Kish S J, Perry T L, Sweeney V P, Hornykiewicz O
Neurosci Lett. 1985 Jul 31;58(2):241-4. doi: 10.1016/0304-3940(85)90171-5.
We measured gamma-aminobutyric acid (GABA) and benzodiazepine binding in autopsied frontal cortex of 8 patients dying with dialysis encephalopathy (DE). No alteration in [3H] GABA binding was observed. However, a mild reduction (-23%, P less than 0.05) of [3H] flunitrazepam-binding density was found in DE cortex. The magnitude of this reduction was similar to that observed in frontal cortex of amygdala-kindled rats [10]. We suggest that a reduction in benzodiazepine receptor number, in combination with markedly reduced GABA concentration in DE cerebral cortex may contribute to some of the clinical features (especially seizures) characteristically observed in this syndrome.
我们检测了8例死于透析性脑病（DE）患者尸检额叶皮质中的γ-氨基丁酸（GABA）和苯二氮䓬结合情况。未观察到[³H]GABA结合有改变。然而，在DE皮质中发现[³H]氟硝西泮结合密度轻度降低（-23%，P<0.05）。这种降低的幅度与在杏仁核点燃大鼠的额叶皮质中观察到的相似[10]。我们认为，苯二氮䓬受体数量减少，再加上DE大脑皮质中GABA浓度显著降低，可能导致了该综合征中一些典型的临床特征（尤其是癫痫发作）。
