Cheng J T, Schallert T, De Ryck M, Teitelbaum P
Proc Natl Acad Sci U S A. 1981 May;78(5):3279-83. doi: 10.1073/pnas.78.5.3279.
Localized lesions or local applications of gamma-aminobutyric acid (GABA) in the nucleus reticularis tegmenti pontis (NRTP) of rats cause rapidly accelerating forward locomotion. Such "festination" can coexist with blockade of the dopamine system. We suggest that (i) the akinesia produced by dopamine deficiency results at least in part from release of excessive inhibition of locomotion by a neural system whose final common inhibitory path includes the region of the NRTP and (ii) when it occurs in addition to nigrostriatal damage, destruction in the region of the NRTP might be the cause of a form of festination seen in some patients suffering from Parkinsonism.
在大鼠脑桥被盖网状核（NRTP）中，γ-氨基丁酸（GABA）的局部损伤或局部应用会导致向前运动迅速加速。这种“慌张步态”可与多巴胺系统的阻断同时存在。我们认为：（i）多巴胺缺乏所产生的运动不能至少部分是由于一个神经系统对运动的过度抑制作用的释放所致，该神经系统的最终共同抑制路径包括NRTP区域；（ii）当除黑质纹状体损伤外还发生这种情况时，NRTP区域的破坏可能是一些帕金森病患者出现的一种慌张步态的原因。
