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The effects of central myorelaxants on synaptically‐evoked primary afferent depolarization in the immature rat spinal cord in vitro

1 In the immature rat in vitro hemisected spinal cord preparation the dorsal root‐evoked depolarizing potential recorded from an adjacent dorsal root DR‐DRP had a mean peak amplitude (± s.e.mean, n = 27) of 2.9 ± 0.2 mV and a mean latency to peak amplitude of 106 ± 3 ms. The DR‐DRP amplitude was maximal with a stimulus intensity of four times the threshold intensity required to activate the lowest threshold fibres. The peak amplitude and/or integral over a time‐source of 0.5 s were used to assess the effects of applied drugs. 2 The DR‐DRP was abolished by baclofen (mean IC50 190 ± 46 nm, n = 7). The depressant effect of baclofen was reversed by CGP35348 (1 mm). The mean apparent Kd value calculated from dose‐ratios was 16.7 ± 6.4 μm (n = 3). 3 At a maximally effective concentration, tizanidine (1 μm) produced at the most only a 14% depression of the DR‐DRP (n = 4). Clonidine (0.3 μm) had an effect similar to that of tizanidine. These depressant effects were reversed by idazoxan (1 μm). 4 The DR‐DRP was potentiated by diazepam in a flumazenil (1 μm)‐reversible manner. A maximal potentiation of 23.2 ± 2.7% (n = 5) was produced by 1 μm diazepam. 5 Diazepam (1 μm) induced a mean bicuculline‐ (10 μm, n = 2) and flumazenil‐ (1 μm, n = 8) sensitive depolarization in the dorsal root of 0.25 ± 0.03 mV (n = 8). However, diazepam failed to depolarize dorsal roots (n = 3) which had been excised from the spinal cord. 6 Comparison of the above effects with previously reported depressant effects of these drugs on the synaptic output from ventral roots suggests that actions on presynaptic inhibition, as reflected in the DR‐DRP, are of subsidiary importance in explaining the muscle relaxant actions of tizanidine or diazepam.