The primary mode of action of local anesthetics is through sodium channel and axonal conduction blockade. Local anesthetics have also extensive effects on pre-synaptic calcium channels that must function to stimulate the release of neurotransmitters. Thus, interference with calcium channel conductance may enhance spinal anesthesia with local anesthetics. The present study was designed to investigate the effect of the intrathecal calcium channel blocker, nifedipine, or GABAB agonist, Baclofen, which is a blocker of pre-synaptic calcium channels on the spinal anesthesia induced by lidocaine. Male Sprague-Dawley rats were chronically implanted with lumbar intrathecal catheters. Tail-flick (TF) test was used to assess thermal nociceptive threshold, motor functions were assessed using a modified langerman’s scale. Intrathecal lidocaine alone showed the prolongation of (TF) latency, and the increase in motor function scale in a time-and dose-dependent manner. But intrathecal nifedipine (50-200 ?g), or baclofen (10, and 20 ?g) alone demonstrated neither sensory nor motor block. The combination of lidocaine (10, 20, 50, 100, and 200 ?g, i.t.) and nifedipine (50 ?g, i.t.) or baclofen (10 ?g, i.t.) produced more potent and prolonged antinociception and motor block when compared with local anesthetics alone. We interpreted these results to indicate that the intrathecal calcium channel blocker, nifedipine, or GABAB agonist, baclofen, potentiate anesthesia with local anesthetics.