The effects of calcium channel blocker, nifedipine on spinal monosynaptic reflexes were investigated in spinal cats. Nifedipine was administrated-locally (10, 50, 100s μmol/l) and intraperitoneally (5; 10, 20 mg/kg). Adult cats (n=10), weighing 1.5-3 kg were anesthetized with ketamine (50 mg/kg, I.M.) and artificially ventilated. Animals were spinalized at C1 level. A laminectomy was performed in the lumbosacral region. The ventral and dorsal roots of segment L5 were isolated and a pouch of skin was formed at the site of the dissection, to allow the exposed tissues to be covered with liquid paraffin, which was kept at 38.5 ± 0.5°C with a heating pad. A polyethylene cannula was introduced into the left carotid artery to monitor blood pressure, which was kept above 100 mmHg. The dorsal root of segment L5 was placed on a silver-silver chloride wire electrode for stimulation through an isolating unit. The reflex potentials were recorded from the ipsilateral L5 ventral root, mounted on a silver-silver chloride wire electrode. Both systemic and local application of nifedipine produced a dose-dependent decrease in the amplitude of the monosynaptic reflexes (p < 0.05). Moreover, the latency of the monosynaptic reflexes was increased after administration of the drug (p < 0.005). These results show the presence of voltage-dependent calcium channels in the spinal cord and these channels may play an important role to regulate reflex respond
