Horváth E J, Fekete M I, Palkovits M
Institute for Drug Research, Budapest, Hungary.
Brain Res Mol Brain Res. 1997 Apr;45(1):141-4. doi: 10.1016/s0169-328x(96)00293-8.
Neurotoxin (AMPA)-induced lesions in the caudate nucleus as well as unilateral surgical transection of the striato-nigral pathway strongly depleted the binding of a homophthalazine (formerly called 2,3-benzodiazepines) girisopam (GYKI-51189, EGIS 5810) selectively in the substantia nigra of the rat, ipsilateral to the lesions. In contrast to this, AMPA injections into the substantia nigra failed to effect on girisopam binding to either components of the nigro-striatal system. Data indicate that this homophthalazine may bind to a descending component of the striatum (striato-nigral projecting neurons), or its binding capacity to substantia nigra neurons depends on the integrity of striatal afferent pathways to the substantia nigra.
神经毒素（AMPA）诱导的尾状核损伤以及纹状体 - 黑质通路的单侧手术横断，强烈地耗尽了大鼠黑质中一种高酞嗪（以前称为2,3 - 苯二氮卓类）吉立帕泮（GYKI - 51189，EGIS 5810）的结合，损伤同侧黑质中的结合量明显减少。与此形成对比的是，向黑质注射AMPA未能影响吉立帕泮与黑质 - 纹状体系统任何组分的结合。数据表明，这种高酞嗪可能与纹状体的下行组分（纹状体 - 黑质投射神经元）结合，或者其与黑质神经元的结合能力取决于纹状体至黑质传入通路的完整性。
