Robin M M, Palfreyman M G
Neuropharmacology. 1982 May;21(5):479-82. doi: 10.1016/0028-3908(82)90035-1.
Unilateral application of gamma-aminobutyric acid (GABA) antagonists on the motor cortex of conscious rats produces myoclonic movements. Paradoxically, the same behaviour can be observed with high concentrations of some GABA-transaminase (GABA-T) inhibitors. Since the GABA conjugate homocarnosine is increased in the brain following GABA-T inhibition and since homocarnosine is known to displace [3H]-GABA from its binding sites at high concentration, we investigated whether homocarnosine might explain the dyskinetic movements produced by these GABA-T inhibitors. We found that homocarnosine produces dyskinesia similar to that observed with GABA antagonists and GABA-T inhibitors when applied directly to the cortex. However, this property of homocarnosine is unlikely to be the basis of the dyskinetic effect of GABA-T inhibitors since we found no relationship between brain homocarnosine levels and the appearance of abnormal movements following GABA-T inhibition.
在清醒大鼠的运动皮层单侧应用γ-氨基丁酸（GABA）拮抗剂会产生肌阵挛运动。矛盾的是，高浓度的一些GABA转氨酶（GABA-T）抑制剂也能观察到同样的行为。由于GABA-T抑制后大脑中GABA共轭物高肌肽增加，且已知高肌肽在高浓度时会从其结合位点置换[3H]-GABA，我们研究了高肌肽是否可以解释这些GABA-T抑制剂产生的运动障碍。我们发现，直接应用于皮层时，高肌肽产生的运动障碍与GABA拮抗剂和GABA-T抑制剂所观察到的相似。然而，高肌肽的这一特性不太可能是GABA-T抑制剂运动障碍效应的基础，因为我们发现大脑高肌肽水平与GABA-T抑制后异常运动的出现之间没有关系。
