Davidoff R A, Hackman J C
Neurology. 1978 May;28(5):488-94. doi: 10.1212/wnl.28.5.488.
The superfused in vitro frog spinal cord preparation was used to investigate the effects of pentylenetetrazol (PTZ) on the spinal cord. PTZ depressed monosynaptic, but augmented polysynaptic reflexes, and decreased primary afferent deplorization. Concurrently, in Ringer's solution containing sufficient magnesium or cobalt ions to block synaptic transmission, PTZ antagonized the hyperpolarizing effects on motoneurons and the depolarizing effects on primary afferent fibers of the inhibitory amino acids GABA, beta-alanine, taurine, and glycine. PTZ did not affect responses to the excitatory amino acids glutamic acid and aspartic acid. Furthermore, PTZ did not alter high affinity uptake by cord slices, K+ -evoked release of [3H]GABA from them, or the spinal concentration of GABA. These data suggest that PTZ may produce its excitatory effects by postsynaptic blockade of inhibitory processes mediated by GABA (and possibly by other amino acids).
采用体外灌流的蛙脊髓标本研究戊四氮（PTZ）对脊髓的作用。PTZ抑制单突触反射，但增强多突触反射，并减少初级传入去极化。同时，在含有足够镁离子或钴离子以阻断突触传递的林格氏液中，PTZ拮抗抑制性氨基酸GABA、β-丙氨酸、牛磺酸和甘氨酸对运动神经元的超极化作用以及对初级传入纤维的去极化作用。PTZ不影响对兴奋性氨基酸谷氨酸和天冬氨酸的反应。此外，PTZ不改变脊髓切片的高亲和力摄取、钾离子诱发的[3H]GABA从切片中的释放或脊髓中GABA的浓度。这些数据表明，PTZ可能通过对由GABA（可能还有其他氨基酸）介导的抑制过程进行突触后阻断而产生兴奋作用。
