Marek G J, McMaster S E, Gormezano I, Harvey J A
Brain Res. 1984 May 14;299(2):215-29. doi: 10.1016/0006-8993(84)90703-0.
Electrolytic and knife-cut lesions were employed in the rabbit to examine the role of the VIth cranial nerve, and of the motoneurons in the abducens (ABD) and accessory abducens (ACC) nuclei that supply the VIth nerve, in the reflex extension of the nictitating membrane. The nictitating membrane response (NMR) was elicited by tactual stimulation of the cornea with a puff of air or by electric shock delivered to the skin over the paraorbital region of the head. Total destruction of the VIth nerve or interruption of all ACC inputs to the VIth nerve (while leaving ABD inputs intact) produced a large and comparable reduction in the magnitude of the NMR elicited by air puff, although a small residual NMR of less than 1 mm could still be detected. In contrast, the magnitude of the NMR elicited by shock was not affected by ACC isolation and only reduced by 50% after VIth nerve lesions. Total isolation of ABD inputs to the VIth nerve (while leaving ACC inputs intact) had no effect on NMR magnitude elicited by either air puff or shock. The small residual NMRs to air puff and the larger NMRs to shock remaining after total destruction of the VIth nerve were not eliminated by the removal of all extraocular muscles (while leaving the retractor bulbi muscle intact). However, knife cut lesions that interrupted all ACC inputs to the VIth nerve and transected the VIIth (facial) nerve completely eliminated NMRs elicited by both air puff and shock. The results of this study indicate that NMRs elicited by tactual stimulation of the cornea are primarily mediated by retractor bulbi motoneurons in the ACC nucleus via the VIth nerve. In contrast, NMRs elicited by electric shock delivered to the skin over the paraorbital region of the head are produced by contraction of the retractor bulbi muscle via the VIth nerve and by contraction of the orbicularis oculi muscle via the VIIth nerve which then squeezes the nictitating membrane over the cornea.
在兔子身上采用电解和刀切损伤的方法，以研究第六对脑神经以及供应第六对脑神经的展神经核（ABD）和副展神经核（ACC）中的运动神经元在瞬膜反射性伸展中的作用。瞬膜反应（NMR）通过用一股气流轻触角膜或通过电击头部眶周区域的皮肤来引发。第六对脑神经的完全破坏或所有ACC对第六对脑神经的输入中断（同时保留ABD输入完整），会使气流引发的NMR幅度大幅且相当程度地降低，尽管仍能检测到小于1毫米的小残余NMR。相比之下，电击引发的NMR幅度不受ACC分离的影响，仅在第六对脑神经损伤后降低50%。第六对脑神经的ABD输入完全分离（同时保留ACC输入完整）对气流或电击引发的NMR幅度没有影响。在第六对脑神经完全破坏后，对气流的小残余NMR和对电击的较大NMR，在切除所有眼外肌（同时保留眼球退缩肌完整）后并未消除。然而，切断所有ACC对第六对脑神经的输入并完全横断第七对（面神经）的刀切损伤，完全消除了气流和电击引发的NMR。本研究结果表明，角膜触觉刺激引发的NMR主要由ACC核中的眼球退缩运动神经元通过第六对脑神经介导。相比之下，电击头部眶周区域皮肤引发的NMR是由眼球退缩肌通过第六对脑神经收缩以及眼轮匝肌通过第七对脑神经收缩产生的，然后眼轮匝肌挤压角膜上的瞬膜。
