[Action of benzodiazepines on spinal dorsal root reflex potentials in cats]

Effects of benzodiazepines on spinal reflex potentials, especially on the dorsal root reflex potentials (DRR), were studied in the spinal preparation of cats. All benzodiazepines used in this study (diazepam, chlordiazepoxide, bromazepam, flurazepam, medazepam, nitrazepam, oxazepam, oxazolazepam, lorazepam, estazolam and triazolam) were administered into the duodenum via a rubber tube implanted previously. These drugs consistently increased the amplitude of DRR. Presynaptic inhibition was increased, but postsynaptic inhibition was not affected by the drugs. DRR was decreased gradually by intravenous administration of semicarbazide, and pretreatment with semicarbazide completely blocked the spinal effect of diazepam. Pyridoxine given intravenously recovered the amplitude of DRR and restored the effect of diazepam on the spinal cord. Pretreatment of AOAA potentiated the increasing effect of diazepam on DRR. Occlusion of the thoracic aorta for 47 min with simultaneous clamping of the mammary arteries produced permanent hind-limb rigidity in cats (Murayama-type rigid cats). The ischemic spinal rigidity is characterized by an enhanced monosynaptic reflex and markedly reduced polysynaptic reflex potentials. Furthermore, DRR was not grossly detectable in the preparation. In these ischemic spinal rigid cats, diazepam administered intravenously or intraduodenally did not enhance DRR at all. These results suggest that the effect of diazepam is closely related with GABA content. Normal levels of GABA in the spinal cord are required for the increasing effect of diazepam on DRR and presynaptic inhibition. These benzodiazepines may act on the releasing mechanism of GABA from the spinal interneuron, or they presumably enhance the sensitivity of the GABA receptor in the spinal cord.