not earlier than, the change in neuronal size. Results from the fourth experiment showed that sound-driven cell divisions appeared in the auditory system. Result on double-labeling the divided cells with GFAP was inconclusive, although information derived from the size histograms of cell nuclei suggested that dividing cells might come from both glia and neurons. The elevated level of the VEGF is consistent with a possible causal relationship with the observed sound-driven changes in neurons and blood vessels. Our findings represent the first evidence that over-activity with sound stimulation promotes both neuronal and micro-vascular development in the central auditory system in a temporally-specific and modality-dependent manner. Results on the rather concomitant plastic changes in neurons and blood vessels are consistent with the tightly-coupled nature of the neuro-vascular system in the young adult brain.

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