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上丘的去抑制作用可恢复猫偏盲视野中对视觉刺激的定向能力。

Disinhibition of the superior colliculus restores orienting to visual stimuli in the hemianopic field of the cat.

作者信息

Ciaramitaro V M, Todd W E, Rosenquist A C

机构信息

Department of Neuroscience, University of Pennsylvania, Philadelphia 19104, USA.

出版信息

J Comp Neurol. 1997 Nov 3;387(4):568-87. doi: 10.1002/(sici)1096-9861(19971103)387:4<568::aid-cne7>3.0.co;2-0.

DOI:10.1002/(sici)1096-9861(19971103)387:4<568::aid-cne7>3.0.co;2-0
PMID:9373014
Abstract

Following unilateral removal of all known visual cortical areas, a cat is rendered hemianopic in the contralateral visual field. Visual orientation can be restored to the blind hemifield by transection of the commissure of the superior colliculus or by destruction of the superior colliculus (SC) or the substantia nigra pars reticulata (SNpr) contralateral to the cortical lesion. It is hypothesized that a mechanism mediating recovery is disinhibition of the SC ipsilateral to the cortical lesion. The ipsilateral nigrotectal projection exerts a robust inhibitory tone onto cells in the SC. However, ibotenic acid destruction of SNpr neurons, which should decrease inhibition onto the SC, does not result in recovery. The failure of ipsilateral SNpr lesions to produce recovery puts into question the validity of SC disinhibition as a mechanism of recovery. We directly tested the disinhibition hypothesis by reversibly disinhibiting the SC ipsilateral to a visual cortical lesion with a gamma-aminobutyric acid (GABA)A antagonist, bicuculline methiodide. In accordance with the hypothesis, transient disinhibition of the SC restored visual orienting for several hours in three of eight animals. Recovery was not a volume or pH effect and was distinct from the release of irrepressible motor effects (i.e., approach and avoidance behaviors) seen within the first hour after injection. Thus, in the absence of all visual cortical areas unilaterally, disinhibition of the SC can transiently restore the ability of the cat to orient to visual stimuli in the previously "blind" hemifield.

摘要

在单侧切除所有已知的视觉皮层区域后,猫会在对侧视野出现偏盲。通过切断上丘连合、破坏与皮层损伤对侧的上丘(SC)或黑质网状部(SNpr),视觉定向功能可恢复到盲侧半视野。据推测,介导恢复的机制是对皮层损伤同侧的上丘进行去抑制。同侧黑质 - 上丘投射对SC中的细胞施加强烈的抑制性张力。然而,用鹅膏蕈氨酸破坏SNpr神经元(这应会减少对SC的抑制)并未导致恢复。同侧SNpr损伤未能产生恢复,这使人质疑SC去抑制作为恢复机制的有效性。我们通过用γ-氨基丁酸(GABA)A拮抗剂甲磺酸荷包牡丹碱可逆性地解除对视觉皮层损伤同侧SC的抑制,直接检验了去抑制假说。与假说一致,在八只动物中的三只中,SC的短暂去抑制使视觉定向恢复了数小时。恢复并非体积或pH效应,且与注射后第一小时内出现的不可抑制的运动效应(即趋近和回避行为)的释放不同。因此,在单侧没有所有视觉皮层区域的情况下,对SC的去抑制可暂时恢复猫在先前“盲”侧半视野中对视觉刺激进行定向的能力。

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