GABAB receptors modulate glycinergic inhibition and spike threshold in Xenopus embryo spinal neurones.

1. The actions of GABAB receptors in the generation of the neuronal pattern underlying swimming in the Xenopus embryo have been investigated using the agonist baclofen. 2. Baclofen (10-100 microM) greatly reduced the length of swimming episodes and ventral root spike amplitude in a reversible manner. These effects were blocked by CGP 35348 (200-300 microm) and hydroxysaclofen (200-300 microM). 3. Baclofen (10-100 microM) reduced the amplitude of glycinergic IPSPs in motoneurones during fictive swimming. 4. Strychnine-sensitive spontaneous miniature inhibitory postsynaptic potentials (mIPSPs) were recorded from motoneurones. While baclofen (10-100 microM) had no effect on the amplitude of the mIPSPs it greatly decreased their frequency of occurrence. 5. GABAB receptors may therefore be present on the terminals of commissural interneurones, the only glycinergic neurones in the Xenopus embryo's nervous system, and act to reduce neurotransmitter release. 6. Baclofen reduced the reliability of action potential firing in motoneurones during fictive swimming without an apparent effect on excitation. 7. Baclofen increased the threshold to action potential firing in response to the injection of depolarizing current in motoneurones. 8. The current-voltage relationships of motoneurones were investigated. Baclofen (10-100 microM) did not change the resting membrane potential, slope conductance or the membrane rectification.