Deficits in smooth-pursuit eye movements after muscimol inactivation within the primate's frontal eye field.
Deficits in smooth-pursuit eye movements after muscimol inactivation within the primate's frontal eye field.
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灵长类动物额眼区域内蝇蕈醇失活后，平滑追踪眼球运动出现缺陷。
DOI：
10.1152/jn.1998.80.1.458
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Bruce,CJ
中科院分区：
文献类型：
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作者：
Shi,D;Friedman,HR;Bruce,CJ
史德修，哈里特·r·弗里德曼，查尔斯·j·布鲁斯。灵长类动物前眼野肌素失活后眼球平滑追踪运动的缺陷。中国生物医学工程学报，2009,31(2):457 - 464。为了评估灵长类动物额眼场（FEF）的平滑追踪（SP）功能，采用显微注射γ-氨基丁酸（GABA）激动剂muscimol来可逆地失活额眼场的生理特征位点。位于猕猴弓状沟眼底和后缘的FEF平滑眼动区（FEFsem）的失活使SP严重受损。这些SP缺陷在注射muscimol后立即出现，并持续数小时，但在第二天恢复。与注射部位引发的平滑眼动方向或其神经元反应的最佳SP方向相似的方向，SP的损害最为严重和持续。在这些方向上运动的目标，通常与注射的半球同侧，在注射muscimol后主要用扫视来追踪，峰值SP速度仅为注射前速度的10-30%。其他方向（包括对侧）SP受影响较小。响应目标运动开始的初始SP加速度也显着降低，通常与峰值SP速度的比例大致相同。相比之下，在FEFsem中，注射muscimol对扫视基本没有影响；当FEF （FEFsac）的眼跳区控制位点失活时，SP也不会立即受到影响，尽管FEFsac注射后30-60分钟经常出现SP缺陷，这可能反映了muscimol向邻近FEFsem的扩散。FEFsem中肌肉分子失活产生的可逆性SP缺陷与FEF大吸入病变引起的永久性SP缺陷相似，表明FEFsem是决定FEF病变是否损害SP的关键因素。这里发现的可逆性缺陷的严重程度表明FEFsem对正常高增益SP是多么关键。
Shi, Dexiu, Harriet R. Friedman, and Charles J. Bruce.Deficits in smooth-pursuit eye movements after muscimol inactivation within the primate's frontal eye field.J. Neurophysiol.80: 458–464, 1998. To evaluate smooth-pursuit (SP) function in the primate frontal eye field (FEF), microinjections of muscimol, a γ-aminobutyric acid (GABA) agonist, were used to reversibly deactivate physiologically characterized sites in FEF. SP was severely impaired by deactivation at sites in the FEF's smooth eye movement region (FEFsem) located in the fundus and posterior bank of the macaque monkey's arcuate sulcus. These SP deficits were apparent immediately after the muscimol injection and persisted for several hours but recovered by the next day. SP was most drastically and consistently impaired for directions similar to the injected site's elicited smooth eye movement direction or to the optimal SP direction for its neuronal responses. Targets moving in these directions, usually ipsilateral to the injected hemisphere, were tracked primarily with saccades after the muscimol injection, the peak SP velocity being only 10–30% of preinjection velocity. SP in other directions, including contralateral, was less strongly affected. Initial SP acceleration in response to target motion onset was also significantly diminished, generally by approximately the same proportion as peak SP velocity. In contrast, saccades were largely unaffected by muscimol injections in FEFsem; nor was there an immediate effect on SP when control sites in the saccadic region of FEF (FEFsac) were deactivated, although a SP deficit often appeared 30–60 min after FEFsac injections, possibly reflecting diffusion of muscimol into neighboring FEFsem. These reversible SP deficits produced by muscimol inactivation within FEFsem are similar to permanent deficits caused by large aspiration lesions of FEF and indicate that inclusion of FEFsem is the critical factor determining whether FEF lesions impair SP. The severity of the reversible deficits found here indicates how extremely critical FEFsem is for normal highgain SP.