• baclofen;
  • locomotion;
  • presynaptic inhibition


The in vitro newborn rat isolated brain stem/spinal cord preparation was used to study the involvement of presynaptic inhibition in the control of the synaptic locomotor drive. The recording chamber was partitioned with Vaseline walls to separate the L1–L2 locomotor network from the motoneurons in the lower segments. When locomotor like activity was induced by bath applying a mixture of N-methyl-d-l-aspartate and serotonin to the L1–L2 segments, intracellular recordings of L3–L5 motoneurons show an alternating pattern of monosynaptic excitatory glutamatergic and inhibitory glycinergic inputs known as the locomotor drive. Gamma-aminobutyric acid (GABA), baclofen and muscimol (respectively GABAB and GABAA agonists) superfused on the L3–L5 segments depressed the synaptic locomotor drive of motoneurons during the ongoing activity. On the contrary, the GABAB receptor antagonist CGP35348 enhanced the locomotor drive, which suggests that an endogenous release of GABA occurs during locomotor-like activity. Baclofen, unlike muscimol and GABA, did not affect the passive membrane properties and the firing discharge of synaptically isolated motoneurons. Baclofen and muscimol acted on the two phases (inhibitory and excitatory) of the synaptic drive. The effects of GABAergic agonists on the whole locomotor activity were tested. When superfused on the L3–L5 part of the cord, they affected only the L5 burst amplitude. When bath-applied to the L1–L2 network, GABA and muscimol decreased the amplitude of the L2 and L5 bursts and increased the locomotor period while baclofen had significant effects only on the period. It was concluded that GABA modulates the information conveyed by the L1–L2 network to its target motoneurons presynaptically via GABAB and possibly GABAA receptors and postsynaptically, via GABAA receptors.